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THE 

DIAGNOSTICS  OF 
INTERNAL  MEDICINE 


A  CLINICAL  TREATISE  UPON  THE  RECOGNISED 

PRINCIPLES  OF  MEDICAL  DIAGNOSIS, 

PREPARED   FOR    THE  USE  OF 

STUDENTS  AND  PRACTITIONERS  OF  MEDICINE 


GLENTVVORTH   REEVE   BUTLER,   A.M.,  M.  D. 

Chief  of  the  Second   Medical    Division,   Methodist   Episcopal    Hospital ; 

Attending  Physician  to  the  Brooklyn  Hospital ;  Consulting  Physician 

to  the  Bushwick  Central  Hospital ;  formerly  Associate  Physician, 

Departments  of  Diseases  of  the  Chest  and  Diseases  of  Children, 

St.  Mary's  Hospital,  Brooklyn,  N.  Y.  ;  Fellow  of  the  New 

York  Academy  of  Medicine  ;  Member  of  the  Medical 

Society  of  the  County  of  Kings,  etc. 


IV/T//  FIVE  COLOURED  PLATES  AND  TWO  LLUNDRED  AND 
FORTY-SIX  ILLUSTRATIONS  AND    CHARTS  IN   THE    TEXT 


NEW    YORK 

D.    APPLETON     AND     COMPANY 

1902 


Copyright,  1901, 
By  D.   APPLETON  AND  COMPANY 


PREFACE 


This  book  has  been  written  from  the  point  of  view  of  practical 
clinical  work.  The  physician  meets  primarily  symptoms  and  signs 
— the  evidences  of  disease ;  subsequently  it  is  decided  that  the 
symptoms  found  indicate  the  presence  of  a  specific  ailment.  This 
volume,  therefore,  naturally  divides  itself  into  two  parts :  first,  a 
study  of  spnptoms  and  their  indications ;  and,  second,  a  study  of 
diseases  and  their  characteristics. 

Part  I — The  Evidences  of  Disease — comprises :  (1)  A  brief  con- 
sideration of  the  clinical  anatomy  and  physiology  of  certain  organs 
and  systems ;  practical  points  of  everyday  utility.  (2)  A  description 
of  the  approved  methods  of  examination.  It  has  been  well  said  by 
a  capable  reviewer  that  "the  basis  of  the  art  of  diagnosis  is  a 
thorough  knowledge  of  clinical  methods."  (3)  A  careful  considera- 
tion of  the  many  signs  and  symptoms  encountered  in  the  practice  of 
internal  medicine.  (4)  A  statement  of  the  diagnostic  significance 
of  each  sign  and  symptom — i.  e.,  the  disease  or  diseases,  the  pres- 
ence of  which  is  more  or  less  strongly  suggested  by  the  finding  of  a 
given  sign  or  symptom.  While  a  prominent  symptom  seldom  leads 
directly  to  the  discovery  of  a  disease,  yet  it  is  of  importance  to 
know  the  diagnostic  value  of  individual  symptoms. 

Part  II — Diagnosis,  Direct  and  Differential — contains  :  (1)  Suc- 
cinct descriptions  of  recognised  diseases  and  their  symptoms,  with 
(2)  special  reference  to  the  diagnosis,  direct  and  differential,  of  each 
disease.  The  qualifying  terms  applied  to  diagnosis  are  scientifically 
indefensible,  but  clinically  useful. 

The  two  parts  are,  indeed,  complementary.  For  example,  if  in 
Part  I  it  is  stated  that  the  finding  of  a  persistently  rapid  pulse  may 
be  explained  by  the  presence  of  exophthalmic  goitre ;  or  of  a  dry 
tongue  and  an  inordinate  thirst,  by  diabetes,  one  can  turn  to  Part  II 
and  compare  his  case  with  the  symptom-group  of  the  disease  in 
question.  Conversely,  when  in  Part  II  a  high-tension  pulse  is 
mentioned  as  a  symptom  of  angina  pectoris,  or  Kernig's  sign  of 
meningitis,  a  reference  to  Part  I  will  discover  the  method  of  esti- 
mating high  tension  or  of  eliciting  Kernig's  sign. 


iv  PEEFACE 

It  is  hoped  that,  owing  to  its  choice  of  material  and  method  of 
arrangement,  the  book  contains  between  two  covers  practically  all 
that  is  essential  for  the  making  of  a  diagnosis,  and  that  no  helpful 
clew  in  obscure  cases  has  been  overlooked.  The  value  of  modern 
laboratory  methods  has  been  fully  appreciated ;  so  also  has  the 
importance  of  symptoms,  subjective  and  objective. 

Xo  one  can  write  upon  the  subject  of  this  book  without  lying 
under  obligations  for  the  major  portion  of  his  material  to  the  Mas- 
ters of  Internal  Medicine,  but,  as  space  forbids  detailed  references, 
this  brief  acknowledgment  must  stand  as  a  very  inadequate  voucher 
for  a  heavy  debt.  Everything,  indeed,  has  been  subordinated  to  tlie 
main  purpose  of  the  book,  which  is  to  facilitate  in  a  practical  way 
the  making  of  a  thorough  examination  and  a  correct  diagnosis.  It 
is  believed  that  the  Synopsis  of  Examinations,  which  immediately 
precedes  the  body  of  the  book,  will  be  found  useful. 

Special  care  has  been  taken  to  secure  clearness  of  arrangement 
by  the  liberal  use  of  italics  and  bold-face  type  to  catch  the  eye ;  and 
to  promote  ease  of  reference  by  varying  the  odd-page  headings,  as 
well  as  by  the  provision  of  an  ample,  but  not  too  bulky,  index. 

Plates  III  and  IV  are  composed  of  selections  reproduced  (with 
the  kind  permission  of  the  authors  and  publishers)  from  the  excel- 
lent illustrations  in  Cabot's  Examination  of  the  Blood  and  Simon's 
Clinical  Diagnosis,  mainly  from  the  former ;  Plate  V  of  similar 
selections  from  Thayer's  fine  drawings  of  the  malarial  parasite.  A 
large  proportion  of  the  illustrations  are  either  original  or  redrawn, 
without,  it  is  believed,  sacrificing  utility  for  originality.  Mr. 
Howard  J.  Shannon  has  put  my  rough  sketches  into  workmanlike 
and,  so  far  as  compatible  with  the  subject,  artistic  form.  For  his 
aid  I  am  indebted  to  the  liberality  of  the  publishers,  Avhose  imprint 
is  a  guarantee  of  good  work  and  good  material. 

The  bulk  of  the  volume  (pages  1  to  908)  is  from  my  own  pen. 
Of  the  remainder.  Dr.  Frank  W.  Shaw,  my  associate  at  the  Metho- 
dist Episcopal  Hospital,  has  prepared  the  sections  on  Parasites  and 
the  Intoxications ;  Dr.  Henry  G.  Webster,  my  associate  at  the 
Brooklyn  Hospital,  those  on  Diseases  of  the  Kidney  and  Constitu- 
tional Diseases ;  Dr.  Henry  P.  De  Forest,  of  Brooklyn,  that  on  Dis- 
eases of  the  Blood  and  Ductless  Glands ;  and  Dr.  Smith  Ely  Jelliffe 
and  Dr.  A.  B.  Bonar,  of  Manhattan,  that  upon  Diseases  of  the  Xer- 
vous  System — assistance  kindly  given  and  gratefully  received.     Dr. 

J.  P.  Warbasse  has  made  valuable  criticisms. 

G.  K.  B. 

229  Gates  Avexue.  BoRouon  of  Brooklyn, 
City  of  New  York. 


CONTENTS 


Schedule  of  Examinatioxs 
Preliminary  Considerations 
Diagnosis 
Difficulties  in 
Obtaining  evidence 
Keeping  case  histories 


PAGK 

xiz 
1 
1 
3 
5 
6 


PART  I 

THE  EVIDENCES  OF  DISEASE 

Section  I.    Considerations  which  may  suggest  or  qualify  a  Diagnosis    .        .  13 

Family  history 13 

Age 15 

Sex 16 

Nationality 17 

Occupation 18 

Residence 19 

Habits 20 

Previous  diseases 20 

Section  II.     History  of  Present  Illness 23 

Section  III.    Diagnostic  Indications  from  the  General  Appearance       .        .  24 

Dress  and  behaviour 24 

Height  and  weight 25 

Amount  and  character  of  adipose  and  muscular  tissue       ....  26 

Conformation  of  body 27 

Diatheses  and  cachexias 28 

Section  IV.     Posture  in  Bed — Mode  of  Moving — Gait — Station      ...  30 

Section  V.    Pain 35 

Tenderness 52 

Parfesthesias 54 

Section  VI.    Vertigo 58 

Section  VII.     Temperament — Psychical  Condition — Insomnia       ...  60 

Section  VIII.     Disturbances  of  Consciousness 66 

Diagnostic  significance  of  coma 66 

Diagnosis  of  the  varieties  of  coma 67 

Section  IX.     General  Convulsions 71 

Section  X.     Cutaneous  Surface 75 

Colour  of  skin        . 75 

Heat  of  skin 81 

V 


vi  CONTENTS 

PAOB 

Moisture  of  skin 83 

Rash  or  eruption 83 

Cicatrices 86 

Dropsy,  oedema,  anasarca 87 

Condition  of  veins 91 

Emphysema  of  skin 92 

Condition  of  joints 93 

Section  XI.    The  Temperature  of  the  Body 95 

Fever 100 

Terminology  of 102 

Diagnostic  classification  of 106 

Chills Ill 

Section  XII.    General  Diagnostic  Evidence  from  the  Digestive  and  Genito- 
urinary Systems 112 

Appetite 112 

Thirst 113 

Vomiting  and  gross  character  of  the  vomitus 113 

Indications  from  presence  of  vomiting 116 

Indications  from  macroscopic  character  of  vomitus        ....  122 

Defecation  and  gross  character  of  the  stools 125 

Constipation 126 

Diarrhoea 128 

FjEcal  incontinence            130 

Painful  defecation 130 

Rectal  tenesmus 132 

Character  and  abnormal  contents  of  stools 132 

Urination 139 

Symptoms  belonging  to  the  genitalia  .        .        .        .        .        .        .        .  144 

Males 144 

Females 146 

Section  XIII.  Symptom  Groups  of  Clinical  Significance 149 

Coma :  Dyspnoea :  Fever 149 

Hyperpyrexia :  Internal  hemorrhage 150 

Shock  or  collapse 151 

Syncope :  Weakness  or  debility 152 

Irritant  poisoning :  Jaundice :  Obstructed  portal  circulation :  Suppura- 
tive or  hectic  fever :  Pyaemia :  Tympanites :  Typhoid  status  .        .  153 

Section  XIV.    Head  and  Face 154 

Size  and  contour 154 

Fontanels  and  sutures 158 

Cranial  bones 160 

The  fa«ies  of  disease 160 

Colour  of  the  face 163 

Skin  of  the  face 164 

The  hair 165 

CEdema  or  swellings  of  the  face 166 

Abnormal  movements  of  the  head 166 

Abnormal  fixity  of  the  head 167 

Facial  spasm 167 

Facial  spasm 169 


CONTENTS  vii 

PAGE 

Section  XV.    The  Ear 175 

Section  XVI.    The  Eye 180 

The  eyelid 180 

The  conjunctiva,  sclerotic,  and  cornea 183 

The  pupil 185 

The  eyeball .  190 

Vision .        .        .        ,202 

Section  XVII.    The  Nose 211 

Section  XVIII.    The  Mouth 218 

Lips 218 

Buccal  cavity 219 

Gums 222 

•    Teeth 223 

Tongue 225 

Section  XIX.    The  Palate,  Tonsils,  and  Pharynx 233 

Section  XX.    Dysphagia 237 

Section  XXI.    Examination  of  Larynx 238 

Laryngeal  paralysis 240 

Section  XXII.     Voice  and  Speech 243 

Aphasia 246 

Section  XXIII.    Cough 256 

Section  XXIV.    Sputum  and  its  Gross  Characters 259 

Section  XXV.    The  Neck 263 

Section  XXVI.  The  Extremities 271 

Nails 271 

Hand  and  fingers 272 

Arm 278 

Foot  and  leg 279 

Section  XXVII.    The  Back 284 

Section  XXVIII.    Theory  and  Practice  of  Palpation,  Auscultation,  and  Per- 
cussion           286 

Section  XXIX.    The  Chest  (Thorax) 296 

Section  XXX.  Anatomical   Landmarks  and  Topographical    Areas  of   the 

Thorax 304 

Section  XXXI.  Examination  of  the  Circulatory  System 308 

Pathological  physiology  of  valvular  defects 312 

Topographical  anatomy  of  the  heart  and  its  valves 318 

Physical  examination  of  the  heart  and  its  neighbourhood ....  321 

Inspection  and  palpation 321 

Percussion  of  the  heart 330 

Auscultation  of  the  heart 339 

Endocardial  sounds  (murmurs) 347 

Exocardial  sounds 360 

Physical  examination  of  the  blood  vessels  (including  the  pulse)        .        .  363 

The  pulse 367 

The  sphygmograph 378 

Section  XXXII.    Examination  of  the  Lungs  and  Pleurae        ....  382 

Topographical  anatomy 382 

Physiology  of  the  lungs 384 

Inspection  and  palpation  with  reference  to  the  lungs         ....  386 


viii  CONTENTS 

FA6B 

Percussion  of  the  lungs 396 

Technic 396 

Results  of  percussion  in  normal  lungs 398 

Results  of  percussion  in  disease  of  lungs  or  pleurae,  or  of  neighbouring 

organs 399 

Auscultation  of  lungs   .      " 409 

Technic 409 

Varieties  and  characteristics  of  the  normal  breath  sounds      .        .        .  410 

The  breath  sounds  in  disease 413 

The  voice  sounds  in  health  and  disease 417 

Adventitious  sounds  or  accompaniments 418 

Section  XXXIII.     The  Abdomen.     Methods  and  Results  of  its  General  Ex- 
amination      423 

Topographical  marks,  areas,  and  anatomy  of  the  abdomen        .        .        .  423 

Methods  and  general  results  of  abdominal  inspection         ....  427 

Methods  and  results  of  general  abdominal  palpation  and  percussion         .  430 

Section  XXXIV.    Examination  of  the  Digestive  System         ....  444 

The  esophagus 445 

The  stomach 447 

Anatomy  and  surface  relations         . 447 

Physical  examination 448 

Interpretation   of  the  results  of    the    physical  examination  of  the 

stomach 455 

Intestines  and  peritoneum 456 

Topographical  anatomy  of  intestines        . 456 

Examination  of  intestines 457 

The  liver  and  gall  bladder 461 

Topographical  anatomy  of  liver 461 

Physical  examination  of  liver  and  gall  bladder 463 

Diagnostic  results  of  physical  examination  of  liver  and   gall  blad- 
der         467 

The  pancreas 470 

Section  XXXV.    Examination  of  the  Spleen 471 

Topographical  anatomy 471 

Physical  examination 471 

Results  of  examination 474 

Section  XXXVI.     Examination  of  Kidneys,  Ureters,  and  Bladder         .        .  475 

Kidneys 475 

Topographical  anatomy 475 

Physical  examination 476 

Diagnostic  results  of  physical  examination 479 

Bladder  and  ureters 480 

Section  XXXVII.     Examination  of  the  Nervous  System         ....  481 

Physiological  and  anatomical  data 481 

Degeneracy 507 

Examination  of  the  muscles  with  reference  to  their  nutrition,  tone,  and 

motor  power 509 

Motor  disturbances    , 514 

Spasm 514 

Paralysis 520 


CONTENTS  ix 

PAOK 

Sensory  disturbances 527 

Methods  of  examination 528 

Diagnostic  significance  of 531 

The  reflexes 536 

Superficial 536 

Deep 537 

Electro-diagnosis  (nerve  and  muscle) 542 

Apparatus  and  technic 542 

Diagnostic  indications  from 547 

Vasomotor  and  trophic  disturbances 549 

Cranial  nerve  functions 550 

Cerebral  localization .  553 

Summary  of  diagnostic  points 555 

Section  XXXVIII.     Examination  of  the  Blood 559 

Technic  of  clinical  examination  of  the  blood 559 

Counting  red  cells 559 

Counting  white  cells 564 

Estimating  the  haemoglobin 567 

Microscopical  examination  of  the  blood 571 

Order  of  procedure  in  the  clinical  examination  of  the  blood  .        .        .  574 
The  results  and  diagnostic  significance  of  the  clinical  examination  of 

normal  and  abnormal  blood 575 

The  red  cells 576 

The  leucocytes 579 

Blood  plates  and  Miiller's  blood  dust 587 

Parasites  in  the  blood 587 

Plasmodium  malaricB 587 

SpirochcBtm  of  relapsing  fever  .        .        . 591 

Filaria  homiiiis  sanguinis 591 

Serum  test  (Widal)  for  typhoid  fever 592 

Blood  tests  for  diabetes 593 

Iodine  reaction  in  suppuration 594 

Results  of  hi-emanalysis  in  special  diseases 595 

Sectiox  XXXIX.     Microscopical  Examination  of  the  Sputum         .        .        .  596 

Section  XL.    Examination  of  the  Stomach  Contents 604 

Physiology  of  digestion 604 

The  chemical  examination  of  the  stomach  contents,  and  the  determi- 
nation of  the  motor  power  of  the  stomach 604 

Test  meals 605 

The  chemical  tests  and  their  technic 606 

Testing  the  motor  power  of  the  stomach 612 

The  microscopic  examination  of  the  stomach  contents   ....  613 

Diagnostic  value  of  an  examination  of  the  stomach  contents     .        .        .  614 

Section  XLI.     Microscopical  Examination  of  the  Fa?ces 618 

Section  XLII.     Diagnostic  Inferences  from  the  Results  of  Urinalysis    .        .  621 
Evidence  from  physical  examination  of  urine  (quantity,  colour,  odour, 

consistence,  specific  gravity,  deposits,  etc.) 621 

Evidence    from    chemical    examination  of    urine  (reaction,    chlorides, 
phosphates,  oxalates,  sulphates,  indican.  urea,  uric  acid,  albumin, 

blood  and  its  compounds,  the  diazo-reaction,  etc.)    ....  626 


X  CONTENTS 

PAGE 

Evidence  from  microscopical  examination  of  urine  (fat,  pus,  red  cells, 

epithelial  cells,  tube  casts,  etc.) 639 

Collective  results  of  urinalysis  in  special  diseases  and  conditions      .        .  645 

Section  XLIII.    Diagnostic  Puncture  and  the  Evidence  derived  therefrom  .  648 

Technic  of  puncture 648 

Examination  of  fluid 649 

Characters  of  the  fluid  according  to  its  source 650 

Section  XLIV.    The  Uses  of  the  Rontgen  Light  in  Medical  Diagnosis  .        .  654 

PAET  II 
DIAGNOSIS,  DIRECT  AND  DIFFERENTIAL 

SECTION  I. — Infectious  Diseases 

Typhoid  fever 655 

Typhus  fever        .        .        .        .        . 668 

Relapsing  fever 670 

Dengue 671 

Cerebro-spinal  meningitis 672 

Influenza 675 

Whooping  cough 677 

Epidemic  parotitis  (mumps)         . 678 

Smallpox  (variola) .        .        .        .        .        .  679 

Vaccinia  (cowpox) 683 

Varicella  (chicken  pox) 683 

Dysentery 700 

Cholera  Asiatica 703 

Bubonic  plague 705 

Malarial  fever 705 

Rheumatic  fever 710 

Lobar  pneumonia 712 

Tuberculosis 723 

Syphilis 737 

Gonorrhoeal  rheumatism 742 

Anthrax 743 

Glanders  (farcy) 744 

Scarlet  fever  (scarlatina) 684 

Measles  (rubeola) 688 

Rubella  (rotheln) 689 

Diphtheria 690 

Erysipelas 693 

Toxajmia,  septicaemia,  pyaemia 694 

Yellow  fever .699 

Actinomycosis 745 

Leprosy 745 

Tetanus 746 

Hydrophobia 747 

Beri-beri 748 

Mountain  fever  and  sickness 749 

Ephemeral  fever — febrieula 749 


CONTENTS  xi 
SECTION  II, — Diseases  of  the  Digestive  System 

PAGE 

Diseases  of  the  mouth 750 

Diseases  of  the  tongue 752 

Diseases  of  the  salivary  glands 753 

Diseases  of  the  pharynx 753 

Diseases  of  the  tonsils 755 

Diseases  of  the  esophagus 757 

Diseases  of  the  stomach 760 

Diseases  of  the  intestines 776 

Diseases  of  the  liver,  gall  bladder,  and  bile  ducts 800 

Diseases  of  the  pancreas 816 

Diseases  of  the  peritoneum 820 

SECTION  III. — Diseases  of  the  Respiratory  System 

Diseases  of  the  nose 828 

Diseases  of  the  larynx 830 

Diseases  of  the  bronchi 833 

Diseases  of  the  lungs 841 

Diseases  of  the  pleura  (and  mediastinum) 856 

SECTION  IV. — Diseases  of  the  Circulatory  System 

Diseases  of  the  pericardium 870 

Diseases  of  the  heart 875 

Diseases  of  the  arteries 900 

SECTION  V. — Diseases  of  the  Blood  and  Ductless  Glands 

Anaemia 908 

Leucjemia 911 

Pseudo- leucaemia 913 

Purpura 916 

Hi-emophilia 918 

Scurvy 918 

Addison's  disease 922 

Diseases  of  the  spleen 923 

Diseases  of  the  thyroid  gland 925 

Diseases  of  the  thymus  gland 929 

SECTION  VI.— Diseases  of  the  Kidney 

Movable  kidney 929 

Renal  congestion 930 

Uriemia 930 

Acute  Bright's  disease 932 

Chronic  Bright's  disease 933 

Amyloid  kidney 935 

Pyelitis 936 

Hydronephrosis 937 

Nephrolithiasis 938 

Tumours  of  the  kidney 939 

Cysts  of  the  kidney 940 

Perinephritic  abscess 941 


xii  CONTENTS 

SECTION  VII.— Diseases  of  the  Nervous  System 

The  neuroses:  Diseases  of  undetermined  pathogeny.  pjiok 

A.  Sensori-motor  neuroses 942 

B.  Motor  neuroses 950 

C.  Trophoneuroses 956 

Diseases  of  the  peripheral  nervous  system. 

A.  Diseases  of  the  peripheral  sensory  neurones 958 

B.  Diseases  of  the  peripheral  motor  neurones 963 

Diseases  of  the  spinal  cord  and  bulb 972 

Systemic  cord  diseases 985 

Inflammation  of  the  spinal  meninges 990 

Inflammation  of  the  membranes  of  the  brain 992 

Diseases  of  the  cerebral  substance 994 

Syphilis  of  the  nervous  system 1004 

SECTION  VIII.— Diseases  of  the  Muscles 

Myositis 1005 

Myotonia .  1007 

Myoclonia 1007 

SECTION  IX.— Constitutional  Diseases 

Chronic  rheumatism 1007 

Muscular  rheumatism 1008 

Diabetes  insipidus 100& 

Diabetes  mellitus  . 1009 

Gout 1010 

Arthritis  deformans 1012 

Rickets 1014 

Obesity 1015 

SECTION  X. — The  Intoxications:  Sunstroke 

Alcoholism 1016- 

Morphinism 1018 

Acute  opium-poisoning .  1018- 

Lead-poisoning 1019- 

Arsenical-poisoning 1023 

Food-poisoning 10t2i) 

Sunstroke 1025 

SECTION  XI. — Diseases  due  to  Animal  Parasites 

Distomiasis 1027 

Nematodes 1027 

Cestodes 1020 

Parasitic  arachnida 103^ 

Parasitic  insects 103$ 


PLATES,   CHARTS,   AND  ILLUSTRATIONS 


PLATE 

L 


II. 


III. 
IV. 
V. 


I. 
II. 

III. 

IV. 

V. 

VI. 

VII. 

VIII. 

IX. 

X. 

XI. 

XII. 

XIII. 

XIV. 

XV. 

XVI. 

XVII. 

XVIII. 

XIX. 

XX. 

XXI. 

XXII. 


FACING 
PAOE 

The  Shape  and  Relations  of  the  Thoracic  and  Abdominal  Vis- 
cera, Anterior  Aspect  (Semi-diagrammatic) .             ...  1 
The  Shape  and  Relations  of  the  Thoracic  and  Abdominal  Vis- 
cera, Posterior  Aspect  (Semi-diagrammatic)     ....  1 

Red  Corpuscles,  Normal  and  Abnormal 578 

The  varieties  of  Leucocytes 582 

The    Plasmodium    Malaria,    selected    and    reproduced    from 

Thayer's  Plates 588 

PAGE 

Abortive  pneumonia      .        .        .        . 97     < 

Types  of  fever.    Continued,  remittent ;  quotidian  and  tertian  types 

of  intermittent .        .        .        .  103 

Types  of  fever.    Intermittent,  quartan  type ;  suppurative  and  hectic 

fev«r 103 

Diagnostic  indications  from  a  sudden  invasion  of  fever.    No.  1 .        .  106 

Diagnostic  significance  of  a  gradual  rise  of  temperature      .        .        .  107 

Diagnostic  significance  of  a  gradual  termination  of  fever  .        .        .  107 

Diagnostic  indications  from  a  sudden  invasion  of  fever.    No.  2.        .  108 

Diagnostic  indications  from  a  sudden  fall  of  temperature  .        .        .  109 

Blood  chart  and  hsemanalysis  card  for  recording  examinations  .        .  560 
Typhoid  fever.     Showing  typical  temperature  curve  and  prominent 

symptoms  . <557 

Typhoid  fever.     Fatal  hemorrhage 662 

Typhoid  fever.     Bathing  chart.     Recovery 663 

Typhus  fever 669 

Relapsing  fever 670 

Smallpox 679 

Varioloid 681 

Varicella 683 

Scarlet  fever 685 

Measles 688 

Pyiemia,  post-operative,  with  pulmonary  gangrene     ....  697 

liObar  pneumonia.     Pulse,  respiration,  and  temperature    .        .        .  712 

Broncho-pneumonia 845 

xiii 


xiv  PLATES,  CHARTS,  AND  ILLUSTRATIONS 

FIGURB  PAOB 

1.  Example  of  a  case-history  card — cardiac 7 

2.  Example  of  a  case-history  card — gyna;cological 8 

3.  Box  for  keeping  history  cards 9 

4.  Card  for  recording  urinalysis 10 

5.  Showing  the  location  of  transferred  pains 39 

6.  Showing  the  location  of  transferred  pains 41 

7.  General  indications  from  seat  of  pain  in  head  and  face     ....  42 

8.  Causes  of  localized  headache  according  to  its  site 43 

9.  Causes  of  localized  headache  according  to  its  site 44 

10.  Showing  the  causes  of  pain  in  the  trunk  and  extremities,  according  to 

its  locality 45 

11.  The  same 46 

12.  The  same 47 

13.  The  same 48 

14.  The  same      . .        .49 

15.  The  same 50 

16.  The  same 51 

17.  Diagram  of  vomiting  centre  in  medulla 115 

18.  Congenital  hydrocephalus 155 

19.  Rachitic  head 155 

20.  Sporadic  cretinism 156 

21.  Face  of  acromegaly 157 

22.  Face  of  myxcedema 157 

23.  Facial  hemiatrophy 158 

24.  Leontiasis  ossea 159 

25.  Leontiasis  ossea 159 

26.  Varieties  and  causes  of  facial  paralysis 170 

27.  Base  of  the  brain 172 

28.  Base  of  the  skull  and  exits  of  nerves 173 

29.  Communications  between  superior  longitudinal  and  external  sinuses  and 

external  veins 181 

30.  Communications  between  lateral  and  cavernous  sinuses  and  external  veins  182 

31.  Nervous  mechanism  of  the  iris 187 

32.  Showing  ocular  muscles  and  their  innervation 196 

33.  Structures  in  right  cavernous  sinus 200 

34.  Showing  optic  tracts,  visual  fields,  and  causes  of  hemiopia       .        .        .  204 

35.  Visual  colour  field,  right  eye 207 

36.  lihinoscopic  view  of  posterior  nares 213 

37.  Syphilitic  "screw-driver"  teeth 224 

38.  L^nilateral  atrophy  of  tongue 226 

39.  Showing  motor  and  sensory  supply  of  tongue 227 

40.  View  of  normal  larynx  in  mirror 239 

41.  Showing  paralyses  of  the  vocal  cords 241 

42.  Showing  localization  of  cerebral  motor  and  sensory  functions,  outer  sur- 

face, left  hemisphere  .        .        . 249 

43.  Showing  principal  convolutions  and  fissures,  outer  surface,  left  hemisphere  249 

44.  Showing  functions,  convolutions,  and  fissures,  inner  aspect,  right  hem- 

isphere          250 

45.  Showing  association  tracts,  left  hemisphere 251 

46.  Gland  groups  of  head  and  neck 266 


PLATES,  CHARTS,  AND  ILLUSTRATIONS 


xr 


FIGURE  PAGK 

47.  Diagram  of  right  external  and  internal  jugulars 268 

48.  Diagram  showing  systolic  and  presystolic  jugular  pulse   ....  270 

49.  Normal  hand  (cast  drawing) 273 

50.  Spade  hand 27a 

51.  Claw  hand 27S 

52.  Morvan's  disease 274 

53.  Hand  of  pulmonary  osteo-arthropathy 275 

54.  Skiagraph  of  hand  in  Fig.  53 275 

55.  Hands  of  arthritis  deformans 276 

56.  Hand  showing  Heberden's  nodes 277 

57.  Skiagraph  of  hand  in  Fig.  56 277 

58.  Gland  groups  in  groin 270 

59.  Sabre-shaped  tibia 280 

60.  Pesequinus 282 

61.  Pes  varus 283 

62.  Pes  calcaneus 283 

63.  Paralysis  of  serratus  magnus 285 

64.  Diagram — varying  force  of  percussion 291 

65.  Diagram — auscultatory  percussion 292 

66.  Diagram — lines  of  percussion 292 

67.  Section  of  emphysematous  chest 290 

68.  Sections  of  healthy  and  rachitic  chests 300 

69.  Section  of  unilaterally  contracted  chest 302 

70.  Section  of  scoliotic  chest 302 

71.  Topographical  areas  of  thorax,  anterior  aspect 306 

72.  Topographical  areas  of  trunk,  posterior  aspect 307 

73.  Showing  events  of  cardiac  cycle  and  sounds  of  heart        ....  309 

74.  Nervous  mechanism  of  the  heart 310 

75.  Diagram  explanatory  of  ai'terial  tension 311 

76.  Showing  vasomotor  nervous  mechanism 312 

77.  Semi-diagrammatic  section  of  heart 313 

78.  Diagram  showing  insuflBciency  and  stenosis 314 

79.  Showing  indirect  effects  of  valvular  lesions 317 

80.  Showing  relations  of  heart  to  chest  walls 319 

81.  Normal  boundaries  of  heart  and  great  vessels 320 

82.  Position  of  apex  beat  and  other  pulsations 326 

83.  Site  and  rhythm  of  thrills  and  friction  fremitus 329 

84.  Exposed  and  covered  dulness  of  normal  heart 332 

85.  Percussion  lines  for  determining  cardiac  dulness 333 

86.  Sansom's  plexi  meter 334 

87.  Normal  area  of  entire  cardiac  dulness 336 

88.  Dulness  in  hypertrophy  of  left  ventricle 336 

89.  Dulness  in  hypertrophy  and  dilatation  of  right  heart        ....  336 

90.  Dulness  in  dilatation  and  hypertrophy  of  both  ventricles ....  337 

91.  Dulness  due  to  large  pericardial  eflfusion 337 

92.  Dulness  due  to  moderate  pericardial  effusion 337 

93.  Heart  valves  and  their  areas  of  audibility 340 

94.  Two  variations  from  normal  cardiac  rhythm 346 

95.  Chronological  types  of  murmurs 349 

96.  Relative  frequency  of  anaemic  murmurs 351 


XVI 


PLATES,  CHARTS,  AND  ILLUSTRATIONS 


FIOURK 

97.  Diagram — mitral  presystolic  murmurs 

98.  Diagram — varieties  of  murmur  of  mitral  stenosis 

99.  Diagram — mitral  systolic  murmur    . 

100.  Diagram — aortic  systolic  murmur 

101.  Diagram — aortic  diaijtolic  murmur  . 

102.  Diagram — tricuspid  presystolic  murmur  . 

103.  Diagram — tricuspid  systolic  murmur 

104.  Diagram — pulmonary  systolic  murmur     . 

105.  Diagram — combined  murmurs  .        .        . 

106.  Diagram — combined  murmurs  . 

107.  Sphygmograms — diagrammatic  and  actual 

108.  Sphygmograms — actual      .... 

109.  Dudgeon's  sphygmograph  .... 

110.  Showing  lobes  of  right  lung 

111.  Showing  lobes  of  both  lungs  posteriorly   . 
113.  Diagram  of  the  respiratory  centre     . 

113.  Showing  auscultatory  areas  of  apices 

114.  Showing  relative  resonances  of  thorax 

115.  Showing  variations  of  lessened  resonance. 

116.  Dulness  of  fluid  in  reflected  pleura  (left)  . 

117.  Conditions  causing  hyper-resonance  . 

118.  Percussion  and  auscultation  above  consolidations  or 

119.  Findings  over  open  cavities  or  pneumothorax 

120.  Gerhardt's  and  Winti'ich's  phenomena 

121.  Coin  percussion  .        .        . 

122.  Normal  bronchial  and  broncho- vesicular  breathing, 

123.  Normal  bronchial  and  broncho-vesicular  breathing, 

124.  Varieties  of  breathing  and  vocal  resonance  in  disease 

125.  Results  of  auscultation  over  pleural  effusion    . 

126.  Adventitious  respiratory  sounds 

127.  Surface  and  bony  landmarks  of  abdomen 

128.  Showing  nine  topographical  areas  of  abdomen 

129.  Quadrants  of  abdomen.     Locating  lesions 

130.  Contents  of  topographical  areas  of  abdomen     . 

131.  Central  tympanicity  and  lateral  dulness  of  fluid 

132.  Dulness  of  both  flanks  in  ascites,  dorsal  posture 

133.  Change  of  line  of  flatness  in  ascites  . 

134.  Dulness  and  tympanicity  in  abdominal  tumours 

135.  Cross  section  explanatory  of  Fig.  134 

136.  Cross  section  of  tympanitic  abdomen 

137.  Showing  tumour  areas  of  abdomen  . 

138.  Possible  findings  in  hepatic  and  appendical  areas 

139.  Possible  findings  in  splenic  and  sigmoid  areas. 

140.  Possible  findings  in  gastric  and  pelvic  areas     . 

141.  Possible  findings  in  umbilical  area    . 

142.  Shape  and  relations  of  the  normal  stomach 

143.  Auscultatory  percussion  of  stomach  . 

144.  Auscultatory  percussion  of  gastric  tumour 

145.  Showing  gastroptosis  and  gastrectasia 

146.  Topographical  relations  of  colon  and  appendix 


effusions 


anteriorly 
posteriorly 


PLATES,  CHARTS,  AND  ILLUSTRATIONS 


xvii 


noCRE 

147.     Auscultatory  percussion  of  colon 

V-shaped  colon 

Auscultatory  {jercussion  of  tumour  of  colon     . 
Determining  size  and  position  of  normal  liver 
Surface  relations  of  liver,  right  lung,  and  pleura 
Results  of  percussion  of  normal  liver 

}  Determining  by  auscultatory  percussion  whether  a 

f  connected  with  the  liver  . 


148. 
149. 
150. 
151. 
153. 
153. 
154. 
155. 
156. 
157. 
158. 
159. 
160. 
161. 
162. 
163. 
164. 
165. 
166. 
167. 
168. 
169. 
170. 
171. 
172. 
173. 
174. 
175. 
176. 
177. 
178. 
179. 
180. 
181. 
182. 
183. 
184. 
185. 
186. 
187. 
188. 
189. 
190. 
191. 
192. 
193. 
194. 
195. 


tumour 


Showing  the  relations  of  the  pancreas 

Topography  of  the  spleen  .... 

Tympanicity  of  colon  over  tumour  of  kidney 

Anterior  surface  relations  of  kidney . 

Posterior  surface  relations  of  kidney 

Section  through  kidney  and  lumbar  muscles 

Diagram  of  the  neurone     .... 

Diagram  of  motor  pathways 

Diagram  of  sensory  pathways    . 

Relation  of  spinal  cord  to  dorsal  surface  of  trunk 

Relation  of  spinal  segments  and  nerves  to  the  spinous  processes 

Tracts  of  spinal  cord  and  their  names 

Functions  of  tracts  of  spinal  cord 

Functions  of  fibres  of  anterior  and  posterior  roots 

Columns  of  cord  and  diseases  affecting  them    . 

Location  of  spinal  segments  for  sensibility  and  motion  . 

Relation  of  skin  areas  to  spinal  segments  (anteriorly) 

Relation  of  skin  areas  to  spinal  segments  (posteriorly)     . 

Relation  of  skin  areas  of  head  and  neck  to  spinal  segments 

Sensory  supply  of  skin  of  trunk  and  leg  (anteriorly) 

Sensory  supply  of  skin  of  trunk  (posteriorly) 

Sensory  nerves  of  skin  of  arm  (anteriorly) 

Sensory  nerves  of  skin  of  arm  (posteriorly) 

Sensory  nerves  of  skin  of  leg  (posteriorly) 

Sensory  nerves  of  skin  of  foot    . 

Showing  arteries  of  base  of  brain 

Arterial  supply  of  cerebral  hemispheres    . 

Infantile  spinal  paralysis  of  left  leg  . 

Pseudo-muscular  hypertrophy   . 

Wrist-drop 

Foot-drop 

Athetoid  movements 

Hand  of  tetany 

Contractures  of  hand 

Relative  positions  of  cranial  nerve  nuclei,  posterior  aspect 
Relative  positions  of  cranial  nerve  nuclei,  lateral  aspect . 
Effects  of  lesions  of  motor  path  in  brain  and  cord  . 

Showing  hemiana?sthesia 

Mono-anaesthesia,  bilateral  anassthesia,  hysterogenic  zones 

Showing  disseminated  anaesthesia 

Showing  segmental  localization  of  reflexes  and  automatic  centres  in 

spinal  cord 

2 


is  not 


PAOB 

458 
459 
460 
461 
462 
464 

466 
470 
472 
473 
476 
477 
479 
482 
484 
485 
486 
487 
488 
489 
490 
490 
491 
498 
499 
500 
501 
502 
504 
504 
504 
505 
506 
506 
509 
510 
512 
513 
516 
518 
519 
522 
523 
525 
531 
532 
533 

537 


xviii  PLATES,  CHARTS,  AND  ILLUSTRATIONS 

FIGURE  PAGE 

196.  Showing  re-enforcement  of  percussing  finger 538 

197.  Showing  mechanism  of  deep  reflexes,  and  two  main  types  of  paralysis  ,  540 

198.  Motor  points  of  head  and  neck 542 

199.  Motor  points  of  arm 543 

200.  Motor  points  of  arm 544 

201.  Motor  points  of  thigh,  anteriorly 545 

202.  Motor  points  of  thigh  and  leg,  posteriorly 546 

203.  Motor  points  of  leg,  laterally 547 

204.  Sensory  supply  of  skin  of  face  and  neck 551 

205.  Thoma-Zeiss  pipettes 561 

206.  Blood  counting  slide,  plan 562 

207.  Blood  counting  slide,  elevation 562 

208.  Group  of  sixteen  squares  under  microscope 563 

209.  Von  Fleischl's  haemometer 568 

210.  Gowers'  haemometer 569 

311.     Resting  attitudes  of  culex  and  anopheles 588 

212.  Filaria  alive  in  blood 591 

213.  Elastic  tissue,  from  lung,  in  sputum 598 

214.  Bronchial  cast  from  case  of  plastic  bronchitis 599 

215.  Curschmann's  spirals  in  sputum 599 

216.  Charcot-Leyden  crystals 600 

217.  Echinococcus  hooklets 600 

218.  Actinomyces  in  sputum 601 

219.  Microscopical  view  of  vomited  matter 613 

220.  Ovaofentozoa 619 

221.  Amoeba  dysenterije 620 

222.  Emphysematous  chest 851 

223.  Parts  first  attacked  in  muscular  dystrophies  and  atrophies     .        .        .  96& 

224.  Mode  of  rising  in  pseudo-muscular  hypertrophy 970 


"I  do  not  know  ...  I  will  investigate." — Pasteur. 
"First  tell  me  what  I  am  to  look  for."— Faeadat. 


SYNOPSIS  (OR  SCHEDULE)  OF  EXAMINATIONS 

CONSTITUTING  AN  ORDER  OF   PROCEDURE,  AND  A  SYMPTOM- 
GUIDE;    WITH   REFERENCES  TO  PART  I  OF  THIS  BOOK 

To  insure  completeness  in  the  examination  of  patients  and  for 
purposes  of  record,  it  is  desirable  to  have  a  definite  and  comprehen- 
sive order  of  procedure.  The  subjoined  schedule,  which  may  be 
modified  according  to  personal  requirements,  is  based  partly  on  sci- 
entific necessities,  partly  on  clinical  convenience.  Incidentally,  the 
symptoms  indicating  disease  of  a  particular  viscus  or  system  are 
grouped,  in  order  to  direct  attention  to  the  organ  at  fault.  Further- 
more, for  convenience,  references  are  given  to  the  pages  upon  which 
special  symptoms,  signs,  or  methods  of  examination  are  described  in 
detail. 

The  three  main  divisions  of  the  schedule  comprise : 
I.  The  History  or  Anamnesis. 

II.  The  General  Examination  )  Present  Condition  or 
III.  The  Special  Examinations  )      Status  Praesens. 

I.    THE    HISTORY   OR    ANAMNESIS 

Ascertain  the  name,  age,  sex,  civil  condition  (single,  married, 
widow,  widower),  nationality,  occupation,  and  residence.  K^ote  the 
date  of  examination. 

Family  History. — Inquire  concerning  the  diseases  which  have 
prevailed  and  the  causes  of  deaths  (if  such  have  occurred)  among 
father,  mother,  brothers,  sisters,  or  children  ;  also  as  to  the  diseases, 
if  any,  which  prevail  among  the  living.  Consider  whether  or  not 
the  stated  ailments  are  of  an  hereditary  character  (pages  13  to  15). 

Previous  Personal  History. — Bear  in  mind  the  diseases  which 
predominate  : 

(1)  At  the  age  period  of  the  patient  (pages  15,  16). 

(2)  In  the  sex  (pages  16,  17);  and  if  the  patient  is  a  woman, 
inquire  regarding  the  menstrual  life,  pregnancies,  and  miscarriages. 

(3)  In  the  race  or  nationality  (page  17). 

(4)  What  is  the  character  of  the  occupation,  and  does  it  predis- 
pose toward  special  diseases  (pages  18,  19)  ? 


XX  SYNOPSIS  OF  EXAMINATIONS 

(5)  Consider  the  residence,  bearing  in  mind  the  geographical  dis- 
tribution of  disease  (pages  19,  20). 

(6)  Inquire  concerning  the  habits :  of  men,  with  reference  to  the 
daily  amount  and  kind  of  alcoholic  beverages  taken,  whether  before 
or  after  meals ;  tobacco,  kind,  amount,  and  manner  of  using ;  sexual 
indulgence,  frequency ;  of  both  men  and  women,  with  reference  to 
the  amount  and  strength  of  tea  and  coffee  taken. 

(7)  Inquire  with  reference  to  previous  injuries  and  diseases 
(pages  20,  21),  ascertaining  their  date,  duration,  character,  and 
whether  or  not  recovery  was  considered  to  have  been  complete.  Are 
the  previous  diseases  of  such  a  nature  that  a  second  attack  is  prob- 
able ;  or  is  it  unlikely ;  or  are  sequelae  to  be  expected  ?  Search 
especially  for  previous  gonorrhoea,  syphilis,  nephritis,  rheumatism, 
or  malaria. 

History  of  Present  Illness. — Inquire  regarding  the  possible  cause 
of  the  illness ;  the  date  and  manner  of  its  onset,  never  failing  to  fix 
in  mind  the  nature  of  the  earliest  symptoms,  and,  if  possible,  the 
organ  or  system  to  wliich  they  belong — e.  g.,  stomach,  circulatory 
apparatus — the  subsequent  symptoms  and  their  order  of  appearance 
to  the  present  time ;  the  symptoms  now  present ;  and  the  previous 
treatment,  if  it  can  be  ascertained  (pages  22  to  24). 

II.    THE    GENERAL    EXAMINATION 

1.  Observe  the  dress  and  general  behaviour  (pages  24,  25). 

2.  Estimate  (or  measure)  the  height  and  weight,  and  note  the 
amount  and  character  of  the  adipose  and  muscular  tissue  (pages  25 
to  27). 

3.  Study  the  shape  and  general  configuration  of  the  body  (pages 
27,  28). 

4.  Note  the  complexion,  and  colour  of  hair  and  eyes  (pages  28, 
165). 

5.  So  far  as  possible,  determine  the  diathesis  (usually  done  at 
the  end  of  the  examination),  and  note  the  presence  of  any  cachexia 
(pages  28  to  30). 

6.  Observe  the  posture  and  manner  of  moving  (pages  30  to  32). 

7.  If  practicable,  test  the  station  or  power  of  standing,  and  ob- 
serve the  gait  or  manner  of  walking  (pages  32  to  34). 

8.  Pain. — If  pain  is  a  subject  of  complaint,  make  due  allowance 
for  susceptibility  (page  35)  and  manner  of  statement  (pages  35,  36). 
Can  any  diagnostic  inference  be  drawn  from  the  character  (pages 
36,  37)  or  the  seat  (pages  38  to  52)  of  the  pain  ? 

9.  Tenderness. — Is  there  tenderness  (pain  on  pressure),  and  is  its 
location  significant  (pages  52  to  54)  ? 


HISTORY  AND  GENERAL   EXAMINATION 


XXI 


10.  Paraesthesias.  —  Are  there  abnormalities  of  sensation  not 
amounting  to  pain  (paresthesias)  ?  If  so,  consider  the  site,  variety, 
and  possible  significance  (pages  54  to  58). 

11.  Vertigo. — Inquire  for  the  existence  of  vertigo,  having  in  mind 
both  its  common  and  less  frequent  causes  (pages  58  to  60). 

12.  Temperament. — What  is  the  temperament  (mainly  psychical) 
of  the  patient  (pages  61,  62)  ? 

13.  Psychical  State. — What  is  the  present  psychical  state  of  the 
patient  as  shown  by  the  facial  expression  (pages  62,  63) ;  the  emo- 
tional state  (page  63) ;  and  the  condition  of  intellection  (pages  63  to 
65) ;  the  abnormalities  of  the  latter,  embracing  mental  dulness,  loss 
of  memory,  delusions,  or  delirium  ?     Inquire  as  to  sleep  (page  65). 

14.  Consciousness. — Is  the  patient  fully  conscious  ?  If  not,  what 
is  the  degree  of  disturbance  (page  66) ;  what  may  it  signify  in  gen- 
eral (pages  66,  67) ;  and  to  what  is  it  due  in  this  particular  case 
(pages  67  to  71)  ? 

15.  Convulsions. — If  general  convulsions  have  occurred  or  are 
present,  to  what  may  they  be  attributed  (pages  71  to  74)  ? 

16.  Cutaneous  Surface. — Observe  and  examine  the  cutaneous  sur- 
face with  reference  to  colour  (pages  75  to  81),  heat  (pages  81,  82), 
moisture  (pages  82,  83),  rash  or  eruption  (pages  83  to  86),  scars 
(pages  86,  87),  dropsy  (pages  87  to  90),  condition  of  the  veins  (page 
91),  and  emphysema  (page  92). 

17.  Pulse. — Take  the  pulse  (pages  367  to  369).  Observe  its  fre- 
quency,'rhythm,  tension,  and  other  qualities.  Note  the  condition  of 
the  arteries.  If  variations  from  the  normal  are  found,  consider  their 
significance  (pages  369  to  378). 

18.  Respiration. — Take  the  respiration.  Observe  its  frequency, 
type,  rhythm,  and  other  characteristics  (pages  386  to  394). 

19.  Temperature. — Take  the  temperature  of  the  body  (pages  95 
to  100).  If  fever  is  present,  consider  its  height,  type,  manner  of 
invasion,  course,  and  termination  (pages  102  to  105).  What  diag- 
nostic inferences  may  be  drawn  from  these  observations  (pages  105 
to  111)?  Has  the  fever  been  preceded  or  accompanied  by  chills 
(page  111)  ?  If  the  temperature  is  subnormal  what  may  it  indicate 
(page  111)? 

20.  Inquire  concerning  the  appetite  and  thirst  (pages  112,  113); 
vomiting  (pages  113  to  121)  and  the  gross  characters  of  the  vomltus 
(pages  122  to  125) ;  defecation  (pages  125  to  132)  and  the  gross  char- 
acters of  the  stools  (pages  132  to  139) ;  the  character  and  frequency 
of  urination  (pages  139  to  144) ;  and  certain  genital  symptoms  in  men 
and  women  (pages  144  to  149). 


xxii  SYNOPSIS  OF  EXAMINATIONS 


III.    SPECIAL    EXAMINATIONS 

By  means  of  a  more  or  less  discursive  examination,  as  just  out- 
lined, the  observer  obtains  a  conception  of  the  general  condition  of 
the  patient ;  and  also,  in  the  majority  of  cases,  an  indication  for  a 
special  examination  of  a  particular  part,  organ,  or  system.  The  spe- 
cial examinations  embrace  the  signs  and  symptoms  which  occur  in 
connection  with  various  parts  of  the  body — e.  g.,  head  and  face, 
tongue ;  or  which  belong  to  an  organ — e.  g.,  spleen ;  or  a  system — 
e.  g.,  respiratory, 

1.  Head  and  Face. — Observe  the  size  and  contour  of  the  head 
and  face ;  in  infants,  the  condition  of  the  fontanels  and  sutures ; 
and  the  consistence  and  surface  of  the  cranial  bones  (pages  154  to 
160).  Study  the  expression  of  the  face  and  consider  whether  it  is 
indicative  of  certain  diseases  (pages  160  to  163),  Xote  the  colour  of 
the  face,  and  the  state  of  the  skin  of  the  face  (pages  163,  164). 
What  is  the  colour  of  the  hair,  and  is  it  abundant,  or  scanty  (page 
165)  ?  Is  there  general  or  circumscribed  swelling  of  the  face  (page 
166)?  Are  there  abnormal  movements  of  the  head,  or  does  it  lack 
normal  mobility  (pages  166,  167)  ?  Are  the  facial  muscles  in  a  state 
of  clonic  or  tonic  spasm  (pages  167  to  169),  or  are  they  paralyzed 
(pages  169  to  174)  ? 

2.  Bar. — Has  the  patient  complained  of  pain  in  the  ear  (page 
175)?  What  is  the  colour  and  shape  (pages  175,  176)  of  the  ear? 
Is  there  a  discharge  from  the  external  meatus  (page  176)?  Does 
the  patient  complain  of  tinnitus  (pages  176, 177)  ?  Does  the  patient 
hear  well ;  is  he  deaf,  and,  if  so,  is  the  deafness  due  to  nerve  lesions 
or  aural  lesions  (pages  177  to  179)  ?  Is  the  hearing  hyperacute 
(page  180)  ? 

3.  Eye. — Are  the  eyelids  swollen  or  ulcerated;  in  a  state  of 
spasm;  too  widely  opened;  or  abnormally  drooping  (pages  180  to 
183)  ?  What  is  the  colour  of  the  sclerotic,  the  state  of  diyness  or 
moisture  of  the  eye,  and  the  condition  of  the  cornea  (pages  183  to 
185)  ?  Are  the  pupils  large  or  small,  equal  or  unequal ;  do  they 
respond  to  light  and  to  accommodation  (pages  185  to  190)?  Are 
the  eyeballs  painful ;  do  they  protrude,  or  are  they  more  sunken  than 
normal ;  what  is  their  position  (pages  190  to  193)  ?  Are  the  eyeballs 
normally  mobile,  or  are  there  symptoms  of  ocular  paralysis ;  and  if 
ocular  paralysis  is  found,  what  is  its  cause  (pages  192  to  202)  ?  Does 
the  patient  complain  of  any  abnormality  of  sight  (page  202)  ?  If 
alterations  in  the  shape  or  size  of  the  visual  fields  have  been  found, 
what  may  be  their  significance  (pages  202  to  208)  ?    If  an  ophthal- 


SPECIAL  EXAMINATIONS  xxWi 

moscopic  examination  of  the  eye  grounds  has  been  made,  do  the 
findings  indicate  extra-ocular  disease  (pages  208  to  211)  ? 

4.  Nose.— The  following  symptoms  demand  an  examination  of 
the  nose  :  Pain  in  or  around  the  nose  (page  213),  frontal  headache^ 
or  trigeminal  neuralgia.  Mouth-breathing  and  its  typical  facial  ex- 
pression due  to  nasal  stenosis  (page  162).  Snoring  and  restless  sleep. 
Nasal  voice.  Nasal  discharges  (page  215),  epistaxis  (pages  215,  216), 
or  had  odour  of  the  expired  air  (pages  219,  220).  Deafness.  Cough 
or  bronchial  asthma. 

To  Examine  the  Nose. — Having  noted  the  shape  and  colour  of  the 
nose,  together  with  such  other  points  as  may  be  observed  by  ordinary 
inspection,  examine  the  nasal  chambers  (using  the  probe)  by  anterior 
and  posterior  rhinoscopy  (pages  211  to  213).  Test  the  sense  of  smell 
(pages  21G  to  218). 

5.  Mouth.. — Examine  the  lips,  buccal  cavity,  gums,  and  teeth 
(pages  218  to  225).  Note  the  condition  of  the  tongue  with  reference 
to  colour,  size,  spasm,  tumour,  paralysis,  scars,  fissure,  ulcers,  etc. 
(p  ges  225  to  230).  Does  the  tongue  present  an  appearance  which  is 
of  general  diagnostic  value  (pages  230  to  232)  ?  Test  the  sense  of 
taste  (pages  232,  233). 

6.  Examine  the  palate,  tonsils,  and  pharynx  (pages  233  to 
237).  What  is  the  shape  of  the  palate ;  is  it  paralyzed,  anaesthetic, 
or  otherwise  abnormal  ?  Are  the  tonsils  acutely  swollen,  chronically 
enlarged,  ulcerated,  or  covered  with  exudate  ?  What  is  the  colour 
of  the  pharynx;  is  there  exudate  or  ulceration;  is  there  bulging 
posteriorly ;  is  it  paralyzed  or  anaesthetic  ? 

7.  Does  the  patient  complain  of  dysphagia,  and,  if  so,  to  what 
may  it  be  due  (pages  237,  238)  ? 

8.  Larynx. — The  following  symptoms  demand  an  examination 
of  the  larynx :  Pain^  burning^  or  soreness  over  and  around  the 
larynx.  Alterations  in  the  character  of  the  voice  sounds^  viz.,  apho- 
nia or  hoarseness  [dysphonia).  Inspiratory  dyspnoea,  especially  if 
accompanied  by  stridulous  {wheezing  or  squeaMng)  respiration. 
Cough,  particularly  of  the  laryngeal  type  {tight  or  croupy).  Dysphor 
gia,  difficulty  or  pain  in  stcallowing. 

To  Examine  the  Larynx.— (See  pages  238  to  243).  Do  not  omit 
an  inspection  of  the  lingual  tonsil. 

9.  Cough.— Has  the  patient  a  cough  ?  If  so,  observe  its  char- 
acter and  consider  its  causes  (pages  256  to  259).  Examine  the  spu- 
tum (if  any)  with  reference  to  its  character  (pages  259  to  261  and 
596  to  603).     Has  he  had  haemoptysis  (pages  261  to  263)  ? 

10.  Speech.— Xote  alterations  in  the  voice  or  the  manner  of 
speaking  (pages  243  to  246).     Is  there  aphasia  (pages  246  to  255)  ? 


xxiv  SYNOPSIS  OF   EXAMINATIONS 

11.  Neck. — Observe  the  shape  of  the  neck ;  is  it  rigid  ?  Are 
the  sterno-mastoids  or  clavicles  prominent ;  is  the  thyroid  gland 
enlarged  or  atrophied  (pages  263,  264)  ?  Does  the  trachea  descend 
with  inspiration,  or  can  tracheal  tugging  be  felt  (page  265)  ? 
"What  is  the  condition  of  the  cervical  glands  (pages  265  to  267) ; 
of  the  arteries  of  the  neck  (page  267) ;  of  the  veins  of  the  neck 
(pages  267  to  271)  ? 

12.  Extremities. — Examine  the  nails  (pages  271,  272) ;  the 
hand  and  fingers  (pages  272  to  278)  ;  the  arm  (page  278) ;  the  foot 
and  leg  (pages  279  to  283). 

13.  Back. — Examine  the  back  for  alterations  of  shape,  promi- 
nence of  the  scapulae,  stiffness,  and  swellings  or  bulgings  (pages 
284  to  286). 

14.  Chest. — Examine — perhaps  measuring  and  outlining — the 
chest  with  reference  to  bilateral  or  unilateral  deformities,  flexibility 
of  ribs,  and  the  presence  of  enlarged  veins  (pages  296  to  303). 

15.  Heart  and  Blood-vessels. — The  following  symptoms 
demand  an  examination  of  the  heart  and  blood-vessels :  Dyspnoea 
{perhaps  ortliopncea),  especially  if  made  worse  hy  physical  exertion  or 
accompanied  by  cyanosis.  (Edema,  especially  of  the  feet  and  ankles. 
Palpitation,  prcecordial  pain,  anxiety,  or  distress,  particularly  if  in- 
creased by  exertion.  Sudden  vertigo.  Restless  sleep,  dreaming,  start- 
ing during  sleep.  Cough,  especially  if  chronic;  or  an  unusually 
persistent  attack  of  bronchitis.  Chronic  digestive  disturbances. 
Hemorrhoids.     Great  obesity. 

If  such  symptoms  are  present  inquire  further  (with  reference  to 
causation)  concerning :  Prolonged  and  severe  muscular  exertion. 
Many  years  of  constant  mental  excitement  or  anxiety.  Excessive 
eating  and  drinking,  especially  of  rich  food  and  alcoholic  beverages  ; 
these,  and  the  foregoing,  partly  with  reference  to  arteriosclerosis. 
Excessive  use  of  tobacco,  tea,  and  coffee  {in  relatioyi  to  cardiac  tieu- 
roses).  Previous  attacks  of  chorea,  gout,  rheumatic  fever,  or  other, 
usually  acute,  infectious  diseases,  especially  scarlatina,  diphtheria, 
typhoid  fever,  tonsilitis,  syphilis.  The  family  history :  does  it  reveal 
rheumatism,  gout,  angina  pectoris,  apoplexy,  or  organic  cardiac 
disease  ? 

To  Examine  the  Heart. — Inspect  and  palpate  the  thorax,  noting, 
if  present,  distended  veins,  pulsating  jugulars,  epigastric  pulsation, 
and  pulsating  liver.  Xote,  as  of  prime  importance,  the  position, 
character,  and  extent  of  the  apex-beat  (pages  321  to  329).  Percuss 
the  heart  (pages  330  to  339).  Auscultate  the  heart  with  reference 
to  the  intensity  and  character  of  the  sounds  (pages  339  to  347),  and 
the  presence  of  adventitious  sounds,  either  endocardial  (pages  347  to 


SPECIAL  EXAMINATIONS  XXV 

3G0)  or  exocardial  (pages  360  to  363).     Examine  the  pulse  (pages  367 
to  378).     Use  the  sphygmograph  (pages  378  to  382). 

To  Examine  the  Blood-vessels.— Inspect,  palpate,  and  auscultate 
the  accessible  arteries  and  veins  (pages  363  to  367).  Xote  any  ab- 
normal capillary  pulsation  (page  271). 

16.  Lungs  and  Pleurae. — The  following  symptoms  demand  an 
.  examination  of  the  lungs  and  pleuras :  Cough^  with  or  without  expecto- 
ration.    Hcemoptysis  or  spitting  of  Mood.     Pain  in  the  aide  of  the 
chest.     Dyspnoea.     Night  sweats.     Loss  of  flesh  and  strength. 

Additional  evidence  should  be  sought  for,  viz.,  a  family  history 
of  consumption^  asthma,  hronchitis,  or  scrofulous  {tuberculous)  dis- 
eases ;  and  a  personal  history  of  enlarged  cervical  glands,  or  tuber- 
culous disease  of  bone,  or  association  with  a  consiimptive,  or  an  occu- 
pation predisposing  toward  pulmonary  disease. 

To  Examine  the  Lungs. — Inspect  and  palpate  the  chest  with 
reference  to  its  shape  (pages  296  to  303).  Measure  it.  Count  the 
respiration  (page  386)  ;  determine  its  type,  degree  of  expansion 
and  retraction,  and  its  rhythm  and  other  characters  (pages  386  to 
394).  Is  fremitus  obtained  (pages  394  to  396)  ?  Is  dyspnoea  pres- 
ent ?  If  so,  what  is  its  character  ?  Percuss  the  lungs — front,  sides, 
and  back  (pages  396  to  409).  Auscultate  the  lungs — front,  sides, 
and  back,  determining  the  character  of  the  breath  sounds  (pages 
409  to  416)  and  the  presence  and  variety  of  adventitious  sounds 
(pages  418  to  422). 

17.  Abdomen. — If  complaint  is  made  of  abdominal  pain  or  dis- 
comfort,  inspect  the  abdomen  (pages  427  to  430).  Palpate  and  per- 
cuss the  abdomen  (pages  430  to  444).  Auscultate  the  abdomen 
(page  444). 

18.  Stomach. — The  following  symptoms  require  an  examination 
of  the  stomach  :  Fulness,  sinking  feelings,  pain  or  discomfort  in  epi- 
gastrium, loiver  sternum,  between  the  scapulm.  Increased  or  lessened 
appetite  or  increased  thirst.  Nausea  or  vomiting  {of  stomach  contents, 
or  blood).  Pyrosis,  eructations,  or  flatulence.  Mental  depression. 
Rapid  emaciation. 

To  Examine  the  Stomach. — Incidentally  inspect  the  lips,  mouth, 
gums,  teeth,  and  tongue.  If  the  food  is  arrested  in  the  throat,  or 
before  it  enters  the  stomach,  and  is  regurgitated,  palpate,  auscul- 
tate, and  instrumentally  examine  the  esophagus  (pages  445,  446). 
Inspect  and  palpate  the  stomach  (pages  448,  449).  Percuss  the 
stomach  by  ordinary  and  auscultatory  percussion  (pages  450  to  453). 
Inflate  the  stomach  (page  453).  Obtain  the  contents  of  the  stomach 
(pages  453  to  455)  after  a  test  meal,  and  examine  by  chemical  and 
microscopical  methods  (pages  604  to  618). 


xxvi  SYNOPSIS  OF  EXAMINATIONS 

19.  Intestines. — Consfipatioti,  diarrhoea,  and  abdominal  pain 
are  the  symptoms  which  require  an  examination  of  the  intestines. 

To  Examine  the  Intestines. — Inspect  the  stools  (pages  132  to  139). 
Inspect,  palpate,  percuss,  and  auscultate  the  abdomen  in  general 
(pages  427  to  444),  and  the  intestines  (including  a  digital  examina- 
tion of  the  rectum)  in  particular  (pages  457  to  461). 

20.  Liver  and  Gall  Bladder. — The  following  symptoms  de- 
mand an  examination  of  the  liver  and  gall  bladder :  Pain,  of  the 
hepatic  type,  over  the  right  hypochondrium.  Jaundice,  darh  urine, 
clay-coloured  stools.  Irregular  chills  and  fever.  Cutaneous  pruritus. 
Hcematemesis.     Digestive  disturbances. 

If  such  symptoms  are  present,  inquire  further  (with  reference  to 
causation)  concerning:  Previous  attacks  of  jaundice  ivith  or  loithout 
hepatic  colic.  Previous  catarrh  of  the  stomach,  or  acute  indigestion 
{catarrh  of  bile  ducts).  Strong  emotions  {anger  or  fright).  Chronic 
alcoholism  {hepatic  cirrhosis).  Syphilis,  tuberculosis,  or  long-con^ 
tinned  suppuration  {amyloid  disease).  Possibility  of  phosphorus 
poisoning. 

To  Examine  the  Liver  and  Gall  Bladder, — Rarely  inspection  and 
auscultation  are  of  use ;  ordinarily  palpation  and  percussion  (pages 
463  to  470)  are  to  be  relied  upon. 

21.  Spleen. — The  size,  shape,  and  position  of  the  spleen  should 
be  determined,  mainly  by  palpation  and  percussion  (pages  471  to 
475),  in  the  following  conditions  and  diseases:  Emphysema,  left 
pleural  effusion,  and  left  pneumothorax.  Ascites,  tympanites,  and 
large  abdominal  tumours.  In  all  acute  infectious  diseases  {e.  g., 
typhoid  fever,  malarial  fever).  Leuccemia.  Cirrhosis  or  amyloid 
disease  of  the  liver. 

22.  Kidneys. — The  following  symptoms  demand  a  physical 
examination  of  the  kidneys,  and  a  chemical  and  microscopical  exami- 
nation of  the  urine :  Pain  in  the  posterior  lumbar  region,  especially 
if  of  the  renal  tyj)e.  (Edema  or  puffiness  of  the  face,  es]yecially  about 
the  eyelids  in  the  morning.  General  oedema  {anasarca).  Painful 
or  frequent  urination.  SmoJcy  or  turbid  urine ;  notable  increase 
or  diminution  in  its  amoutit.  Headache,  drowsiness,  nausea,  and 
vomiting.  Dyspnoea  or  asthma,  without  other  discoverable  cause. 
Dimness  of  vision.  Convulsions  or  paralyses.  Irregular  chills  and 
fever  {pyelitis). 

If  such  symptoms  are  present,  inquire  further  (with  reference  to 
causation)  concerning :  A  family  history  of  nephritis,  apoplexy,  or 
gout.  A  personal  history  of  alcoholism,  gout,  lead-poisoning,  renal 
colic,  chilling  of  the  surface  of  the  body,  acute  infectious  diseases 
(such  as    scarlet  fever,  malaria,   tonsilitis,   diphtheria),  and    long- 


SPECIAL  EXAMINATIONS  xxvii 

continued  suppuration,  tuberculosis^  tertiary  syphilis^  and  malaria 
{amyloid  disease). 

To  Examine  the  Kidneys. — Inspect  and  palpate  anteriorly;  in- 
spect, palpate,  and  percuss  posteriorly  (pages  475  to  480).  Examine 
also  the  heart  and  blood-vessels  for  cardiac  hypertrophy  and  general 
arteriosclerosis.  Examine  the  urine  physically,  chemically,  and  mi- 
croscopically (pages  621  to  648).  If  necessary,  examine  the  bladder 
and  ureters. 

23.  Nervous  System. — The  following  symptoms  require  an 
examination  of  the  nervous  system :  Frequent  or  continuous  headache. 
Frequent  vomiting.  General  convulsions,  or  localized  spasm.  Paral- 
yses {ocular  or  skeletal).  Vertigo.  Speech  disturbances.  Difficulty 
in  standing  or  walking  if  not  due  to  iveakness,  injury,  or  disease  of 
joints.     Mental  disturbances.     Dysphagia  {sometimes). 

If  such  symptoms  are  present,  inquire  further  (with  reference  to 
etiology)  concerning  :  A  family  history  of  psychoses  {insanity),  hys- 
teria, chorea,  epilepsy,  neurasthenia,  paralysis,  convulsions,  or  hered- 
itary syphilis.  A  personal  history  of  alcoholism,  syphilis,  injury ; 
discharge  from  the  ear  ;  any  of  the  acute  infectious  diseases  ;  poison- 
ing from  lead,  mercury,  arsenic,  tobacco,  or  naphtha ;  and  exposure 
to  cold. 

To  Examine  the  Nervous  System. — Xote  the  presence  of  the  stig- 
mata of  degeneration  (pages  507  to  509).  Examine  the  muscles 
with  reference  to  their  nutrition,  tone,  and  motor  power  (pages  509  to 
514).  Are  there  motor  disturbances  ?  If  so,  is  there  increased  mo- 
tility (spasm,  pages  514  to  519),  or  decreased  motility  (paralysis,  pages 
520  to  527)  ?  Are  there  disturbances  of  sensation  (pages  527  to  535)  ? 
What  is  the  condition  of  the  superficial  reflexes  (pages  536,  537) ;  of 
the  deep  reflexes  (pages  537  to  542)  ?  "What  is  the  electrical  reaction 
of  the  muscles  and  nerves  (pages  542  to  549)  ?  Are  there  vasomotor 
and  trophic  disturbances  (pages  549,  550)  ?  What  is  the  condition 
of  the  cranial  nerve  functions  (pages  550  to  553)  ?  What  are  the  find- 
ings from  an  examination  of  the  eye  grounds  (pages  208  to  211)  ? 

24.  Blood. — The  following  symptoms  require  an  examination  of 
the  blood :  Dyspnoea  and  palpitatioii  upon  exertion.  Pallor  of  the 
skin  and  mucous  membranes.  Headache  and  vertigo.  Debility.  Dis- 
turbances of  digestion  and  gastric  pain.     (Edema  of  the  feet. 

If  such  symptoms  are  present,  inquire  further  (with  reference  to 
causation)  concerning:  Hereditary  or  personal  hwmophilia.  Loss  of 
blood  {injury,  menorrhagia,  bleeding  piles,  hwmoptysis,  hmmatemesis, 
etc.).  Malaria,  rheumatic  fever,  lead-poisonitig.  Chronic  gastric  or 
intestinal  catarrh  ;  or  a  long-continued  diarrhoea.  Worry  and  men- 
tal excitement.     Wasting  diseases. 


xxviii  SYNOPSIS  OF  EXAMINATIONS 

To  Examine  the  Blood. — Count  the  red  and  white  cells  (pages  559 
to  567).  Estimate  the  haemoglobin  (pages  567  to  571).  Stain  a  dried 
specimen  of  the  blood  and  make  a  differential  count  of  the  leucocytes 
(pages  571  to  586).  Examine  a  fresh  specimen  of  the  blood  (espe- 
cially for  the  malarial  organism,  pages  587  to  591). 

25.  Diagnostic  Puncture. — If  desirable,  obtain  fluid  by  punc- 
ture (pages  648,  649)  from  cavities  or  cysts ;  examine  the  fluid,  and 
from  its  character  endeavour  to  determine  its  source  (pages  649 
to  653). 


PLATE   I. 


The  Shape  and  Relations  of  the  Thoracic  and 

Abdominal  viscera, 

.Anterior  Aspect  (Semi-diagrammatic) 


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PLATE   I. 


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ThL   bHArt  AND   RELATIONS  OF    I  Ht    I  HOKACIC  AND 

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PLATE  II. 


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The  Shape  and  Relations  of  the  Thoracic  and 

Abdominal  Viscera, 

Posterior  Aspect  <Semi-diagrammatic) 


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PLATE  II. 


The  Shape  and  Relations  of  the  Thoracic  and 

Abdominal  Viscera. 

Posterior  Aspect  (Semi-diagrammatic) 


THE  DIAGNOSTICS  OF  INTERNAL  MEDICINE 


PRELIMmARY  CONSIDERATIONS 

Diagnosis. — This,  in  its  narrowest  sense,  consists  in  bestowing 
a  name  upon  a  certain  assemblage  of  pathological  phenomena.  It 
should  include  also  a  knowledge  of  the  causal  factors  of  the  disease ; 
a  determination  of  its  character  with  reference  to  type  and  severity ; 
an  estimate  of  the  amount  and  kind  of  damage,  both  general  and 
local,  which  has  been  sustained  by  the  organism ;  a  forecast  of  the 
probable  course  and  duration  of  the  morbid  process ;  and  a  cogni- 
zance of  the  personal  characteristics  of  the  patient,  whether  psychic 
or  physical,  inherited  or  acquired.  Its  final  object  is  to  be  able 
to  treat  disease  intelligently,  and  the  application  of  scientific  meth- 
ods to  the  completest  discrimination  and  recognition  of  disease  con- 
stitutes the  art  of  diagnosis. 

A  diagnosis  is  made  by  means  of  symptoms,  which  constitute  the 
evidence  upon  which  is  based  a  judgment  as  to  the  nature  of  the 
case.  Symptoms,  the  phenomena  caused  by  morbid  processes,  are 
divided  into  subjective,  those  which  can  be  appreciated  only  by  the 
patient,  and  objective,  comprising  those  which  are  detected  by  the 
personal  examination  made  by  the  physician.  The  term  physical 
signs  is  by  common  consent  applied  to  the  objective  symptoms 
revealed  by  special  methods  of  examination,  used  mainly  in  deter- 
mining the  condition  of  the  organs  contained  in  the  chest  and 
abdomen. 

In  addition  to  a  knowledge  of  the  symptoms,  subjective  or  objec- 
tive, which  may  exist  at  the  time  of  examination,  it  is  necessary  to 
ascertain  the  presence  or  absence  of  hereditary  taints  or  tendencies, 
to  know  something  about  the  habits  and  occupation  of  the  patient, 
to  learn  of  past  illnesses  or  injuries,  and  to  obtain  a  clear  idea  of  the 
manner  of  onset  and  subsequent  evolution  of  the  present  disease. 
Finally,  it  is  well  to  study  the  temperament  and  personal  character- 
istics, mainly  psychical,  of  the  individual  patient  so  far  as  practicable. 

The  family  and  personal  history,  the  history  of  the  present  illness, 
and  the  results  of   the  examination  constitute  the  evidence  upon 

1 


2  THE  DIAGNOSTICS  OF  INTERNAL  MEDICINE 

which  the  final  judgment  as  to  the  nature  of  the  ease  is  to  be  based. 
A  necessarily  heterogeneous  collection  of  facts  must  be  classified 
with  reference  to  their  relative  value  and  significance  and  compared 
with  the  previous  knowledge  and  experience  of  the  diagnostician, 
after  which  a  judgment  may  be  rendered  as  nearly  as  possible  in 
accordance  with  the  facts.  This  constitutes  the  second  and  final 
step  in  the  making  of  a  diagnosis.  The  process  is  thus  seen  to  con- 
sist of  two  elements — observation,  in  its  broadest  sense,  and  reason- 
ing, applied  to  the  results  of  the  observation. 

Certain  terms  of  some  practical  value  and  convenience  are  used 
to  qualify  a  diagnosis,  as  follows  (the  definitions  are  largely  from 
Foster) : 

LIST  OF  DESCRIPTIVE  TERMS   EMPLOYED  WITH   REFERENCE  TO 
DIAGNOSES,  SYMPTOMS,  AND  SIGNS 

Diagnoses : 

1.  Anatomical. — Based  on  a  knowledge  not  only  of  symptoms  or 

phenomena,  but  also  of  definite  anatomical  alterations  on 
which  the  phenomena  depend  ;  or  a  post-mortem  diagnosis. 

2.  Clinical. — Based  upon  the  symptoms  manifested  during  life. 

3.  By  Exclusion. — Keached  by  a  deductive  process,  all  the  affec- 

tions which  present  salient  points  of  similarity  with  the  one 
to  be  diagnosticated  being  reviewed  in  turn,  and  each  suc- 
cessively discarded  as  one  or  more  of  its  essential  features 
are  missed  in  a  given  case,  until  but  one  possibility  remains, 
which  is  accepted  as  the  true  one. 

4.  Differential. — The  process  of  distinguishing  between  different 

diseases  which  resemble  one  another  more  or  less  closely. 

5.  Direct. — The  symptoms  are  of  such  a  nature  that  they  point 

to  the  presence  of  one  special  disease,  and  are  not  capable 
of  misinterpretation. 

6.  Patliological. — Of  the  nature  of  a  lesion,  without  regard  to  its 

situation. 

7.  Physical. — By  means  of  physical  (objective)  signs,  irrespec- 

tive of  subjective  symptoms,  as  by  palpation,  auscultation, 
etc, 

8.  Presumptive. — Not  regarded  as  certain. 

9.  Retrospective. — Of   some   antecedent    disease  or    injury,  the 

nature  of  which  can  be  deduced  only  from  the  history 
given  and  from  the  persistent  effects, 

10,  Symptomatic. — Consisting  simply  in  the  determination  of  the: 

most  striking  symptoms. 

11,  Topographical. — Of  the  seat  of  a  lesion. 


PRELIMINARY  CONSIDERATIONS  3 

Symptoms : 

1.  Constitutional. — Those  that  may  result  from  unbalancing  of 

the  organism  as  a  whole,  and  are  common  to  affections  of 
many  kinds. 

2.  Direct. — Those  that  depend  directly  upon  the  disease. 

3.  General. — Constitutional.     (See  above.) 

4.  Indirect. — Which  are  the  indirect  consequences  of  the  disease. 

5.  Local. — Which  result  from  localized  disease,  and  are  usually 

confined  to  the  site  of  the  diseased  organ  or  tissue. 

6.  Negatively  Pathognomonic. — Which  seldom  or  never  occur  in 

a  certain  disease,  and  consequently,  if  present,  show  that 
the  case  is  not  one  of  that  disease. 

7.  Pathognomonic. — Which  undeniably  indicate  the  existence  of 

a  certain  disease. 

8.  Reflex. — Which  are  caused  by  local  disease,  but  manifest  them- 

selves by  means  of  the  nervous  system  in  an  otherwise  unre- 
lated organ  or  part  of  the  body. 

9.  Sympathetic. — Which  appear  with  the  essential  ones,  but  for 

the  presence  of  which  no  cause  can  be  assigned  except  that 
of  sympathy. 
Signs : 

1.  Physical. — Already  defined. 

2.  Rational. — Signs  and  symptoms,  subjective  or  objective,  cor- 

responding to  the  alterations  in  structure  and  mechanical 
conditions  discovered  by  physical  examination. 

3.  Stethoscopic. — Those  discovered  by  auscultation. 

Difficulties  in  Diagnosis. — For  various  reasons  it  may  be 
difficult  or  impossible  to  make  a  diagnosis.  The  most  important  of 
these  reasons  are  as  follows  : 

(1)  The  subjective  symptoms  may  be  puzzling  or  incongruous. 

(2)  The  objective  symptoms  and  signs  may  be  ill-defined,  obscure, 
or,  if  present,  as  discovered  later,  may  be  impossible  of  detection  by 
the  most  searching  examination — e.  g.,  a  beginning,  small  peri- 
nephritic  abscess  in  an  unusually  obese  patient,  which  can  not  be 
palpated  until  it  reaches  a  certain  size. 

(3)  Certain  symptoms  essential  to  a  diagnosis  may  not  appear 
until  the  disease  has  advanced  to  a  certain  stage — e.  g.,  the  splenic 
enlargement  and  rose  rash  of  typhoid  fever. 

(4)  Several  diseases,  each  of  which  in  other  cases  may  constitute 
the  sole  morbid  process,  may  co-exist,  one  as  the  primary  or  main 
disease,  the  others  attending  as  complications  or  sequel*.  One  or 
more  of  the  secondary  lesions  may  be  recognised,  and  the  underlying 
or  primary  disease  or  condition  be  overlooked — e.  g.,  pleurisy  with 


4  THE  DIAGNOSTICS  OP  INTERNAL  MEDICINE 

effusion  occurring  as  a  result  of  previously  unrecognised  pulmonary 
tuberculosis,  and  masking  the  primary  lesion  in  the  lungs. 

(5)  The  rarity  of  a  disease  may  lead  to  its  non-recognition  be- 
cause of  unfamiliarity  with  its  history  and  symptomatology,  and 
perhaps  the  consequent  failure  to  elicit  all  the  diagnostic  data. 

(6)  The  lack  of  a  full  and  accurate  history  is  at  times  a  serious 
hindrance  in  making  a  diagnosis.  The  patient  may  be  deaf  and 
dumb  or  speak  an  unfamiliar  tongue,  or  he  may  be  unconscious, 
delirious,  mentally  unsound,  or  so  ignorant  and  stupid  that  no  reli- 
able information  can  be  obtained  from  him,  and  intelligent  friends 
or  relatives  may  not  be  available.  On  the  other  hand,  in  conse- 
quence of  a  variety  of  motives,  essential  facts  may  be  concealed  by 
the  patient  or  the  friends. 

(7)  Drug  symptoms,  unless  known  and  due  allowance  made  for 
them,  may  so  disguise,  add  to,  or  simulate  certain  diseases  that  the 
diagnosis  may  be  shrouded  in  uncertainty. 

(8)  The  diagnostician  must  be  a  good  observer,  and  at  the  same 
time  be  able  to  reason  correctly.  As  Huxley  well  says  :  "  Scientific 
reasoning  differs  from  ordinary  reasoning  in  just  the  same  way  as 
scientific  observation  and  experiment  differ  from  ordinary  observa- 
tion and  experiment — that  is  to  say,  it  strives  to  be  accurate  ;  and  it 
is  just  as  hard  to  reason  accurately  as  it  is  to  observe  accurately.  In 
scientific  reasoning  general  rules  are  collected  from  the  observation 
of  many  particular  cases ;  and,  when  these  general  rules  are  estab- 
lished, conclusions  are  deduced  from  them,  just  as  in  everyday  life. 
If  a  boy  says  that  '  marbles  are  hard,'  he  has  drawn  a  conclusion  as 
to  marbles  in  general  from  the  marbles  he  happens  to  have  seen  and 
felt,  and  has  reasoned  in  that  mode  which  is  technically  termed 
induction.  If  he  declines  to  try  to  break  a  marble  with  his  teeth,  it 
is  because  he  consciously,  or  unconsciously,  performs  the  converse 
operation  of  deduction  from  the  general  rule  '  marbles  are  too  hard 
to  break  with  one's  teeth.'  .  .  .  The  man  of  science,  in  fact,  simply 
uses  with  scrupulous  exactness  the  methods  which  we  all,  habitually 
and  at  every  moment,  use  carelessly." 

While  medicine  is  to  a  certain  extent  a  science,  and  requires  sci- 
entific modes  of  reasoning,  medical  art  is,  in  a  large  proportion  of 
cases,  obliged  to  reason  from  probabilities  as  premises,  and  its  final 
results  can  not  be  expressed  in  the  exact  formulas  of  the  mathema- 
tician. In  obedience  to  some  law  which  we  do  not  yet  know,  2 
and  2  do  not  always  make  4  in  the  reactions  of  the  human  body, 
otherwise  patients  would  not  be  encountered  who  present  serious 
symptoms  after  a  medicinal  dose  of  morphine,  or  blaze  out  with 
urticaria  after  eating  strawberries. 


PRELIMINARY  CONSIDERATIONS  5 

To  study  and  to  compare  ;  to  approach  a  case  with  a  mind  open 
to  impressions,  and  without  preconceived  or  fixed  ideas  as  to  its 
nature,  based  upon  previous  hearsay  ;  to  review  and  balance  the 
evidence  from  time  to  time  in  the  course  of  the  disease ;  to  ques- 
tion one's  self  "  Is  there  any  other  disease  or  condition  which  may 
l)etter  explain  these  symptoms  than  that  which  I  have  already 
assigned  ?  " — these  and  other  habits  of  thought  make  the  difference 
between  the  man  who  sees  without  learning  and  he  who  learns  by 
seeing. 

Obtaining  Evidence.— The  diagnostician  acquires  the  facts 
upon  which  he  is  to  form  an  opinion  :  (1)  By  Ititerrogation — in- 
quiry of  the  patient  or  his  friends ;  (2)  by  Observation— dm  ex- 
amination, mainly  objective,  of  the  patient.  Information  obtained 
by  interrogation  is  called  the  History  or  Anamnesis  (remembrance) ; 
that  derived  from  observation,  the  Present  Condition  or  Status 
Prwsens. 

From  a  purely  scientific  and  diagnostic  point  of  view,  the  first 
questions  addressed  to  the  patient  will  be  with  reference  to  his  an- 
cestry ;  next,  in  regard  to  his  personal  history  antecedent  to  the 
present  disease  ;  then  as  to  the  existing  disease,  followed  by  a  care- 
ful and  systematic  examination,  first  of  the  general  condition,  then 
of  special  organs,  one  by  one,  together  with  such  chemical,  micro- 
scopical, bacteriological,  and  other  investigations  as  appear  to  be 
demanded.  But  for  obvious  reasons  this  order  of  pursuing  the  inves- 
tigation is  for  the  most  part  impracticable,  and  consumes  an  un- 
necessary amount  of  time. 

In  the  vast  majority  of  cases  the  facts  are  acquired  by  the  physi- 
cian in  the  reverse  order.  The  first  question  asked  is,  "  In  what 
way  do  you  feel  ill  ?  "  "  Of  what  are  you  complaining  ?  "  Or,  the 
patient  will  volunteer  a  statement  as  to  his  subjective  sensations. 
The  question  or  the  statement  will  direct  attention  at  once  to 
the  probable  or  possible  seat  or  nature  of  the  disease.  Further  in- 
quiries are  put  as  to  the  duration  and  character  of  the  morbid 
sensations.  During  these  interrogations  the  physician  attentively 
scrutinizes  the  general  aspect  of  the  patient  in  search  of  obvious 
objective  symptoms.  The  pulse,  respiration,  and  temperature  are 
taken.  The  organ  or  part  which  appears  to  be  most  at  fault  is 
first  examined,  after  which  due  attention  is  paid  to  other  por- 
tions of  the  body.  Finally,  the  family  and  social  history  may  be 
ascertained. 

This  is  the  logical  order  of  investigation,  as  conditioned  by  actual 
circumstances.  It  is  a  matter  of  indifference  as  to  the  sequence  in 
which  the  symptoms  are  learned,  provided  that  the  examination  is 
3 


6  THE  DIAGNOSTICS  OF  INTERNAL  MEDICINE 

sufficiently  intelligent  and  systematic  to  be  sure  of  eliciting  all  the 
facts,  and  that  the  facts  when  obtained  are  so  arranged  in  the  mind 
of  the  physician  that  they  form  a  clear  and  coherent  picture,  and 
are  capable  of  being  recorded  in  an  orderly  manner.  It  is  to  be 
remembered  in  this  connection  that  in  many  cases  it  is  just  as  neces- 
sary to  note  negative  facts — i.  e.,  the  absence  of  certain  symptoms  or 
signs — as  it  is  to  ascertain  the  presence  of  others. 

Keeping  Case  Histories. — This  habit  promotes  accuracy  of 
observation,  completeness  in  examination,  and  affords  trustworthy 
material.  The  physician  who  keeps  adequate  records  acquires  facil- 
ity in  describing  symptoms,  signs,  and  morbid  conditions.  The 
drawbacks  are  the  time  consumed  and  the  amount  of  work  involved, 
but  by  late  methods  the  time  and  labour  required  are  reduced  to  a 
minimum.  To  accomplish  this  requires  certain  materials  and  acces- 
sories. The  essential  elements  (Dickinson)  of  the  outfit  are  of  two 
kinds :  (1)  Cards  made  and  handled  according  to  the  card  cata- 
logue system,  and  (2)  rubber  stamps  made  to  suit  individual  re- 
quirements. 

(1)  Card  Outfit. — Eecords  are  made  (Figs.  1  and  2)  upon  cards- 
(6  by  6f  inches),  one  or  more  being  used  for  each  case,  standing  on 
edge  in  a  box  or  drawer  and  ranged  under  an  alphabetical  index, 
each  letter  printed  on  a  buff  Bristol  card  (guide  or  index  cards) 
which  stands  higher  than  the  history  cards. 

The  size  of  the  history  card  is  such  that,  by  folding  once  (the 
line  of  the  fold  must  be  vertical),  it  will  fit  into  the  pocket-book 
or  visiting  list.  The  cards  are  kept  in  a  box  with  a  sliding  top, 
or  with  a  lid  which  is  the  upper  third  of  the  box  (Fig.  3).  When 
Mr.  A.  or  Mrs.  S.  enters  the  consulting  room,  the  cards  under  A  or  S- 
are  picked  up  and  shuffled  through  until  the  desired  one  is  found. 
The  necessary  record  or  entry  is  made  and  the  card  returned  to- 
its  proper  place.  For  patients  ill  at  home,  cards  are  picked  out  and 
placed  in  the  pocket-book  before  starting  on  morning  rounds.  Cards 
of  convalescents  are  dropped.  If  two  or  more  cards  are  found  to  be 
necessary  for  a  long  case,  they  may  be  fastened  together  with  a  brass 
clip. 

Cards  differing  in  colour  are  useful  for  special  purposes,  i.  e.,  buff- 
coloured  cards  for  consultation  cases,  salmon  colour  for  surgical  cases, 
and  the  like.  Another  method  of  special  classification  is  to  have  two- 
or  more  alphabetical  indexes,  the  cards  which  belong  to  a  special 
class  of  cases  being  ranged  under  the  corresponding  separate  index, 
in  the  same  box  or  drawer.  Loose  notes,  letters,  or  sketches  may  be 
pasted  to  the  case  card  or  kept  in  envelopes  of  the  same  size  as  the 
cards  and  filed. 


'     PRELIMINARY   CONSIDERATIONS  9 

Temperature  cards  (Chart  1),  urinalysis  cards  (Fig.  4),  and  cards 
for  blood  examinations  (Chart  IX)  have  been  devised  by  De  Forest. 

(2)  /Rubber  Stamps. — These  are  of  two  kinds — outline  stamps  and 
stamp  forms  for  recording  special  data. 

Outline  Stamps. — These,  as  the  name  indicates,  are  rubber  stamps 
representing  in  more  or  less  detail  various  regions  or  organs  of  the 
body,  and  employed  when  it  is  desired  to  represent  by  the  graphic 
method  any  changes  of  structure,  the  exact  location  and  character  of 
physical  signs,  the  outline  of  tumours,  etc.     An  ink  pad  is  required, 


Fig.  3. 


preferably  red  or  blue.  The  case  card  is  placed  upon  a  level  surface, 
the  stamp  inked,  and  adjusted  on  the  desired  place,  and  a  quick, 
light  blow  given  with  the  palm  of  the  hand.  On  the  outline  thus 
printed  may  be  sketched  or  written  with  pen  or  pencil  whatever 
abnormalities  it  is  desired  to  represent.  Further  changes  which 
occur  may  be  entered  on  tlie  same  outline,  the  date  being  appended, 
or  a  new  print  may  be  made.  The  use  of  the  outline  stamp  has 
proved  invaluable,  because  of  the  increased  accuracy  of  observation 
to  which  it  leads,  even  leaving  out  of  consideration  its  value  as  a 
record.     (See  Figs.  1  and  2,  red  outlines.) 


PkMtii     %.  t. 


3/^9& 


aUANTITV    IN    24    HOURS 


REACTION 


SPECIFIC    GRAVITV 


sex.     ACE.    NATIONALITV. 

Urinalysis 


f^^ 


CHLORIDES 


PEPTONES 


6e:«>0SIT  on  8TANDIN& 


/Yt>^.</-y 


CRYSTALS 


ADVENTITIOUS     ELEMENTS 


MORPHOLOGIC     ELEMENTS 


^'U^.-a^   K^  CU^S-  tU^  -d^c^ 


n^tc-d-tC     U^aJUJ^^  ^  i^^%x:Jie£i^JL^ 


DIAGNOSIS 


^outH    cCa^jx^'-^^  7Lfcy»^->£:z^'vr 


Fig.  4. 


PRELIMINARY  CONSIDERATIONS  H 

Type  Stamps. — These  are  used  in  noting  any  set  of  answers  which 
require  frequent  asking,  or  which  may  be  involved  in  special  investi- 
gations, like  the  following  example  : 

SHORT  MED  TALL  FT  IN  :  STOUT  THIN  WEIGHT  LBS: 

BLON  BRU  INDETER:  EYES  BLU  BR  BLK  :  SLIGHTLY  VERY  NEUROTIC: 
MENTALITY  HIGH  MED  LOW:  SLEEPS  WELL  POORLY:  APPT  GOOD 
POOR:  VOMITG  ERUCTS  FULNESS  DISCOMF  PAIN  IMMED  HRS 
AFTcR  BEFORE  EATING  :  BOWELS  HABITUAL  OCCAS  CONSTIP  LOOSE 
REG  FLATULENCE:  URINATION  NOT  FREQ  PAINFUL:  URINE  AMT 
INCREAS  DIMIN  :  MENSES  PAIN  SLIGHT  SEVERE  NOT  REG  FREE 
SCANTY  VAG  DISCH  LABOURS  SEVERE  NO  FEVER  :  TOBACCO  HABIT 
OCCAS  MOD  EXCESS:  COFFEE  TEA  BOTH  HABIT  OCCAS  MOD  EXCESS: 
PULSE  RATE  NOT  REG  TENSION  HIGH  LOW  :  ARTERIES  HARD  SOFT: 
RESP  RATE  COSTAL  ABDOM   EXPANS  GOOD   POOR  :  TEMP 

A  large  amount  of  writing  is  saved  by  this  device.  The  imprint 
is  made  in  the  same  manner  as  with  the  outline  stamps.  The  words 
required  are  underlined,  special  emphasis  indicated  by  double  under- 
lining, and  doubtful  points  followed  by  a  question  mark.  Any  de- 
sired set  of  words  can  be  made  to  suit  individual  requirements.  The 
set  should  not  cover  a  space  greater  than  14^'  X  3",  or  2"  X  4',  as  a 
larger  size  will  not  print  evenly.  The  stamp  may  be  a  self-inker  or 
a  hand  stamp.  The  hand  stamp  is  less  expensive  and,  with  care  in 
printing,  answers  perfectly. 


PART   I 
THE  EVIDENCES   OF  DISEASE 


SECTION  I 

CONSIDEEATIOXS,    NEITHER    SYMPTOMS    NOR    SIGNS, 
WHICH    MAY   QUALIFY   OR  SUGGEST   A   DIAGNOSIS 

The  considerations  which  may  qualify  or  suggest  the  diagnosis 
in  a  given  case  relate  to  the  family  history  or  hereditary  tendencies, 
and  the  personal  history  up  to  the  date  of  the  present  illness.  The 
personal  history  includes  age,  sex,  nationality,  occupation,  residence, 
hahits,  and  previous  diseases  or  injuries.  Such  considerations  em- 
brace also  the  chronological  occurrence,  seasonal  or  diurnal,  of  cer- 
tain diseases,  and  the  comparative  infrequency  of  others. 

I.  Family  History. — The  family  history  of  the  patient  is  of  much 
importance,  because  of  the  light  which  may  be  cast  by  it,  not  only 
upon  the  present  illness,  but  also  upon  the  constitution  and  tenden- 
cies of  the  patient. 

Unfortunately,  it  is  not  always  possible  to  obtain  a  complete  and 
accurate  family  history.  It  is  usually  necessary  to  cross-examine  the 
patient  with  some  particularity,  inquiring  into  the  symptoms  and 
duration  of  illnesses  attributed  to  ancestors,  and  bearing  in  mind  the 
approximate  meanings  of  various  popular  terms,  such  as  "gastric 
fever,"  "  dropsy,"  "  blood-poisoning,"  "  teething,"  "  cold,"  "  nervous 
prostration,"  which  latter  may  cover  insanity  or  hysteria.  "  Old 
age  "  is  frequently  assigned  as  a  cause  of  death,  which  has,  of  course, 
little  meaning.  "  Childbirth,"  when  assigned  as  a  lethal  cause,  not 
infrequently  proves  to  be  a  rapid  phthisis  pulmonalis. 

Inquiries  regarding  certain  diseases  should  be  made  very  cau- 
tiously, because  of  the  possibility  of  arousing  feelings  of  shame  or 
fear  in  the  patient.  It  is  better  to  ask  if  there  is  "  lung  trouble  "  in 
the  family  than  to  use  the  word  "  consumption."  So,  too,  it  is 
strongly  advisable  to  ask  after  the  symptoms  without  mentioning 
the  names  of  suspected  syphilis,  tuberculosis,  or  cancer.  There  is 
a  certain  reproach  to  family  or  personal  pride  in  the  acknowledg- 
ment of  the  existence  of  some  ailments,  which  may  lead  to  the  con- 
cealment of  important  information. 

13 


u 


THE  EVIDENCES  OF  DISEASE 


A  full  statement  of  the  family  history  includes  the  nature  of  the 
illnesses  (with  the  age  of  the  living)  and  the  causes  of  deaths  (with 
the  age  at  death)  which  may  have  occurred  in  the  patient's  parents, 
paternal  and  maternal  grandparents,  brothers  and  sisters.  It  is 
requisite  at  times  to  ascertain  similar  facts  with  reference  to  aunts, 
uncles,  and  cousins.  It  should  be  borne  in  mind  that  transmissible 
tendencies  may  pass  over  one  generation. 

It  is  important  during  this  inquiry  to  bear  in  mind  that  certain 
diseases  are  either  frequently  associated  or  are  manifestations  of  a 
common  cause.  In  some  cases  there  is  a  curious  alternation  between 
two  diseases,  one  replacing  the  other — e.  g.,  migraine  and  epilepsy. 
This  may  occur  in  the  individual,  or  in  alternating  generations. 

Heredity  may  be  direct,  the  offspring  showing  the  lesions  of  the 
disease  at  birth,  as  in  syphilis.  In  the  majority  of  cases,  a  certain 
stamp  or  type  of  tissue  and  organization  is  transmitted  which  ren- 
ders the  individual  vulnerable  to  special  micro-organisms,  as  in 
tuberculous  subjects,  or  liable  to  perversions  of  the  nervous  system, 
or  prone  to  degenerations  and  disturbances  of  metabolism. 


HEREDITARY  DISEASES  OR  CONDITIONS 


Rheumatism. 
Cardiac  diseases. 
Chorea. 
Nephritis. 
Renal  calculus. 
Emphysema. 
Bronchitis. 
Psoriasis. 

Tuberculosis. 
Phthisis  pulmonalis. 
Tuberculous  glands. 
Tuberculous  disease  of  bones. 
Tuberculous  peritonitis. 
Tuberculous  meningitis. 
Hydrocephalus. 


Insanity. 

Hysteria. 

Hypochondria. 

Epilepsy.  ; 

Migraine. 

Neuralgias. 

Many  neuroses. 

Gout. 

Diseases  of  the  liver. 

Chronic  nephritis,  especially  cirrhotic. 

Renal  calculus. 

Angina  pectoris. 

Cardio- vascular  disease. 

Apoplexy. 

Asthma. 


Haemophilia. 

Diabetes. 

Syphilis. 

Alcoholism. 

Acne. 

Eczema. 

Ichthyosis. 

Leprosy. 


Lichen. 
Naevus. 

Malformations. 

Pseudo-hypertrophic  paralysis. 
Progressive  muscular  atrophy. 
Huntington's  chorea. 
Thomsen's  disease. 
Friedreich's  ataxia. 


AGE— INFANCY   AND  CHILDHOOD  15 

A  list  of  diseases  and  conditions  which  are  considered  to  be  trans- 
missible in  varying  degrees  is  given  on  the  preceding  page.  The 
bracketed  groups  are  composed  of  those  which  have  afl&liations  either 
of  conjoint  occurrence  or  common  causes. 

II.  Age. — Anatomical  structure  varies  with  age,  and  physiological 
processes  have  peculiarities  which  are  characteristic  of  different 
periods  of  life.  Moreover,  the  effects  of  environment,  occupation, 
habits,  the  beginning  and  end  of  sexual  life,  and  the  wearing  out  of 
the  organism  by  constant  friction,  are  necessarily  manifested  at  vary- 
ing ages.  Consequently  there  is  a  distinct  preponderance  in  the 
frequency  of  certain  diseases  or  classes  of  disease  at  special  age  pe- 
riods. The  diseases  of  youth  are  often  the  direct  progenitors  of 
those  of  old  age,  and  the  life  of  the  individual  may  be  a  constant 
struggle  with  diseased  conditions  which  began  in  antenatal  life. 

(1)  Infancy  and  Childhood. — At  this  age  there  is  a  special  liability 
to  digestive  disorders,  because  of  the  relatively  large  amount  of  work 
required  to  meet  the  pressing  needs  of  a  rapidly  developing  organ- 
ism, and  because  of  the  peculiar  susceptibility  to  infection  of  the 
gastro-intestinal  tract  in  children.  Inflammations  of  the  respiratory 
apparatus  are  frequent,  because  oi  the  tendency  of  the  cells  of  the 
mucous  membranes  to  undergo  rapid  proliferation  under  slight  and 
unaccustomed  irritations.  Xervous  diseases  and  reflex  disturbances 
are  common  for  the  reason  that  the  cerebro-spinal  and  sympathetic 
apparatus  is  developing,  and  has  not  yet  settled  into  habits  of  regu- 
lar innervation.  This  is  also  the  age,  above  all  others,  at  which  the 
organism  is  susceptible  to  certain  infectious  diseases — the  exan- 
themata. 

The  following  diseases  are  those  which  are  most  common  at  this 
age  period.  Some  are  congenital.  Diseases  mentioned  under  a  given 
head  may  begin  later  than  the  period  under  which  they  are  classed. 

Post-pharyngeal  abscess.  Endocarditis. 

Amyloid  disease.  Disease  of  the  lymph  glands. 

Bronchitis.  Haemophilia. 

Convulsions.  Hydrocephalus, 

Primary  renal  sarcoma.  Idiocy. 

Cretinism.  Intertrigo. 

Soft  cataract.  Impetigo  contagiosa. 

Chorea.  Intussusception. 

Diarrhoeal  diseases.  Lumbrici. 

Diphtheria.  Laryngismus  stridulus. 

Eczema.  Diphtheria  of  the  larynx. 

Epilepsy  (beginning).  Spasmodic  laryngitis. 


16 


THE  EVIDENCES  OF  DISEASE 


Malformations. 

Measles. 

Meningitis. 

Mumps. 

Naevi. 

Noma. 

Infantile  paralysis. 

Pseudo-hypertrophic  paralysis. 

Pemphigus. 

Lobular  pneumonia. 

Progressive  muscular  atrophy. 

(2)  Puberty  and  Adolescence 
Acne. 

Addison's  disease. 

Anaemia. 

Chlorosis. 

Catalepsy. 

Epilepsy. 

Fever. 

(3)  Middle  Age : 
Aneurism. 
Angina  pectoris. 
Apoplexy. 
Cancer. 
Diabetes. 

Gout. 
Gallstones. 
Hypochondriasis. 
Leucocythemia. 

(4)  Old  Age: 
Aortic  disease. 
Atheroma. 

Cerebral  degenerations. 
Chronic  bronchitis. 


Bachitis. 

Roseola. 

Rotheln. 

Scarlatina. 

Seborrhoea. 

Strophulus. 

Congenital  syphilis. 

Tetany. 

Varicella. 

Variola. 


Hysteria  and  spinal  irritation. 

Exophthalmic  goitre. 

Myxcedema. 

Lobar  pneumonia. 

Acute  rheumatism. 

Acute  tuberculosis. 

Gastric  ulcer. 


Melancholia. 
MoUities  ossium. 
Myxcedema. 
Paralysis  agitans. 
General  paresis. 
Bulbar  paralysis. 
Sciatica. 
Stricture  of  rectum. 


Degenerations  of  the  heart. 
Broncho-pneumonia. 
Prostatic  diseases. 
Gangrene  of  extremities. 


III.  Sex. — Putting  aside  the  diseases  due  to  differences  in  struc- 
ture and  function  between  male  and  female,  there  remain  certain 
maladies  which  occur  more  frequently  in  one  sex  than  in  the  other. 
These  discrepancies  are  caused  mainly  by  the  manner  of  life.  Men 
suffer  especially  from  diseases  induced  by  exposure,  hard  physical  or 
mental  work  and  worry,  and  by  the  acquirement  of  injurious  habits. 


SEX— NATIONALITY 


17 


Women  lead  an  indoor  life,  and  many  are  harassed  by  household 
and  domestic  anxieties.  If  not  occupied  by  domestic  cares,  or  if 
without  definite  aims  and  interests,  a  habit  of  morbid  self-examina- 
tion is  apt  to  be  formed.  Moreover,  the  nervous  system  in  women 
is  normally  more  unstable  in  its  equilibrium.  Because  of  all  these 
factors,  functional  nervous  diseases  (neuroses)  are  much  more  com- 
mon in  women  than  in  men. 

The  following  list,  which  is  by  no  means  exhaustive,  contains 
some  of  the  more  common  diseases,  classified  according  to  sex  fre- 
quency.    The  figures  are  only  approximate. 

(1)  Males  : 


Aneurism  in  general. 

Abdominal  aneurism,  8  to  1. 

Angina  pectoris. 

Progressive  muscular  atrophy,  6 
to  1. 

Locomotor  ataxia. 

Carcinoma  of  the  stomach  or  rec- 
tum, 2  to  1. 

Diabetes,  2  to  1. 

Epilepsy. 

Haemophilia,  11  to  1. 

(3)  Females  : 
Anaemia. 

Arthritis  deformans. 
Catalepsy. 
Chloro-ansemia. 
Chorea. 

Erythema  nodosum. 
Gallstones. 

Goitre  (ordinary  and  exophthal- 
mic). 

In  women  the  regularity,  profuseness,  and  attendant  pain  of  the 
menstruation,  the  number  of  pregnancies  and  miscarriages  and 
their  sequelae  should  be  ascertained,  for  the  reason  that  deviations 
from  the  normal  in  these  respects  may  be  of  much  importance  as 
possible  causes  of  subsequent  disease. 

IV.  Nationality. — The  susceptibility  or  its  opposite,  immunity, 
possessed  by  certain  races  has  been  commented  upon  by  some  ob- 
servers. Among  these  may  be  noted  the  liability  of  the  Jewish  race 
to  diabetes,  of  the  Scandinavian  and  African  to  phthisis  pulmonalis, 
and  the  comparative  immunity  of  the  African  to  yellow  fever. 


Fatty  heart,  2  to  1. 

Gout. 

Chronic  gastritis. 

Hypochondriasis. 

Intussusception. 

Leucaemia,  3  to  1. 

Pseudo-leuc»mia,  3  to  1. 

General  paresis. 

Pseudo-hypertrophic  paralysis. 

Typhoid  fever,  4  to  1. 

Valvular  diseases  of  heart. 

Hysteria. 

Movable  kidney. 

Myxoedema. 

Neuralgias. 

Neurasthenia. 

Osteomalacia,  30  to  1. 

Spinal  irritation  (neurasthenia). 

Ulcer  of  the  stomach. 


18  THE  EVIDENCES  OF  DISEASE 

V.  Occupation. — ^^'ith  reference  to  the  effects  of  occupation  in 
causing  disease,  it  will  be  found  necessary  to  ascertain  the  details  of 
the  patient's  employment,  whether  active  or  sedentary  in  character, 
and  whether  or  not  it  requires  the  handling  or  breathing  of  toxic  or 
irritating  substances.  Possible  overuse  of  the  eyes,  playing  wind 
instruments,  and  the  care  of  domestic  animals,  are  other  details  a 
knowledge  of  which  may  be  useful.  All  previous  occupations  should 
be  ascertained.  It  should  be  remembered  that  the  state  of  health 
sometimes  enforces  the  occupation. 

(1)  Diseases  Incident  to  Active  Occupations : 
Aneurism.  Pneumonia.  Rheumatism. 

(2)  Diseases  Incident  to  Sedentary  Occupations,  including  Mental 
Work  : 

Anaemia.  Gallstones.  Xeuroses. 

Chlorosis.  Haemorrhoids.  Obesity. 

Constipation.  Hysteria.  Ulcer  of  the  stomach. 

Digestive  disorders.  Hypochondriasis. 

(3)  Diseases  Incident  to  Special  Occupations  : 

Pulmonary  phthisis. — Accountants,  book-keepers,  clerks,  compositors, 
printers,  pressmen,  marble  and  stone  cutters. 

Fibroid  phthisis,  from  dust. — Grinders,  file  cutters,  potters,  glass  polishers, 
wool  and  cotton  spinners,  millers. 

Anthrax. — Skin  handlers. 

Internal  anthrax.— Wool  and  rag  sorters. 

Glanders  and  tetanus. — Hostlers. 

Anaemia,  gastric  ulcer,  eczema,  erythema  nodosum. — Domestic  servants 
(female). 

Varicose  veins. — Coachmen,  shop  girls,  and  others  accustomed  to  long 
maintenance  of  the  standing  or  part  standing  position. 

Writer's  cramp  (scrivener's  palsy). — Clerks  and  writers. 

Septic  infection. — Butchers  and  slaughterhouse  employees. 

Conjunctivitis. — Electric-light  workers.     Probably  caused  by  actinic  rays. 

Nystagmus.  — Miners. 

Emphysema. — Players  upon  wind  instruments. 

Insomnia,  dyspepsia,  disease  of  liver  and  kidneys,  neurasthenia,  irritable 
heart,  apoplexy,  and  paralysis. — Brain  workers. 

Typhoid  fever,  pneumonia,  cardio- vascular  and  renal  disease,  morphine  and 
cocaine  habits. — Physicians. 

Lead  poisoning. — Lead  miners  and  smelters,  painters,  gilders,  makers  of 
white  and  red  lead,  seamstresses  (from  silk  thread  loaded  with  acetate  of  lead), 
makers  of  artificial  flowers. 

Mercurial  poisoning. — Cinnabar  miners,  makers  of  cheap  looking  glasses  or 
mirrors,  makers  of  felt  hats  (from  the  bath  of  acid  nitrate  or  mercury  used  to 
promote  felting). 


OCCUPATION— RESIDENCE  19 

Arsenical  poisoning. — Wall-paper  workers  (formerly),  workers  on  artificial 
flowers  and  fancy  glazed-paper  boxes. 

Phosphorus  poisoning.  — Matchmakers. 

Chromium  and  zinc  poisoning. — "Founders'  ague  "  in  brass  foundries. 

Disease  of  hair  follicles. —Operatives  in  oil  refineries  and  paraffin  works. 

VI.  Residence. — A  knowledge  of  the  place  of  residence  may  be  of 
considerable  importance,  if  not  with  regard  to  diagnosis,  at  least  with 
regard  to  the  prophylaxis  of  future  attacks.  In  the  diagnosis  of  sus- 
pected cases  of  cholera,  yellow  fever,  and  the  pernicious  or  severe 
malarial  fevers,  the  fact  of  the  patient  having  visited  or  lived  in 
countries  or  localities  where  they  are  prevalent  may  furnish  a  clew 
otherwise  lacking.  Goitre,  rachitis,  calculus,  cretinism,  dysentery,  and 
lung  diseases  have  at  times  special  affinities  with  certain  localities. 

The  following  list  comprises  the  more  important  geographical 
associations  of  disease,  which  may  be  of  diagnostic  value  in  connec- 
tion with  a  patient  fresh  from  residence  in  the  countries  named : 

Africa. — Dengue,  Guinea- worm  disease. 

Africa,  South. — Bilharzia  hsematobia. 

Africii,  West  Coast. — Yellow  fever,  framboesia. 

America,  South. — Chigoe,  ainhum  (negro). 

AraVia. — Bilharzia  haematobia. 

Canada,  New  Brunsirick,  Cape  Breton. — Leprosy. 

China. — Beriberi,  bilharzia  haematobia. 

Egypt. — Bilharzia  haematobia,  plague. 

England,  Certain  Counties. —Renal  calculus. 

Europe,  Large  Cities. — Rachitis. 

France,  South  of. — -Pellagra. 

India,  East. — Beri-beri,  Delhi  boil,  dengue,  bilharzia  haematobia,  Asiatic 
cholera,  framboesia,  Guinea- worm  disease,  ainhum  (negro). 

West  Indies. — Chigoe,  dengue,  yellow  fever,  framboesia. 

Italy. — Goitre,  cretinism,  pellagra. 

Japan. — Beri-beri,  bubonic  plague,  bilharzia  haematobia. 

Malta. — Malta  fever. 

Morocco. — Plague. 

Naples. — Malta  fever. 

Noncay. — Leprosy. 

Spain. — Pellagra,  goitre  (Pyrenees). 

Switzerland,  Alps. — Goitre,  cretinism. 

Syria. — Plague. 

Tropical  Regions  in  General. — Epidemic  dysentery,  pernicious  intermittent 
and  remittent  fevers,  acute  hepatitis  and  hepatic  abscess,  leprosy,  filaria  san- 
guinis hominis. 

United  States,  Southern  Portion,  especially  the  Gulf  States. — Pernicious- 
intermittent  and  remittent  fevers,  yellow  fever  (epidemic),  dengue,  leprosy, 
filaria  sanguinis  hominis,  ainhum  (negro). 


20  THE  EVIDENCES  OF   DISEASE 

Other  items  embraced  under  the  head  of  residence  concern  the 
effects  of  climate,  city  or  country,  seashore  or  inland  residence,  and 
the  sanitary  condition  of  dwellings  with  reference  to  ventilation, 
drainage,  heating,  cleanliness,  and  water  supply. 

VII.  Habits. — The  habits  formed  by  individuals  are  so  closely 
interwoven  with  age,  occupation,  and  residence  that  it  is  only  neces- 
sary to  include  here  the  possible  existence  of  alcohol,  opium,  cocaine, 
or  other  drug  addiction.  Diet ;  the  use  of  tea,  coffee,  and  tobacco ; 
clothing,  sleep,  and  exercise  are  largely  governed  by  the  social  condi- 
tion and  environment.  In  men,  the  habits  as  to  the  frequency  of 
sexual  intercourse  and  a  history  of  early  self-abuse  require  investiga- 
tion. Ascertain  also  the  kind  and  amount  of  alcoholic  beverages  taken 
and  the  time  of  taking — i.  e.,  before,  during,  or  between  meals  (with 
reference  to  the  causation  of  sclerotic  changes  in  stomach,  liver,  kid- 
neys, arteries,  etc.).  How  much  tobacco  is  used,  of  what  kind,  and  in 
what  manner  (with  reference  to  naso-pharyngeal  catarrh,  nervous- 
ness, cardiac  neuroses). 

Both  men  and  women  should  be  interrogated  as  to  the  amount 
and  strength  of  tea  and  coffee  taken  daily.  The  "  tea-and-bread " 
habit  is  mainly  found  in  women. 

VIII.  Previous  Diseases  or  Injuries. — A  knowledge  of  prior  ill- 
nesses and  injuries  is  of  value,  provided  that  their  date,  nature,  and 
severity  can  be  ascertained,  for  three  reasons  : 

(1)  The  history  of  a  previous  attack  of  certain  diseases  renders 
subsequent  attacks  probable.     Among  such  diseases  are  : 
Apoplexy.  Gallstones. 

Asthma.  Malarial  fevers. 

Bronchitis.  J»[ephritis. 

Colic  (lead).  Neuralgia. 

Convulsions  (infantile  or  epileptic).     Pneumonia. 

Delirium  tremens.  Tonsilitis  (follicular  and  phleg- 

Diphtheria.  monous). 

Erysipelas.  Eheumatism. 

Gout. 

(2)  With  other  diseases,  a  previous  attack,  as  a  rule,  negatives 
its  subsequent  occurrence.     Among  these  are  : 

Measles  (not  uniformly).  Typhus  fever. 

Parotitis  (epidemic).  Variola. 

Pertussis.  Varioloid. 

Kotheln.  Varicella. 

Scarlatina.  Yellow  fever. 
Typhoid  fever. 

(3)  A  history  of  the  previous  existence  of  certain  diseases  or  in- 


PREVIOUS  OR  INFREQUENT  DISEASES  21 

juries  may  throw  light  upon  present  conditions  which  stand  in  the 
relation  of  sequelm  to  the  primary  ailments.  Examples  of  these  are  : 
Syphilis,  followed  by  skin  eruptions,  alopecia,  ulcers,  periostitis, 
gummata,  amyloid  diseases,  affections  of  the  nervous  system,  etc. 
Gonorrhoea^  with  reference  to  gonorrhoeal  rheumatism,  orchitis,  con- 
junctivitis, and  pelvic  tubal  inflammations  in  the  female.  Scarlet 
fever,  with  subsequent  middle-ear  inflammations,  renal  disease, 
and  rheumatism.  Rheumatism,  initiating  chronic  processes  which 
result  in  valvular  cardiac  lesions,  and  renal  disease.  Septic  or  sup- 
purating foci,  leading  to  subsequent  embolic  or  general  inflammations 
of  heart,  lungs,  liver,  pleura,  or  peritoneum. 

A  history  of  a  fall  or  other  injury  may  be  of  some  value  in  con- 
nection with  suspected  meningitis,  disease  of  the  spine,  and  arthritis. 
A  previous  surgical  operation  may  point  to  the  possibility  of  a  recur- 
rence of  the  condition  which  required  operative  interference. 

(4)  There  are  certain  diseases  of  which  a  diagnosis  should  be 
made  with  caution  because  of  the  infrequency  of  their  occurrence,  or 
the  difiiculty  of  their  recognition.  A  provisional  diagnosis  is  justified 
in  many  cases,  but  a  positive  diagnosis  of  the  diseases  in  the  follow- 
ing list  demands  good  evidence,  not  mere  conjecture.  This  list  ap- 
plies to  the  general  practitioner.  The  specialist  in  certain  lines  may 
and  does  have  a  different  experience. 

Acromegaly.  Hydatids  (except  of  liver). 

Actinomycosis.  Hysteria  (in  men). 

Addison's  disease.  Hydrophobia. 

Anthrax.  Leucaemia. 

Aneurism  of  pulmonary  artery  or      Abscess  of  liver. 

of  abdominal  aorta.  Acute  yellow  atrophy  of  liver. 

Athetosis.  Acute  inflammation  of  liver. 

Atrophy  of  brain   and   poren-  Cerebro-spinal    meningitis    (ex- 

cephalus.  cept  when  epidemic). 

Catalepsy.  Mollities  ossium. 

Asiatic  cholera  (except  when  epi-      Myxoedema. 

demic).  Landry's  paralysis. 

Chyluria.  Pancreatitis. 

Malignant  endocarditis.  Raynaud's  disease. 

Glanders.  Amyotrophic  lateral  sclerosis. 

Haemophilia.  Scleroderma. 

Aneurism  of  heart.  Acute  inflammation  of  spleen. 

Abscess  of  heart.  Tetany. 

Disease  of  pulmonary  valve.  Tetanus. 

Primary  disease  of  tricuspid  valve.     Trichinosis. 
Hodgkin's  disease. 
4 


22  THE  EVIDENCES  OF  DISEASES 

(5)  There  is  little  of  diagnostic  value  to  be  gained  from  the  vary^ 
ing  statistics  of  the  seasonal  prevalence  of  disease^  beyond  the  broad 
statement  that  diarrhoea!  diseases  predominate  during  the  summer 
months,  while  pulmonary  disorders  and  rheumatic  affections  are  most 
prevalent  in  the  winter  and  early  spring.  Zymotic  diseases  occur  in 
largest  number  during  the  cold  season,  but  this  is  to  be  explained 
rather  by  the  opening  of  the  schools  and  the  closing  of  house  windows 
than  by  the  effect  of  season  per  se.  Typhoid  fever  has  a  notable 
seasonal  incidence  in  the  autumn  months. 

(6)  It  may  be  mentioned  here  that  certain  diseases  either  begin 
or  show  an  exacerbation  of  symptoms  at  special  diurnal  lyeriods. 
Bronchial  asthma  is  apt  to  make  its  onset  or  to  intensify  in  severity 
in  the  early  morning  hours ;  spasmodic  croup,  as  well  as  diphtheritic 
stenosis  of  the  larynx,  between  10  and  12  at  night.  The  suffering 
from  painful  diseases  is  usually  worse  at  night,  and  in  febrile  disor- 
ders the  temperature  generally  reaches  its  highest  point  between  7 
and  8  p.  m.  The  paroxysms  of  whooping-cough  are  more  frequent 
and  severe  at  night.  The  pain  due  to  diseases  of  the  bones  and  joints 
presents  a  nocturnal  aggravation. 


SECTION   II 
THE  HISTOEY   OF  THE  PRESENT   ILLNESS 

It  is  desirable  to  obtain  a  full  and  accurate  history  of  the  present 
illness,  as  in  all  cases  it  is  more  or  less  necessary,  in  some  absolutely 
essential.  The  greater  part  of  this  history  is  subjective,  but  there 
may  have  been  some  symptoms  sufficiently  objective  to  have  been 
observed  by  the  patient,  such  as  oedema  or  hemorrhages. 

It  is  in  obtaining  this  history  that  the  largest  draughts  are  made 
upon  the  tact  and  experience  of  the  physician.  The  patient  may  be 
one  of  the  odd  people  from  whom  it  is  difficult  to  extract  more  than 
a  monosyllabic  answer,  or  may  be  so  talkative  that  a  question  is 
slipped  in  only  after  patient  waiting  for  a  pause.  Dense  ignorance 
may  be  an  obstacle,  so  also  may  false  modesty  or  shame.  Exaggera- 
tion of  symptoms,  a  not  uncommon  failing, must  be  guarded  against; 
less  often  its  opposite,  a  stoic  pride  in  making  light  of  pain.  These 
and  other  difficulties  (e.  g.,  malingering)  require  the  exercise  of  some 
skill  in  the  art  of  cross-examination. 

Except  in  the  case  of  suspected  malingering,  where  the  answer 
may  flatly  contradict  the  alleged  condition,  leading  questions  are  to 
be  avoided,  especially  with  impressionable  or  ignorant  patients.     For 


THE   HISTORY  OF  THE   PRESEXT  ILLNESS  23 

instance,  it  is  better  to  say,  "  Did  you  have  any  pain  in  the  head  ?  " 
than  "You  had  pain  in  the  head,  did  you  not?"  The  first  ques- 
tion is  a  simple  interrogation,  which  may  elicit  the  reply,  "  Yes  "  or 
"Xo."  The  second  almost  forces  the  answer  "Yes."  Care  is  to 
be  taken  lest  the  patient's  story  should  be  too  narrowly  limited, 
otherwise  a  knowledge  of  important  symptoms  may  not  be  gained. 
It  is  better  to  expend  additional  time  and  patience,  which  may  be 
utilized  in  a  careful  scanning  of  the  general  appearance,  behaviour, 
and  temperament  of  the  patient,  than  to  miss  a  possibly  vital  point 
in  the  history. 

The  physician's  object  in  this  portion  of  the  examination  is  to 
gain  a  clear  conception  of  the  origin  and  course  of  the  disease  up  to 
the  present  time.  The  inquiry  should  therefore  be  conducted  with 
reference  to  the  following  points  : 

(1)  Possible  Exciting  Causes — The  most  important,  with  refer- 
ence to  early  diagnosis,  is  a  known  exposure  to  some  infectious 
disease.  Other  causes  of  consequence  are  fatigue  of  mind  or  body, 
dietetic  imprudences,  toxic  agents,  and  chilling  of  the  body  or  "  tak- 
ing cold."  This  last  factor  is  frequently  assigned  by  patients  as  a 
satisfactory  etiological  explanation  of  the  most  diverse  ailments,  and 
is  a  convenient  substitute  for  other  demonstrable  causes. 

(2)  Date  and  Manner  of  Onset. — A  definite  statement  of  the  time 
of  onset  will  generally  place  the  disease  in  one  of  two  categories, 
acute  or  chronic.  Xevertheless  it  must  not  be  forgotten  that  an 
acute  attack  may  be  an  expression,  perhaps  the  first,  of  some  under- 
lying and  causal  disease  or  condition  ;  for  instance,  uraemic  convul- 
sions in  renal  disease.  As  a  rule,  however,  acute  diseases  begin  sud- 
denly, while  with  chronic  maladies  a  long  period  may  elapse  before 
the  symptoms  force  themselves  upon  the  attention  of  the  patient. 
Lobar  pneumonia  and  cirrhosis  of  the  liver  may  be  cited  as  illustra- 
tions, respectively,  of  acute  and  chronic  diseases. 

The  manner  of  onset  shoiild  be  accurately  ascertained,  strictly 
separating  tlie  symptoms  which  initiated  the  attack  from  those  which 
appeared  at  a  later  period,  for  otherwise  their  relative  importance 
may  not  be  appreciated. 

Closely  connected  with  the  date  and  manner  of  onset  are  the — 

(3)  Subsequent  Symptoms  in  the  Order  of  Appearance  up  to  the 
Present  Time. — The  value  of  a  strict  chronological  history  of  the 
symptoms  which  succeed  the  onset  of  any  disease,  can  not  be  over- 
estimated. In  some,  as  typhoid  fever,  the  diagnosis  may  depend 
largely  upon  the  order  of  evolution  of  the  present  symptoms.  Each 
symptom  should  be  elicited  and  the  time  of  its  appearance  borne  in 
mind. 


24  THE   EVIDENCES  OF  DISEASE 

(4)  Symptoms  now  Present. — The  present  sufferings  and  com- 
plaints of  the  patient  should  be  attentively  listened  to,  as  in  connec- 
tion with  previous  symptoms  they  may  determine  the  direction  of 
the  first  step  in  the  special  objective  examination.  Thus,  a  colicky 
pain  in  the  abdomen  will  prompt  an  immediate  palpation  of  the 
appendical  region.  Moreover,  the  present  condition  may  demand 
instant  palliative  or  other  treatment,  as  in  pulmonary  hemorrhage, 
before  the  physician  is  able  to  proceed  with  his  special  investigations. 

One  thing  more  is  needed  to  complete  the  antecedent  history — 
namely,  information  as  to — 

(5)  Previous  Treatment. — It  is  rarely  possible  to  obtain  reliable 
information  in  regard  to  previous  treatment.  The  statements  of 
patients  with  reference  to  the  therapeutic  agencies  used  by  previous 
physicians  are  ordinarily  quite  untrustworthy.  But,  if  such  knowl- 
edge can  be  obtained  from  authoritative  sources,  it  may  be  of  con- 
siderable value.  Thus,  certain  symptoms,  otherwise  unaccounted 
for,  may  be  explained  as  due  to  the  administration  of  certain  drugs 
(acne  from  bromides,  dilated  pupils  from  atropine,  etc.).  The  "  thera- 
peutic test"  may  have  been  applied,  and  the  result  weigh  for  or 
against  a  certain  diagnosis  (quinine  in  malaria,  in  the  absence  of  a 
blood  examination ;  mercury  and  iodides  in  suspected  syphilis). 


SECTION  in 

DIAGNOSTIC  IXDICATIONS  FEOM   THE   GEXEEAL 
APPEAKAXCE 

The  general  appearance  is  studied  with  reference  to  the  dress, 
height,  and  weight;  amount  and  character  of  adipose  and  muscular 
tissue ;  complexion,  colour  of  hair  and  eyes ;  diathesis  and  cachexia. 

I.  Dress  and  General  Behaviour. — An  occasional  hint  may  be 
derived  from  the  clothing.  Omission  to  use  fastenings  which  may 
be  needed  for  common  decency,  the  coat  or  trousers  buttoned  with 
the  wrong  buttons,  a  vest  soiled  with  droppings  of  food,  may  indi- 
cate the  mental  enfeeblement  of  a  psychosis  or  chronic  alcoholism. 
Clothing  wet  and  of  an  ammoniacal  odour  is  found  in  cases  of  incon- 
tinence of  urine  and  cystitis.  Diabetic  urine  in  drying  may  leave  a 
white  deposit  of  glucose.  The  patient  may  be  so  crowded  and  bulg- 
ing in  his  clothes  as  to  suggest  a  recent  rapid  increase  of  bulk  from 
obesity  or  general  dropsy.  The  shoes  may  be  left  partly  or  entirely 
unfastened  from  forgetfulness,  gout,  rheumatism,  or  oedema ;  or  slit 
for  similar  reasons,  or  because  of  corns,  bunions,  or  injury ;  or  worn 


HEIGHT  AND  WEIGHT 


25 


more  on  one  side,  or  in  front,  or  at  the  heel,  because  of  paralysis, 
deformity,  or  disease  of  the  joints. 

In  meeting  people  unprofessionally  one  forms  an  unconscious 
judgment  of  character  and  peculiarities  based  upon  the  observation 
of  small  details  of  behaviour.  These  judgments  are  often  useful 
outside  of  strictly  technical  lines  in  estimating  the  value  of  infor- 
mation received,  its  reliability,  completeness,  and  freedom  from 
exaggeration.  The  furtive  look  and  the  inability  to  meet  squarely 
the  eye  of  the  physician  may  indicate  mental  weakness,  morbid 
suspicion,  or  an  intention  to  deceive.  This  manner,  however,  is  not 
always  to  be  interpreted  as  stated,  for  there  are  absolutely  upright 
people  who,  because  of  ingrained  timidity  or  bashfulness,  will  present 
a  most  striking  but  quite  baseless  hangdog  manner  and  expression. 

11.  Height  and  Weight  should  be  ascertained,  if  practicable,  by 
actual  measurement,  but  the  statements  of  the  patient,  and  the 
rough  estimate  which  may  be  made  by  the  eye,  are  sufficient  for 
diagnostic  purposes.  Height  is  qualified  by  the  adjectives  dwarfish, 
short,  medium,  tall,  very  tall.  Similar  qualifying  terms  with  refer- 
ence to  weight  comprise  emaciated,  thin,  spare,  medium,  stout, 
obese.  When  emaciation  is  extreme,  and  attended  with  a  general 
failure  of  strength  and  vitality,  it  is  called  marasmus. 

The  relation  of  height  to  weight  is  by  no  means  a  fixed  ratio,  and 
is  of  little  consequence  in  diagnosis.  Very  considerable  variations 
may  exist  without  indication  of  disease  and  without  creating  a  pre- 
disposition thereto.  An  abnormally  large  disparity,  other  things 
being  equal,  shows  that  the  balance  of  nutrition  is  disturbed,  and  in 
consequence  the  chances  of  longevity  are  lessened. 

HEIGHT-WEIGHT    RATIO 

6  feet  0  inches  in  height  should  weigh  115  pounds. 

"  «  120  " 

"  «  125  " 

«  "  130  " 

«  "  135  " 

«  "  140  " 

«  «  145  " 

«  «  150  " 

«  «  ■   155  " 

«  «  160  " 

"  "  165  " 

u  «  170  " 

«  «  175  " 

«  «  180  " 

«  «  185  " 

«  "  190  " 


5 

1      " 

5 

2      " 

5 

3      " 

5 

4      " 

5 

5      " 

5 

6       " 

5 

7      " 

5 

8      " 

5 

"9      " 

5 

10      " 

5 

11       " 

6 

0      " 

6 

1       " 

6 

2      " 

6 

3       '^ 

26  THE  EVIDENCES  OF  DISEASE 

Although  the  weight  of  the  body  at  any  one  time  has  compara- 
tively little  diagnostic  value,  it  is  otherwise  with  increase  or  loss  of 
weight  as  compared  with  former  measurements.  Change  in  the 
weight  of  the  body,  especially  in  some  chronic  diseases,  such  as 
tuberculosis,  is  in  most  cases  a  reliable  index  of  the  tendency  of 
the  malady,  progressive  loss  indicating  an  advance  of  the  disease, 
while  progressive  increase  in  weight  follows  a  lessened  activity.  In 
this  connection  it  is  important  to  remember  that  general  anasarca, 
ascites,  and  bulky  abdominal  or  other  tumours  may  cause  a  mislead- 
ing increase  of  body  weight. 

In  general,  persons  of  moderate  height  and  weight  are  best 
adapted  to  pass  successfully  through  the  ordinary  trials  of  life  and 
the  extraordinary  ordeals  of  disease.  But,  just  as  the  thin,  "  wiry  " 
individual  may  accomplish  an  enormous  amount  of  work  without 
excessive  fatigue  and  emerge  triumphantly  from  severe  illness,  so 
there  are  stout  (in  the  sense  of  obese)  and  hearty  people  who  decline 
to  grow  thin  or  to  be  worn  out  or  to  degenerate,  and  will  live  to  old 
age  in  spite  of  serious  acute  diseases. 

III.  Amount  and  Character  of  Adipose  and  Muscular  Tissue. — The 
subcutaneous  fat  is  a  large  element  in  the  weight.  Normally  it  is 
distributed  quite  equally  over  the  body,  but  may  accumulate  excess- 
ively on  some  particular  part,  especially  the  abdomen.  In  women 
after  the  menopause,  and  in  men  after  the  age  of  45,  there  is  fre- 
quently a  marked  increase  in  its  amount.  This  increase  is  most 
commonly  seen  in  sedentary  persons  who  consume  large  quantities 
of  food,  although  not  uncommonly  it  appears  to  be  an  inherited 
tendency.  The  quality  of  the  subcutaneous  fat  is  to  be  estimated 
by  the  touch :  good,  if  firm  and  elastic ;  poor,  if  soft  and  flabby. 

Loss  of  weight  is  ordinarily  first  observed  as  a  diminution  of  the 
subcutaneous  fat.  When  this  diminution  is  extreme,  the  skin  becomes 
loose,  owing  to  the  loss  of  its  foundation,  is  wrinkled,  and  can  be 
raised  in  folds.  On  the  other  hand,  in  obese  persons  the  skin  may 
be  overstretched,  so  that  lines  resembling  the  familiar  lineee  albicantes 
of  pregnancy  can  be  seen  upon  the  buttocks  and  abdomen. 

The  muscles  may  be  large  or  small  as  compared  to  the  bones. 
Size,  however,  is  not  of  so  much  importance  as  quality.  It  is  better 
to  possess  muscles  which  are  soft  and  of  moderate  bulk,  but  yet  firm, 
elastic,  and  quick-acting.  Flabby,  relaxed,  firm,  large,  small,  are  the 
terms  employed  in  describing  the  quality  of  muscles. 

The  bones,  by  comparison,  may  be  large,  thick,  and  prominent, 
or  small,  slender,  and  inconspicuous.  To  a  considerable  extent,  the 
visibility  of  bony  angularities  depends  upon  the  amount  of  subcuta- 
neous fat.      The   characteristic  rounded   curves   of   well-developed 


THE   DIAGNOSTIC  IMPORT  OP  CHANGES  IN  WEIGHT         27 

women  and  children  arise  not  only  from  the  smaller  bones,  but  also 
from  the  thicker  covering  of  fatty  tissue  which  belongs  normally  to 
the  sex  and  age. 

Special  deformities  and  alterations  in  the  shape  of  the  skeleton, 
eithei'  in  whole  or  in  part,  are  caused  by  certain  morbid  processes, 
and,  with  associated  symptoms,  constitute  recognised  forms  of  dis- 
ease. 

The  Diagnostic  Impoet  of  Changes  in  Weight 

As  alterations  in  weight  are  largely  dependent  upon  changes  in 
the  volume  of  the  subcutaneous  fat  and  the  muscles,  it  is  proper  to 
summarize  the  principal  conditions  in  which  the  weight  progressively 
increases,  progressively  decreases,  or  remains  stationary,  omitting 
normal  conditions  (rich  food,  sedentary  life,  middle  age,  menopause ; 
or  hardships  and  poor  food). 

It  is  stationary  or  increases  slightly  in  chloro-anaemia,  and  slight 
continuous  or  frequently  recurring  hemorrhages,  as  from  bleeding 
hemorrhoids. 

It  progressively  increases  in  pathological  obesity. 

It  progressively  diminishes  in 
Addison's  disease.  Marasmus, 

Hysterical  anorexia,  Stricture  of  esophagus. 

Cancer,  Obstruction  of  pylorus, 

Diabetes,  Ulcer  of  stomach, 

Chronic  diarrhoea,  Chronic  suppurations. 

Long-continued  fevers,  Obstruction  of  thoracic  duct, 

Prolonged  lactation.  Tuberculosis  (all  varieties). 

As  a  symptom,  progressive  emaciation  is  most  important  in  chronic 
diseases,  and  during  convalescence  from  acute  diseases.  Continuing 
loss  of  weight  in  the  latter  case  may  point  to  approaching  or  co- 
existing chronic  disease. 

IV.  The  Conformation  of  the  Body. — From  the  purely  aesthetic 
point  of  view  the  painter  or  sculptor  rarely,  if  ever,  finds  a  figure 
measuring  up  to  the  ideal  which  is  in  his  mind.  Certain  of  the  pho- 
tographs used  as  a  basis  for  illustrative  diagrams  in  this  volume  have 
been  made  from  professional  models  who  have  presumably  cliosen 
their  occupation  because  of  possessing  unusual  symmetry  of  figure, 
and  yet  in  nearly  all  there  are  obvious  defects  when  a  comparison  is 
made  with  the  acknowledged  masterpieces  of  figure  painting. 

From  the  medical  point  of  view  one  may  rather  easily  recognise 
certain  abnormalities  in  the  configuration  of  the  body  which  are  {a) 
congenital  and  predispose  toward  disease,  or  {h)  acquired  as  results, 
and  are  signs  of  disease. 


28  THE  EVIDENCES  OF   DISEASE 

(a)  There  are  two  congenital  types  of  body  which  predispose  to 
disease. 

1.  Tall,  thin  subjects,  with  small  bones,  slender  ribs,  and  a  long, 
narrow  thorax,  are  predisposed  toward  tuberculous  disease  of  the 
lungs. 

2.  Short,  stout,  thick-boned  persons  are  predisposed  toward  obesity 
and  its  attendant  evils.  If  the  thorax  is  wide  and  round,  emphysema 
is  liable  to  occur,  although  this  shape  of  chest  is  more  often  a  con- 
sequence than  a  cause. 

(b)  Certain  abnormalities  of  shape  result  from  the  following  dis- 
eases {q.  V.) :  Eachitis,  acromegaly,  myxoedema,  pulmonary  osteoar- 
thropathy, osteitis  deformans,  and  osteomalacia. 

The  colour  of  the  hair  and  eyes  is  of  little  importance,  but  it  is 
of  service  in  forming  a  complete  conception  of  the  case  to  note  the 
"  complexion."  Light  or  blonde,  dark  or  brunette,  indeterminate, 
may  be  employed  as  qualifying  terms  in  the  white  races.  The  colour 
of  the  hair  and  its  amount  {q.  v.)  as  symptoms  are  considered  else- 
where. 

V.  Diatheses  and  Cachexias. — There  are  some  differences  among 
lexicographers  as  to  the  meaning  of  the  terms  diathesis  and  cachexia. 
Following  and  defining  the  modern  usage,  it  is  to  be  understood  that 
diathesis  refers  to  a  congenital  habit  of  body,  and  cachexia  to  a  con- 
dition of  anaemia  and  debility,  as  follows  : 

1.  Diathesis. — A  diathesis  is  a  congenital  condition  or  habit  of 
body  which  predisposes  to  certain  constitutional  or  local  manifesta- 
tions of  disease. 

The  recognition  of  a  diathesis  is,  as  a  rule,  dependent  upon  the 
presence  of  a  certain  disease,  or  a  history  of  its  past  occurrence  in 
the  individual.  After  the  history  is  taken  and  the  examination  com- 
pleted, it  is  of  service  in  conveying  an  idea  of  the  patient  and  the 
general  trend  of  his  pathological  life,  to  state  the  diathesis  with  its 
qualifying  adjective.     The  qualifications  are  as  follows  : 

{a)  Gouty,  Arthritic,  Uric-acid,  or  LithcBinic  Diathesis. — A  dis- 
position to  gout  and  its  sequent  renal  and  cardio-vascular  changes — 
aneurism,  angina  pectoris,  and  cerebral  hemorrhage.  The  physical 
characteristics  of  the  individual  of  this  diathesis  are  said  to  be  a 
robust,  well-developed  body,  florid  face,  thick  hair,  and  good  teeth, 
hearty  appetite,  good  digestion,  and  a  strong  heart  with  high-pres- 
sured arteries. 

{h)  Tuierculous  {Phthisical,  Strumous,  Scrofulous)  Diathesis. — 
A  habit  of  body  which  is  vulnerable  or  predisposed  to  tuberculous 
disease  of  glands,  bones,  or  other  forms  of  tuberculous  infection. 
The  older  writers  recognised  two  types  which  are  not  infrequently 


DIATHESES  AND  CACHEXIAS  29 

seen  in  classical  perfection — viz.,  tlie  tuberculous,  with  oval  face, 
bright  eyes,  delicate  skin  and  colouring,  and  long,  slender  bones ; 
and  the  strumous,  with  a  heavy,  round  face,  thick,  muddy  skin, 
lumpy  figure,  and  thick  bones. 

(c)  Catarrhal  Diathesis. — There  are  many  persons  who  appear  to 
be  so  liable  to  various  chronic  inflammations  of  mucous  membranes 
that  it  is  convenient  to  characterize  them  as  belonging  to  the  catar- 
rhal diathesis. 

{(1)  Fatty  Diathesis  (Bazix). — A  term  applied  to  those  who  are 
obliged  to  battle,  oftentimes  unsuccessfully,  against  a  tendency  to 
pathological  obesity  and  fatty  overgrowth. 

{e)  Rheumatic  Diathesis. — A  predisposition  to  various  rheumatic 
affections — an  indefensible  but  useful  term. 

(/)  Hemorrhagic  Diathesis. — The  equivalent  of  haemophilia 
{q.  v.). 

(g)  Neuropathic  Diathesis. — A  predisposition,  frequently  hered- 
itary, to  diseases  of  the  nervous  system,  most  commonly  the  various 
neuroses.  It  is  among  this  class  that  drug  idiosyncrasies  are  most 
-apt  to  be  encountered.  The  diatheses  a,  </,  e,  /,  and  g  can  not  be 
^aid  to  present  physical  traits  which  are  in  any  degree  characteristic. 

(//)  Status  Lymphaticus. — Under  diatheses  may  be  classed  the 
status  lymphaticus  (lymphatism),  a  condition  not  often  encountered, 
occurring  mainly  in  children  and  young  persons.  The  lymph  glands, 
•especially  the  pharyngeal,  thoracic,  and  abdominal,  are  universally 
enlarged ;  the  lymphoid  marrow  of  the  bones  is  increased  in  amount 
and  red  marrow  may  replace  the  yellow  marrow  in  young  adults; 
the  thymus  gland  and  the  spleen  are  enlarged ;  and  there  is  defi- 
cient development  (hypoplasia)  of  the  heart  and  aorta.  The  body 
as  a  whole  is  undeveloped,  and  in  shape  retains  many  of  its  infan- 
tile characteristics.  Eachitis  frequently  co-exists.  Such  individuals 
have  a  veiy  small  power  of  resistance,  and  sudden  death  may  occur 
either  without  apparent  cause  or  as  a  result  of  ailments  or  causes 
which  are  ordinarily  attended  by  danger — e.  g.,  unexpected  death 
during  convalescence  from  infectious  diseases ;  sudden  and  inex- 
plicable deaths  in  children  ;  or  while  bathing ;  or  during  anaesthesia ; 
or  following  the  injection  of  diphtheria  antitoxine. 

2.  Cachexia. — A  yellow,  waxy  face,  associated  with  anaemia,  gen- 
eral debility,  and  more  or  less  emaciation,  are  the  characteristic  signs 
of  a  condition  which  is  spoken  of  as  "  cachetic,"  or  a  "  cachexia." 
The  anfemia  and  the  yellow  or  brownish-yellow  colour  of  the  skin  are 
the  indispensable  signs  of  this  condition.  It  is  usually  associated 
ivith  some  grave  organic  disease  or  a  chronic  poisoning  of  the  blood. 
While  the  meaning  of  the  word  is  somewhat  vague,  yet  to  the  physi- 


80  THE  EVIDENCES   OF  DISEASE 

cian  of  considerable  experience,  like  some  other  terms,  as  "  very  ill,"' 
"sinking,"  "collapse,"  it  expresses  very  graphically  a  state  which 
would  otherwise  require  many  words  of  description,  and  the  recogni- 
tion of  which  is  often  of  diagnostic  value. 

The  various  cachexise  of  a  more  or  less  well-defined  character  and 
importance  are  as  follows  : 

(a)  Cancerous  Cachexia. — Debility,  emaciation,  anaemia,  and  a 
dirty  yellowish,  yellowish-broAvn,  or  brownish-green  complexion. 

(b)  SypliiUtic  Cachexia. — Pronounced  anaemia,  with  a  muddy 
pallor,  and  perhaps  a  light  yellowish  tint  of  the  skin  and  conjunc- 
tivae. 

(c)  Malarial  or  Paludal  Cachexia. — Puffy,  pallid  face,  profound 
anaemia,  and  a  greatly  enlarged  spleen  (ague  cake).  There  may  be 
bronzing  and  discoloration  of  the  skin  and  general  cedema. 

{d)  Cachexia  Strumipriva  (Kocher). — A  condition  of  anaemia  and 
myxoedema  resulting  from  the  total  extirpation  of  the  thyroid 
gland,  and  attended  by  peculiar  nervous  phenomena. 


SECTION  IV 
POSTUKE  IN  BED— MODE   OF  MOVIXG— GAIT— STATION 

Inspection  may  reveal  certain  facts  in  regard  to  the  posture 
and  the  movements  of  the  patient,  which  may  be  of  little  value  or 
may  furnish  important  suggestions  as  to  the  general  condition  of  the 
patient  or  the  nature  of  the  disease. 

I.  Posture  in  Bed. — The  patient  usually  takes  to  bed  in  acute  ill- 
ness or  in  chronic  ailments,  because  of  general  weakness  or  some 
special  interference  with  the  use  of  the  limbs,  as  in  certain  diseases 
of  the  nervous  system.  Eemembering  that  many  persons  in  health 
habitually  assume  certain  attitudes  while  in  bed,  and  that  their  cus- 
toms in  this  respect  may  not  be  changed  by  illness,  the  postures 
assumed  in  disease  and  their  diagnostic  associations  are  : 

{a)  The  dorsal  strong  or  active  posture,  in  which  the  patient  lies 
upon  the  back  comfortably  and  without  constraint.  It  is  seen  in 
health,  and  in  slight  illness  unattended  with  great  pain. 

{h)  The  dorsal  inert  or  passive  posture.  The  patient  lies  upon 
the  back,  but  is  constantly  slipping  toward  the  foot  of  the  bed, 
thereby  putting  the  body  in  a  posture  which  is  uncomfortable,  and 
which  interferes  with  the  respiratory  movements.  It  is  observed  in 
conditions  of  great  weakness,  most  frequently  in  the  acute  infectious 
diseases.     It  is  especially  characteristic  of  typhoid  fever,  even  at  an 


POSTURE  IN  BED  31 

early  period,  because  of  the  marked  muscular  weakness  and  mental 
apathy  so  characteristic  of  this  disease. 

(c)  A  rigid  dorsal  position,  with  both  legs  drawn  up,  in  order  to 
diminish  abdominal  tension,  is  the  rule  in  general  peritonitis  and  in 
many  cases  of  pelvic  peritonitis.  In  appendical  peritonitis  the  right 
leg  alone  may  be  flexed. 

(d)  The  patient  may  lie  upon  the  side,  and  the  manner  of  lying 
may  be  active  or  passive,  as  in  the  dorsal  position. 

Patients  suffering  from  acute  affections  of  the  chest  usually  lie 
upon  the  affected  side  in  order  to  limit  the  movements  of  the 
affected  side  and  lessen  the  pain  caused  by  pleural  friction,  as  well 
as  to  afford  greater  freedom  of  compensatory  motion  to  the  healthy 
side.  Moreover,  if  a  large  pleural  effusion  exists,  the  pressure  due  to 
its  weight  will  not  burden  the  heart  and  the  healthy,  uncompressed 
lung.  The  posture  of  a  patient  with  a  cavity  in  the  lung  is  of  some 
significance,  that  position  being  chosen  which  brings  the  opening  of 
the  cavity  uppermost,  thus  allowing  secretions  to  accumulate  and  be 
discharged  at  infrequent  intervals  instead  of  constantly  trickling  into 
the  bronchial  tubes  and  causing  an  incessant  irritating  cough.  The 
rule  of  lateral  decubitus  is  not  invariable,  as  the  patient  may  find 
other  positions  preferable. 

The  lateral  position  with  the  legs  drawn  up  to  meet  the  trunk 
(the  "  coiled  "  posture)  is  seen  in  cerebellar  disease  (due  to  spasm), 
hepatic,  renal,  and  intestinal  colic. 

(e)  Opisthotonus. — This  is  the  name  given  to  an  uncommon  dorsal 
position  in  which  the  body  rests  upon  the  head  and  heels,  the  trunk 
being  arched  upward.  It  is  observed  in  strychnine  poisoning  and 
tetanus,  as  well  as  in  some  peculiar  manifestations  of  hysteria  and 
hystero-epilepsy.  A  modification  of  this  position  is  observed  in  the 
characteristic  contraction  of  the  posterior  neck  muscles  occurring  in 
meningitis,  whereby  the  back  of  the  head  bores  into  the  pillow. 

(/)  Emprosthotonus. — An  attitude  in  which  the  upcurved  body 
rests  face  downward  upon  the  forehead  and  feet.  It  is  the  opposite 
of  opisthotonus  and  is  rarely  seen,  but  may  be  observed  in  tetanus 
and  strychnine  poisoning. 

The  prone  position,  without  tonic  contraction  of  the  muscles,  is 
occasionally  witnessed  in  the  various  forms  of  colic,  the  patient  usu- 
ally lying  with  the  abdomen  resting  upon  a  pillow  or  bolster  in  order 
to  secure  firm  abdominal  pressure  for  mitigation  of  pain.  This  pos- 
ture, without  the  pillow,  is  sometimes  assumed  because  of  the  relief 
afforded  in  erosion  of  the  vertebrae  resulting  from  aneurism,  or  in 
tuberculous  disease  of  the  spine.  Less  frequently  it  may  be  seen  in 
gastric  ulcer. 


32  THE  EVIDENCES  OF   DISEASE 

(g)  OrtJiopncea. — In  diseases  attended  with  excessive  dyspnoea  the 
patient  instinctively  sits  upright,  with  the  hands  or  elbows  resting 
upon  some  point  of  support,  in  order,  by  fixing  the  shoulders,  to 
facilitate  the  action  of  the  accessory  muscles  of  respiration.  If  an 
attempt  is  made  to  assume  the  horizontal  position,  the  feeling  of 
dyspnoea  becomes  so  intense  that  the  upright  attitude  is  quickly 
retaken.  Orthopnoea  attends  spasmodic  asthma,  emphysema,  and 
diseases  of  the  heart  in  their  later  stages.  It  is  common  with  large 
effusions  into  the  pericardial  and  pleural  cavities,  and  is  often  en- 
countered in  abdominal  dropsies  of  sufficient  size  to  press  the  dia- 
phragm upward.  If  the  diaphragmatic  pleura  is  inflamed,  the  patient 
is  apt  to  sit  erect  with  the  trunk  leaning  toward  the  affected  side. 
Extreme  dyspnoea  of  the  inspiratory  type,  requiring  the  sitting  pos- 
ture, attends  obstructive  or  paralytic  disease  of  the  larynx,  as  in 
laryngeal  diphtheria  and  paralysis  of  the  dilators  of  the  glottis. 

II.  Mode  of  Moving. — {a)  In  certain  ailments,  some  of  which  have 
been  mentioned  in  the  preceding  paragraphs,  there  is  unusual  immo- 
bility and  a  striking  look  of  helplessness,  due  to  the  increase  of  pain 
upon  motion,  as  in  rheumatism,  scurvy,  and  rachitis,  or  a  disinclina- 
tion to  move  because  dyspnoea  is  made  worse  by  exertion.  Paralysis 
or  tonic  spasm  of  large  muscular  groups  is  another  cause  of  enforced 
quietude. 

{h)  An  opposite  condition,  restlessness,  exists  in  many  diseases,  as 
in  fevers  and  large  hemorrhages.  Agitated  and  irregular  move- 
ments are  seen  in  chorea,  in  hysteria  with  its  manifold  manifesta- 
tions, and  in  other  diseases  of  the  nervous  system.  Severe  griping 
or  colicky  pain,  gallstone,  or  renal  colic  will  induce  the  patient  to 
throw  himself  about  in  the  hope  of  relieving  his  suffering. 

III.  Station. — One  should  observe  the  manner  in  which  the  pa- 
tient stands ;  whether  or  not  he  is  firm  upon  his  feet ;  the  shape  and 
carriage  of  the  head  and  shoulders ;  whether  he  is  erect  or  bends 
forward  (as  in  paralysis  agitans)  or  backward  (as  in  ascites  or  abdom- 
inal tumour) ;  and  the  position  and  shape  of  the  limbs.  Station,  the 
power  of  standing  more  or  less  steadily,  is  greatly  disturbed  in  some 
forms  of  nervous  disease.  A  healthy  person  standing  with  the  feet 
close  together  and  the  eyes  open  will  sway  forward  and  back  1  inch 
and  from  side  to  side  f  of  an  inch.  In  locomotor  ataxia  the  swaying 
is  extreme,  owing  to  the  loss  of  muscular,  articular,  and  tendonous 
sense,  and  if  the  eyes  are  closed  the  patient  may  fall.  Disease  of  the 
middle  cerebellar  lobe  and  aural  vertigo  (Meniere's  disease)  will  also 
cause  swaying,  and  in  paroxysms  of  the  latter  malady  the  patient 
may  be  absolutely  incapable  of  standing  or  walking.  Loss  of  the 
power  to  stand  steadily  is  called  static  ataxia  {q.  v.). 


GAIT  33 

IV.  Gait. — The  manner  of  walking  is  closely  associated  with  sta- 
tion, and  when  possible  should  be  attentively  observed,  as  it  is  of 
much  importance  in  the  diagnosis  of  certain  conditions  or  diseases. 

When  observing  the  manner  in  which  the  patient  walks,  it  is  very  desirable, 
if  circumstances  permit,  to  have  the  legs  stripped  and  the  patient  in  his  bare 
feet.  In  women  patients  the  nightdress  may  be  pulled  through  from  the  back 
between  the  legs,  snugged  up,  and  pinned  in  front  ;  or  a  T-bandage  may  be 
improvised  out  of  a  couple  of  towels. 

First  eliminate,  by  inquiry  and  examination  of  the  abdomen,  bones,  and 
joints,  the  varioils  causes  of  abnormal  progression  enumerated  in  (a)  and  (6) 
below.  Then  desire  the  patient  to  walk  away  from  and  back  to  the  observer  ; 
to  walk  at  right  angles  to  the  line  of  sight  ;  to  walk  along  a  crack  between  the 
floor  boards  or  a  seam  of  the  carpet.  During  this  time  he  is  to  be  attentively 
watched  in  order  to  discover  any  peculiarities  of  gait,  the  manner  of  putting 
down  and  raising  the  feet,  reeling,  unsteadiness,  or  deviation  from  the  straight 
line. 

The  peculiarities  in  the  manner  of  walking,  and  the  conditions 
in  which  they  possess  more  or  less  diagnostic  importance,  are  as 
follows : 

(a)  In  pregnancy,  ascites,  large  abdominal  tumours,  and  obesity, 
the  body  leans  backward  and  the  feet  are  widely  separated  while 
walking. 

(b)  Painful  or  disabling  affections  of  one  or  both  lower  extremi- 
ties, such  as  rheumatism,  gout,  sciatica,  metatarsal  neuralgia,  hip-  or 
knee-joint  disease  or  injury  (recent  or  old),  give  rise  to  a  limping  or 
hobbling  gait. 

(c)  The  most  characteristic  methods  of  progression  are  seen  in 
diseases  of  the  nervous  system  : 

(1)  Ataxic  Gait. — In  walking,  the  foot  is  raised  suddenly  and  too  high,  the 
leg  is  thrown  forward  with  unnecessary  vehemence,  and  the  foot  is  again 
brought  to  the  ground  heel  first,  or  flat-footed  with  a  stamp.  The  feet  are 
usually  planted  wide  apart,  and  while  they  are  in  the  air  they  move  as  if  the 
patient  was  doubtful  where  to  put  them.  The  body  is  bent  forward,  and  the 
eyes  are  fixed  upon  the  ground  in  order  to  supplement  as  far  as  possible  the  loss 
of  muscular  and  articular  sensation.  This  gait  is  extremely  characteristic  of 
locomotor  ataxia. 

(2)  Cerebellar  Ataxic  Gait. — The  manner  of  progression  resembles  that  of  an 
intoxicated  person.  The  patient  walks  with  his  feet  wide  apart,  staggers,  reels, 
sways  to  and  fro,  and  reaches  a  set  point  by  zigzagging  toward  it.  The  sway- 
ing is  relieved  if  he  is  supported  by  the  hands  of  the  observer  placed  under  the 
armpits.  This  gait  is  significant  of  a  tumour  of  the  vermis  or  middle  lobe  of  the 
cerebellum,  and  is  often  called  the  titubating  gait,  or  simply  cerebellar  ataxia 
(q.  v.).  A  somewhat  similar  gait  is  seen  in  Friedreich's  disease  and  hereditary 
cerebellar  ataxia. 


34  THE  EVIDENCES  OF   DISEASE 

(3)  Steppage  Gait. — This  variety  of  gait  is  due  to  paralysis  of  the  extensor 
muscles  of  the  foot,  whereby,  when  the  foot  is  lifted,  its  anterior  part  tends  to 
hang  or  drop  down.  In  order  to  prevent  the  toes  catching  and  tripping  against 
the  ground,  the  leg  carries  the  foot  somewhat  forcibly  forward,  raising  it  at  the 
same  time  unusually  high,  thus  throwing  the  toes  upward  and  bringing  the  foot 
to  the  ground  heel  first.  It  resembles  the  gait  of  a  man  who  is  walking  through 
thick  grass  or  brushwood,  and  has  been  described  as  "prancing  "or  "high- 
stepping."  It  is  evidence  of  peripheral  neuritis  (diabetic,  arsenical,  alcoholic, 
etc.)  of  the  anterior  tibial  nerve,  and,  because  of  a  certain  resemblance  to  that 
of  locomotor  ataxia,  is  sometimes  termed  the  pseudo-tabetic  gait. 

(4)  Spastic  Gait. — The  legs  are  rigid,  move  stiffly,  and  there  is  apparent 
difficulty  in  bending  the  knees.  In  consequence  the  foot  is  dragged  along,  the 
toes  catching  and  scraping  on  the  ground.  In  some  instances,  owing  to  spasm 
of  the  adductors  of  the  thigh,  the  legs  and  knees  touch  and  can  not  be  sepa- 
rated, causing  cross-legged  progression — i.  e.,  the  legs  and  feet  overlap  at  each 
step.  This  gait  depends  upon  the  excessive  tension  and  spasticity  of  the  mus- 
cles arising  from  lesions  of  the  upper  motor  neurones.  It  is  therefore,  when 
bilateral,  significant  of  sclerosis  affecting  the  lateral  pyramidal  columns  of  the 
cord.  The  mode  of  walking  in  hemiplegia  (q.  v.)  is  a  unilateral  form  of  the 
same  gait.  The  paralyzed  leg,  by  a  tilting  of  the  pelvis,  is  swung  outward  and 
around  to  the  front  ("mowing"  gait),  the  toes  often  scraping  the  ground. 

(5)  Festination. — The  head  and  body  are  bent  forward  and  the  patient 
takes  short,  shuffling,  hurried  steps,  his  speed  tending  to  increase  as  he 
progresses,  exactly  as  if  he  was  being  constantly  pushed  forward  and  was  try- 
ing to  prevent  it.  This  gait  is  termed  festination  or  propulsion.  In  some 
instances,  if  the  patient  is  pulled  rather  suddenly  backward,  he  will  take  a 
number  of  backward  steps  (retropulsion),  although  the  body  remains  in  its  for- 
ward-leaning attitude.     This  gait  is  characteristic  of  paralysis  agitans. 

(6)  Waddling  Gait. — The  shoulders  are  thrown  back,  the  back  is  hollowed 
(lordosis),  and  the  abdomen  protuberant,  the  body  sometimes  actually  leaning 
backward.  In  walking,  the  feet  are  planted  wide  apart  and  the  body  swings 
from  side  to  side  at  each  step— the  "  waddling  "  or  "goose  "  gait.  It  resembles 
somewhat  the  gait  described  under  (a),  and  is  a  very  characteristic  symptom  of 
pseudo-hypertrophic  muscular  paralysis. 


SECTION  V 
PAIX;   TENDEENESS;   PARESTHESIAS 

There  are  certain  subjective  sensations  which  are  of  mucli, 
although  varying,  importance  in  diagnosis.  Although  a  subjective 
symptom  does  not  constitute  decisive  evidence,  it  may  furnish  an 
important  clew  to  the  nature  of  the  disease — e.  g.,  the  "  tender  point  " 
in  appendicitis.  On  the  other  hand,  there  may  be  an  absolute 
absence  of  tenderness  over  the  kidney  in  pyelitis  and  an  occasional 


PAIN  35 

lack  of  pain  in  peritonitis,  gastric  ulcer,  perforating  duodenal  ulcer, 
latent  pleurisy,  and  various  pelvic  lesions,  by  which  a  most  important 
guide  symptom  is  missing. 

The  subjective  symptoms  which  are  considered  in  this  section 
comprise  pain,  tenderness,  and  paraesthesias.  Other  disorders  of 
sensation,  such  as  anaesthesia,  hyperaesthesia,  etc.,  are  dealt  with  else- 
where (Examination  of  the  Nervous  System).  It  is,  of  course,  impos- 
sible within  reasonable  limits  to  describe  all  the  multiple  forms  and 
sites  of  pain  and  other  subjective  sensations.  Only  those  are  con- 
sidered which  may  prove  helpful  in  diagnosis. 

I.    PAIN 

1.  Differences  in  Susceptibility. — As  pain  is  a  purely  subjective 
symptom,  its  intensity  must  be  estimated  by  the  statements  of  the 
sufferer,  by  the  manifestations  of  its  presence,  and  by  the  nature  of 
any  lesion  which  may  be  discovered  as  its  probable  cause.  Much 
depends  upon  the  skill  and  experience  of  the  observer  in  judging 
individual  susceptibility.  The  variations  in  pain  sensibility  are  very 
great,  and  are  racial  as  well  as  individual.  The  Semitic  stock,  and 
the  Celtic  and  Italic  groups,  appear  to  possess  an  average  greater 
'sensibility  to  pain  than  the  Teutonic  and  Slavonic  groups.  The 
most  important  variations,  however,  are  personal  or  individual. 
The  congenitally  neurotic  patient  will  complain  bitterly  of  pain  from 
&  cause  which  in  one  of  dull  sensibilities  will  give  rise  to  simple  dis- 
comfort. It  is  to  be  remembered  that  the  pain  suffered  by  the 
abnormally  sensitive  person  has  as  real  an  existence  in  consciousness 
as  the  slight  discomfort  felt,  from  the  same  cause,  by  those  of  less 
acute  pain  perception. 

2.  Modifications  of  Susceptibility. — The  manner  of  life  and  occu- 
pation may  modify  the  susceptibility  to  pain.  The  habitual  endur- 
ance of  hardship  blunts  the  pain  sense,  and,  conversely,  the  person 
guarded  from  rude  mental  or  physical  contact,  will  be  more  acutely 
sensitive  to  pain.  A  strong  mental  prepossession  (religion,  excite- 
ment of  battle,  etc.)  may  interfere  with  the  registration  of  painful 
impressions  upon  the  consciousness.  The  sensibility  to  pain  is  apt 
to  be  increased  by  its  long  continuance,  and  it  is  a  common  observa- 
tion that  each  recurrence  of  pain,  during  the  course  of  a  disease,  finds 
the  patient  less  able  to  bear  it.  Fright  or  expectant  apprehension 
invariably  increases  pain,  and  sometimes  originates  it. 

3.  Manner  of  Statement. — There  are  also  differences  in  the  manner 
of  statement.  Some  patients  as  a  matter  of  pride  practise  understate- 
ment of  their  subjective  sensations,  while  others  from  various  motives 
habitually  magnify  their  sufferings,  and  in  most  instances  without 


36  THE  EVIDENCES  OP  DISEASE 

the  slightest  intention  of  deceiving  the  physician.  It  arises  largely 
from  the  unconscious  egotism  of  illness  and  a  desire  to  obtain  relief 
by  impressing  the  medical  attendant  with  its  pressing  necessity.  In 
estimating  the  severity  of  pain,  the  facial  expression  and  bodily  mani- 
festations of  pain  are  of  much  value.  A  statement  made  with  a 
cheerfifl  countenance,  that  the  speaker  is  at  the  present  moment 
suffering  "  horrible  agony,"  does  not  square  with  the  facts,  and  this 
combination  is  of  diagnostic  value  as  indicative  of  self-deception, 
hysteria,  or  a  habit  of  chronic  emphasis.  Women,  perhaps  more 
than  men,  are  inclined  to  exaggerate  in  recounting  their  symptoms. 
The  reason  may  be  found  in  the  greater  susceptibility  of  the  feminine 
nervous  system,  and  the  larger  measure  of  sympathy  which  a  woman 
habitually  receives.  This  is  said  without  prejudice  to  the  courage, 
endurance,  and  self-sacrifice  which  are  so  brilliantly  exhibited  in 
many  sick-rooms. 

In  the  majority  of  cases  in  which  really  severe  pain  is  present  the 
respiration  is  rapid,  the  pupils  are  dilated,  the  skin  is  wet  with  per- 
spiration, the  pulse  is  apt  to  be  tense,  there  is  a  feeling  of  faintness, 
and  not  infrequently  a  large  amount  of  limpid  urine  is  passed  within 
a  brief  period — symptoms  some  of  which  can  not  be  simulated. 

In  all  cases  in  which  pain  is  a  symptom  a  careful  investigation' 
should  be  made  in  order  to  discover  any  existing  objective  condition 
which  may  constitute  corroborative  evidence  of  the  truth  of  the 
patient's  statement.  In  view  of  the  fact  that  sad  mistakes  have 
occurred,  it  is  best  not  to  err  on  the  side  of  scepticism,  but  to  credit 
subjective  testimony  until  some  anatomical  incongruity  of  distribu- 
tion is  found  or  some  sudden  shifting  of  the  seat  of  pain  occurs, 
which  is  incompatible  with  the  ascertained  objective  symptoms  and 
signs. 

4.  Varieties  of  Pain. — Pain  varies  in  intensity  from  sharp  or  acute 
to  dull  or  aching  pain.  It  may  be  radiating,  darting  from  its  point 
of  origin  along  the  branches  of  a  nerve  trunk  ;  or  paroxysmal,  remit- 
ting, coming  and  going;  or  shifting,  moving  from  one  locality  to 
another ;  or  possess  the  character  indicated  by  the  terms  gnawing  or 
colicky.  It  may  be  increased  by  motion  or  relieved  by  pressure. 
Two  or  more  varieties  may  co-exist  as  a  single  pain  symptom. 

5.  Diagnostic  Import  of  the  Character  of  Pain— («)  Acute  pain 
is  characteristic  of  acute  inflammations  of  serous  and  synovial  mem- 
branes, as  in  pleurisy  or  joint  inflammations.  Acute  radiating  pain 
marks  the  idiopathic  neuralgias  or  the  nerve  pain  due  to  inflamma- 
tion or  pressure,  as  in  neuritis  or  thoracic  aneurism. 

{h)  Dull  pain^  like  that  of  a  bruise,  usually  attends  inflammations 
of  mucous  membranes  and  the  parenchymatous  viscera  (which  are 


PAIN  37 

poorly  endowed  with  sensory  nerves),  and  many  chronic  inflamma- 
tions. 

(c)  Paroxysmal  ox  remitting  2)(tin  is  characteristic  of  the  neural- 
gias and  colics,  and  the  major  portion  of  the  radiating  pains  just 
mentioned  are  paroxysmal  in  type. 

{d)  Shifting  pain,  more  or  less  sharp,  occurs  in  connection  with 
rheumatism,  hysteria,  locomotor  ataxia,  and  trichinosis. 

{e)  Pain  of  a  gnaiving  or  boring  character  is  encountered  in  dis- 
ease of  the  spinal  column,  thoracic  and  abdominal  aneurism,  perios- 
teal or  osteal  inflammations,  gastric  carcinoma,  and  sometimes  in 
gouty  lesions  and  lithaemic  states. 

(/)  Cramp  is  a  sudden  and  painful  spasm  of  certain  muscles  or 
muscle  groups.  Aside  from  the  cramp  due  to  overuse  of  special  muscles 
(writer's  cramp,  occupation  neuroses),  and  the  cramp  affecting  the 
muscles  of  the  calf  and  the  toes,  the  term  is  frequently  applied  to 
painful  abdominal  spasms  (colic)  due  to  excessive  action  of  the  mus- 
cular walls  of  the  stomach  and  intestines.  Abdominal  cramp  or 
colicky  pain  is  a  frequent  accompaniment  of  flatulence  and  gastro- 
intestinal disease  in  general ;  it  occurs  in  cases  of  intestinal  obstruc- 
tion from  any  cause,  and  as  a  result  of  irritant  poisoning. 

{g)  Other  qualifying  terms  which  are  employed  to  indicate  the 
character  of  pain  are :  burning,  as  in  herpes  zoster  ;  aching,  as  in  a 
moderate  lumbago  or  other  myalgia  ;  throbbing  or  pulsating  with  the 
heart  beat,  as  in  a  circumscribed  phlegmon  or  suppurative  inflamma- 
tion. Tenesmus,  or  tenesmic  pain,  is  that  which  attends  urination 
or  defecation  from  an  inflamed  bladder  or  rectum,  or  the  expulsion 
of  membrane  or  clots  from  the  uterus,  accompanied  with  a  sensation 
of  straining  or  bearing  doAvn.  The  adjectives  stabbing,  darting,  and 
lancinating  are  equivalent  to  sudden,  sharp,  and  acute  radiating 
pain. 

[h)  Pain,  increased  hy  motion,  is  found  in  all  inflammatory  dis- 
eases, myalgias,  serous  inflammations,  the  various  forms  of  articular 
rheumatism,  and  disease  of  the  joints  and  vertebrae.  Some  forms  of 
colic  and  hysterical  pain  may  be  relieved  by  firm  and  even  pressure. 

(/)  The  acuteness  or  chronicity  of  pain  corresponds  largely  to  the 
suddenness  of  occurrence  and  the  persistence  of  its  cause.  Pain  may 
persist  after  the  removal  of  its  factors,  apparently  because  the  pain 
habit  has  been  formed  by  the  affected  nerves  and  their  associated 
centres ;  but,  as  a  rule,  pain  extending  over  a  long  period  of  time  indi- 
cates a  continuance  of  the  pathological  conditions  from  which  it  ori- 
ginated. Pain  may  be  recurrent  or  periodic,  days  or  weeks  elapsing 
between  successive  attacks,  as  with  migraine ;  or  may  be  continuous, 
with  occasional  exacerbations,  as  in  headache  from  eye  strain. 
5 
/ 


38  THE  EVIDENCES  OF  DISEASE 

6.  Diagnostic  Import  of  the  Seat  of  Pain. — As  a  general  rule,  the 
seat  of  pain  corresponds  to  the  location  of  the  causative  lesion.  In 
certain  cases  the  pain  is  reflex  or,  more  properly,  transferred,  being 
assigned  to  the  furthest  peripheral  termination  of  a  nerve,  when  the 
causative  lesion  is  situated  at  one  of  its  terminations  much  nearer 
the  origin  of  the  nerve,  or  an  irritation  at  the  termination  of  one 
branch  is  felt  also  at  the  termination  of  a  branch  situated  in  a  differ- 
ent locality,  or  the  irritation  may  be  at  the  origin  of  the  nerve  trunk 
and  the  pain  referred  to  its  entire  peripheral  distribution.  If  the 
pain  is  extremely  intense,  it  may  be  felt  not  only  in  the  direct  nerve 
supply  of  the  affected  area  but  also  in  areas  indirectly  connected,  a 
phenomenon  assumed  to  be  caused  by  irradiation,  or  an  overflow  of 
the  painful  impression  from  its  accustomed  channels. 

Even  though  the  pain  caused  is  not  intense,  a  source  of  irritation 
may  exist  at  one  point  and  be  felt  at  another  widely  separated  from 
the  actual  seat  of  the  lesion.  In  all  such  cases  the  sensation  is  in 
reality  a  transferred  or  referred  pain,  and  strictly  speaking  can  not 
be  termed  reflex.  The  latter  word  implies  the  travelling  of  an 
afferent  (sensory)  impression  to  a  centre,  which  centre,  in  conse- 
quence of  the  received  impulse,  sends  out  an  efferent  (motor)  im- 
pulse ;  whereas  a  transferred  sensation  is  one  perceived  by  the  sen- 
sorium,  not  as  belonging  to  its  real  source  of  origin,  but  which, 
because  of  the  existence  of  indirect  sensory  connections  along 
which  the  impression  travels,  is  referred  to  an  entirely  different 
portion  of  the  periphery.  The  pain  sometimes  felt  in  the  mammary 
gland  when  disease  of  the  uterus  exists  is  an  illustration  of  this  fact. 
The  well-known  diagrams  of  Dana  represent  graphically  the  more 
important  varieties  of  transferred  pains  (Figs.  5  and  6).  Xot  in- 
frequently there  may  be  pains  felt  in  the  periphery  which  are  due 
to  central  disease  of  the  brain  or  cord,  as  in  meningitis. 

Diseases  of  the  different  viscera  may  manifest  themselves  by  pain  and  dis- 
turbed sensation  referred  to  certain  cutaneous  areas.  The  elaborate  researches 
of  Head  make  it  probable  that  when  a  painful  stimulus  is  applied  to  a  tissue  or 
an  organ  which  normally  possesses  a  low  degree  of  sensibility,  and  which  is 
centrally  in  close  connection  with  a  tissue  or  organ  possessing  a  much  higher 
degree  of  sensibility,  the  pain  produced  is  felt  in  the  part  which  is  relatively 
more  sensitive.  Consequently  the  tenderness  of  the  skin  in  visceral  disease  is 
due  to  the  passing  of  sensory  impulses  from  a  diseased  organ  to  its  correspond- 
ing spinal  segment,  these  impulses  causing  a  disturbance  in  the  segment  of  such 
a  nature  that  any  additional  impulses  coming  from  the  skin  surface  with  which 
this  is  connected  will  be  increased  and  modified  so  as  to  produce  abnormal  or 
painful  impressions,  which  are  referred  in  consciousness  to  the  part  of  higher 
sensitiveness,  the  skin. 

These  painful  cutaneous  areas  are  best  demonstrated  by  using  a  round- 


PAIN 


39 


headed  pin  of  sufficient  size  to  feel  distinctly  blunt  to  the  normal  skin  of  the 
observer.     The  head  of  the  pin  is  then  pressed  with  moderate  force  upon  the 


Pseudo-angina 
of  gastric 
origin 


Dyspepsia  and 
constipation 


Fio.  5. — The  location  of  transferred  pains  (Dana).  Figure  redrawn  in  charcoal  after  an 
imported  photograph.*  These  pains,  through  the  existence  of  more  or  less  indirect  or 
roundabout  sensory  nerve  connections,  are  felt  at  points  of  varying  remoteness  from  the 
source  of  tlie  irritation  which  produces  them.  Thus,  pain  in  the  knee  may  be  due  to 
disease  of  the  hip  joint,  the  les\on  affecting  one  of  the  terminations  of  the  nerve  much 
nearer  to  the  origin  of  the  latter  than  that  in  which  the  pain  is  felt;  or  the  mammary 
gland  may  swell  and  become  painful  when  a  distant  organ — the  uterus — is  tlie  seat  of  a 
pain -producing  process.    See  also  Fig.  6. 

surface  to  be  examined,  using  it  as  if  testing  with  the  point  for  anaesthesia.     If 
a  tender  area  is  present,  the  patient  will  at  once  complain  of  soreness  resembling 

*  With  few  exceptions,  the  photographs  used  for  diagrammatic  purposes  in 
this  book  have  been  imported. 


40  THE  EVIDENCES  OP  DISEASE 

that  of  a  bruise  when  touched ;  and  if  the  point  of  the  pin  is  employed,  it  causes 
pain  greatly  exceeding  that  which  would  be  felt  in  a  normal  skin.  A  rough 
test  may  be  made  without  using  the  pin  by  gently  pinching  up  a  fold  of  skin. 
The  absence  of  tenderness  does  not  negative  the  existence  of  visceral  disease ; 
its  presence  is  simply  confirmatory,  or  in  some  cases  suggestive.  The  clinical 
value  of  this  test  is  at  present  very  slight. 

(a)  Diffuse  Pain. — Pain  or  aching,  general  in  its  distribution,  is 
encountered  in  the  majority  of  febrile  diseases,  especially  during 
their  initial  stage.  Although  present  to  a  greater  or  less  degree  in 
most  fevers,  general  aching  is  apt  to  be  most  pronounced  in  the 
acute  infections,  of  which  epidemic  influenza,  variola,  and  dengue 
are  striking  examples.  Lacunar  tonsilitis  exhibits  it  to  almost  as 
great  a  degree.  It  may  be  associated  with  syphilis,  lithaemia,  rheu- 
matism, and  some  of  the  intoxications,  as  in  poisoning  by  mercury  and 
lead.  General  aching  results,  as  a  rule,  from  the  action  of  a  toxine 
or  other  poison  in  the  circulating  blood  upon  the  central  or  periph- 
eral nervous  system. 

(S)  Headache  and  Pain  in  the  Head. — Pain  in  the  head  is  a  symp- 
tom of  diverse  meaning  and  origin.  Headache  is  defined  as  an  attack 
of  diffuse  pain  affecting  different  parts  of  the  head,  and  not  confined 
to  a  particular  nerve. 

Neuralgia  (toxic,  referred,  pressure)  is  characterized  by  pain  in 
the  course  of  a  nerve  or  nerves,  generally  unilateral.  It  is  func- 
tional in  the  sense  that  no  disease  of  the  nerve  itself  may  be  present. 
Pain  limited  to  a  nerve  tract  may  be  due  to  neuritis.  Migraine 
{q.  V.)  is  a  painful,  periodical  neurosis,  involving  the  trigeminus, 
but  with  certain  symptoms  which  distinguish  it  from  headache  or 
neuralgia. 

In  general,  the  causes  of  pain  in  the  head  are  as  follows,  excluding 
traumatism :  1.  Anaemia  and  sudden  hemorrhages.  Xephritis.  2. 
Constitutional  diseases;  diabetes,  gout,  lithgemia,  rheumatism.  3. 
Specific  infectious  diseases,  mainly  fevers.  4,  Intoxications ;  alco- 
hol, lead,  mercury,  tobacco.  5.  Xeuroses ;  epilepsy,  hysteria,  neu- 
rasthenia, exophthalmic  goitre.  6.  Inflammations  or  organic  diseases 
of,  or  affecting,  the  nervous  system ;  embracing  arteriosclerosis,  dis- 
eases of  cranial  bones,  meningitis,  encephalitis,  neuritis,  syphilis,  and 
tumour  or  abscess.  7.  Reflex  or  referred  pain  from  disease  of  the 
ear,  eye,  nasopharynx,  stomach,  and  sexual  organs.  8.  Fatigue, 
bodily  or  mental ;  impure  air,  acclimation. 

The  character  of  head  pain  varies  with  the  individual  and  the 
cause.  AVe  may  distinguish :  1.  Sharp,  lancinating,  paroxysmal 
pain ;  characteristic  of  neuralgia.  3.  Pulsating  or  throbbing  head- 
ache ;  if  unilateral  and  in  connection  with  other  vasomotor  disturb- 


PATN 


41 


ances,  indicative  of  migraine   or  hemicrania.     3.  Dull,  heavy,  dif- 
fused headache ;  found  in  gastro-intestinal  and  febrile  diseases  of 


Splenitis 


Broad  ligaments 
and  ovaries 


Ovaries 


Neurasthenia 
Spinal  irritation 


Lithsemis 
Neurasthenia 


Fig.  6. — The  location  of  transferred  pains  (Dana).    Figure  after  a  painting  by  Eoyer. 

infectious   origin.     4.  Binding,  pressing,  or  squeezing  headache ;  in 
neurotic  and  neurasthenic  individuals.     5.  Hot,  burning,  sore  head- 


42 


THE   EVIDENCES  OF   DISEASE 


ache ;  associated  with  rheumatism  and  anaemia.    6.  Sharp  and  boring 
head  pains ;  encountered  in  epilepsy  and  hysteria. 

The  location  of  head  pain  is  of  considerable  diagnostic  impor- 
tance.    It  may  be  diffuse  or  in  varying  combinations,  frontal,  tem- 


PARIETAL  AND  AURAL 


Otitis  Media 

Foreign  Body  in  Ear 

Caries  of  Teeth 

Dentition 

Eye  Strain 

Syphilitic  or  Other  Disease  of 

Maxillary  or  Temporal  Bones 
Cancer  or  Irritable  Ulcer  of 

Tongue 
Aneurism  of  Innominate 


VERTEX 


AN/tMIA 

Hysteria 
Neurasthenia 
Epilepsy 

Disease  of  Uterus, 
Ovaries,  Bladder 


OCCIPITAL  AND 
CERVICAL 


Neurasthenia 

Spinal  Irritation 

Epilepsy 

Meningitis 

Cerebellar  Tumour 
OR  Lesion 

Dyspepsia 

Cervico-Occipital  My- 
algia AND  Neuralgia 

Disease    of    Cervical 

VERTEBR/E 

Adenoids  of  Pharynx 
Middle  Ear  Disease 
Eye  Strain 
Carious  Teeth 
Uterine  Disease 


LOWER  JAW 


Dental  Affections 
Neuralgia  of  Inferior 

Maxillary  Nerve 
Parotitis 


FRONTAL  AND 
TEMPORAL 


An/EMia 
Neurasthenia 
Nephritis,  Ur/emia 
Dyspepsia,  Constipation 
Myalgia  and  Rheumatism 

OF  the  Scalp 
Lith/emia 
Eye  Strain,  Glaucoma, 

Iritis 
Disease  of,  or  Foreign 

Body  in.  Nasopharynx 
Disease  of  Frontal 

Sinus 
Syphilitic  Nodes  or 

Periostitis 
l_ 


EYEBALLS 


Migraine 

Neuralgia  of  5th  Nerve 

Ophthalmoplegia  Interna 

CORYZA 

Inflammation  of  Con- 
junctiva, Iris,  Cornea 


UPPER  JAW 


Dental  Affections 
Periostitis 
Disease  of  Antrum 
Cancer 

Neuralgia  of  Superior 
Maxillary  Nerve 


Fig,  7. — The  general  diagnostic  indications  to  be  derived  from  the  seat  of  pain  in  the 

head  and  face. 


poral,  parietal,  vertical,  or  occipital.  Fig.  7  shows  in  a  general  way 
the  diagnostic  indications  to  be  derived  from  the  seat  of  pain  in  the 
head  and  face.  Figs.  8  and  9  afford  a  more  specific  and  detailed 
representation. 


PAIN 


43 


The  more  important  varieties  of  headache  which  possess  some- 
what distinctive  characteristics  are  as  follows : 

1.  Amemic  headache  is  a  sore  and  pressing  pain,  usually  felt  in  the  forehead 
and  orbital  region  or  in  the  vertex,  and  is  often  associated  with  occipital 
pressure.  As  its  name  indicates,  it  is  found  in  connection  with  the  general 
and  special  forms  of  impoverished  blood. 

3.  The  headache  of  nephritis,  excepting  the  sudden  attacks  due  to  uraemia, 
is  in  most  cases  caused  by  the  arteriosclerosis  which  so  often  forms  an  essen- 


Constipation 


-I  Nasal 


Fig.  8. — The  causes  of  localized  headache,  according  to  the  exact  site  of  the  pain. 
Redrawn  after  Collins. 

tial  part  of  the  chronic  nephritides.  The  pain  is  apt  to  be  of  a  throbbing  char- 
acter, somewhat  shifting,  often  accompanied  by  vertigo  and  tinnitus.  I  have 
more  than  once  been  struck  by  the  presence  of  a  vague  fear  on  the  part  of  the 
patient  as  to  the  final  result — forebodings  which  have  in  two  cases  been  uncon- 
sciously realized  by  the  supervention  of  an  apoplectic  attack. 

3.  The  typical  headache  of  hysteria  is  a  pain  as  if  a  nail  was  being  driven 
into  the  top  of  the  head  (clavus),  but  is  of  comparatively  infrequent  occurrence. 

4,  The  headache  of  neurasthenia,  probably  the  most  frequent  of  all  head- 
aches which  require  treatment,  is  of  a  pressive  character,  usually  vertical,  but 
sometimes  described  as  a  band  around  the  head.     It  is  very  characteristic  in 


44 


THE  EVIDENCES  OF  DISEASE 


being  almost  invariably  worse  in  the  morning,  becoming  lighter  or  disappear- 
ing toward  the  latter  part  of  the  day. 

5.  Headache  from  turbinal  pressure^  either  acute  from  rapid  swelling  or 
chronic  from  hypertrophy  or  septal  deviations,  or  perhaps  from  distention  of 
the  accessory  sinuses  of  the  nose,  is  felt  as  a  pain  beginning  at  the  root  of  the 
nose  and  running  directly  backward  to  the  occiput.  It  is  greatly  increased  in 
severity  by  coughing  or  bending  over.  This  variety  of  headache  is  not  at  all 
uncommon. 

6.  Ocular  headaches  are  either  frontal  or  occipital ;  the  pain  comes  on  in  the 
majority  of  cases  after  use  of  the  eyes  in  close  work,  such  as  sewing  or  reading, 
and  the  nightly  rest  of  the  eyes  renders  the  patient  free  from  pain  on  arising. 

7.  Headache  from  constipation  and  disorders  of  digestion  is  usually  of  a 
throbbing,  pulsating  character,  affects  the  frontal  and  orbital  regions,  and  is 
made  worse  by  sudden  movements  of  the  head. 

8.  The  headache  of  uterine  disease  is  usually  occipital,  sharp,  and  radiating. 

Eye  and  teeth  Ansemia  and  neurasthenia 


Neurasthenia 


Fig.  9.- 


-The  causes  of  lociilized  headache,  according  to  the  exact  site  of  the  pain. 
Redrawn  after  Collins. 


As  headache  or  head  pain  is  merely  a  symptom,  a  careful  search 
should  be  made  to  find  the  cause.  It  is  of  especial  importance  to 
examine  with  reference  to  rheumatism  of  the  scalp,  periostitis  or 
caries  of  the  cranial  bones,  the  existence  of  nasal  disease  (particu- 
larly inflammation   of    the    frontal    or    ethmoidal   sinuses),   ocular 


PAIN 


45 


defects,  gastro-intestinal  disorders,  anaemia,  disease  of  the  blood-ves- 
sels (arteriosclerosis),  nephritis,  syphilis,  neuralgia,  migraine,  neur- 
asthenia, hysteria,  epilepsy,  and  finally  organic  disease  of  the  nerv- 


LATERAL  WALL  OF  CHEST 


Anemia 

Intercostal  Neuralgia  (usually  left) 

Pleurodynia 

Pleurisy 

Pneumonia 

Phthisis 

Mediastinal  Tumour 

Enlarged  Bronchial 
Glands 

Disease  of 
Chest- 
Walls 
(Ribs,  Soft 
Tissues) 

Disease  of 

VERTEBR/€ 

Herpes  Zoster 
(usually  right 
side) 


PAIN 


DIAPHRAGM 


Pleurisy 

Violent  Vomiting  or 
Coughing 


PR/ECORDIAL  REGION 


Angina  Pectoris  (radiates  down  left  arm) 

Pseudo-Angina  (an/emic,  gastric,  neurasthenic,  grippal,  toxic) 

Pericarditis 

Gastralgia  (Cardialgia) 

Flatus  in  Splenic  Colon 

Locomotor  Ataxia  (more  common  in  axilla) 


Fm.  10. 


ous  system  (abscess,  tumour,  meningitis,  encephalitis).  Chronic 
headaches  are  usually  due  to  neurasthenia,  less  frequently  to  ocular 
defects,  anaemia,  syphilis,  or  pachymeningitis,  and,  rarely,  the  cause 
remains  conjectural. 

(c)  Pain  in  Chest,  Abdomen,  and  Extremities. — The  diagnostic 
indications  derived  from  the  seat  of  pains  in  the  thorax,  abdomen, 
back,  and  extremities  are  shown  in  Figs.  10  to  16.     As  with  head- 


46 


THE  EVIDENCES  OF  DISEASE 


ache,  the  cause  of  a  given  pain  is  to  be  discovered  by  a  study  of  the 
associated  signs  and  symptoms,  determining  by  means  of  the  lat- 


EPIGASTRIC  REGION 


Gastric  Neuroses 
Gastric  Ulcer 
Gastric  Cancer 
Gastric  Catarrh 
Gastric  Erosions 
and  Hyper- 

>ESTHES1A 

Ulcer   of   the 
Duodenum 


Qastralgia 
Morphine  Habit 
Disease  of  Vertebr/e 

Pneumonia  in  Children 

Cancer  or  Inflammation  of 
Pancreas 


PAIN 


ABDOMINAL  PAIN,   MORE  OR  LESS  GENERAL 
AND  SHARP  OR  COLICKY 


Gastralgia 

Cancer  or  Ulcer  of  Stomach 

Enteralgia 

Enteritis  « 

Lead  Colic 

Arsenical  or  Mercurial  Poisoning 

Floating  Kidney  (Dietl's  crises) 

Mucous  Colic 

Flatulence 

Intestinal  Obstruction 

Intestinal  Perforation 

Appendicitis  (onset) 

Peritonitis  (any  cause) 


HyPEH/€STHES1A 

Rheumatism  of  Abdominal  Walls 

Hernia 

Lumbo-Abdominal  Neuralgia 

Embolism  Superior  Mesenteric  Artery 

Aneurism  (occasional) 

Acute  Pancreatitis 

Locomotor  Ataxia 

Dysmenorrhea 

Diabetes 

RAYNAUD'S  Disease 

PoTT's  Disease  (in  child) 

Pneumonia  (in  child) 


Fir,.  11. 


ter  the  presence  or  absence  of  the  diseases  or  conditions  which  are 
assigned  as  capable  of  producing  the  pain  of  which  complaint  is 
made. 


PAIN 


47 


(d)  The  More  Common  Diseases  or  Conditions  with  which  Pain  is 
Associated. — It  is,  of  course,  impossible  to  mention  in  detail  the  mul- 
tiple pains  which  may  be  encountered  clinically  as  evidences  of  dis- 
ease of  various  organs  or  systems.  Those  here  dealt  with  are  of 
more  or  less  importance  from  a  diagnostic  point  of  view.  There  are 
many  examples  of  pain  which  the  clinician  can  not  rationally  or  to 
his  own  satisfaction  explain. 


PAIN 


Sciatica  (unilateral) 

(track  of  nerve) 
Both  Sciatics 

Locomotor  Ataxia 

Lumbar  Abscess 

Growth  involving  Cord 
or  both  Sciatics  in 
Pelvis 
Impacted  Faeces 
Cancer  or  Ulcer  of  Rectum 


Nervous  System. — There  is  the  sharp,  radiating,  generally  unilateral  pain  of 
the  various  neuralgias  (q.  v.).  There  is,  furthermore,  the  pain  of  neuritis,  mul- 
tiple or  localized  ;  of  neurasthenia  or  hysteria  in  the  back  of  the  neck,  along 


48 


THE  EVIDENCES  OP  DISEASE 


the  spine,  and  sometimes  in  the  heel  ;  of  locomotor  ataxia,  most  atrocious  and 
agonizing  ;  and  the  rare  sharp,  solitary  pain  below  the  knee  which  has  been 
known  as  a  premonition  of  cerebral  hemorrhage. 

Heart  and  Vessels. — The  cardiac  pain  which  is  important  beyond  all  others 
is  that  of  true  angina  pectoris,  closely  simulated  by  the  pseudo-angina  of 
anaemic,  gastric,  hysterical,  or  toxic  origin.  Valvular  disease,  especially  of  the 
aortic  cusps,  may  cause  pain  in  the  right  hypochondrium  and  right  shoulder, 
and  there  may  or  may  not  be  some  sternal  pain  in  pericarditis.  Thoracic  aneu- 
rism may  give  rise  to  pain  beneath  the  sternum  or  between  the  shoulders,  and  in 


PAIN 


RIGHT 
HYPOCHONDR 


Disease  of  Liver, 
Functional, 
Inflammatory,  or 
Suppurative 

Cancer 

Cirrhosis 

Impacted  Hepatic  Colon 

Aneurism  of  Abdominal 
Aorta  or  Mesenteric 
Artery 

Valvular  (esp.  Aortic) 
disease  of  Heart 

Exercise  (esp.  when  con- 
stricted BY  corset) 

Subphrenic  Abscess 

Tender  point  at,  in 
Hepatic  Colic  and 
Empyaema,  Impaction  or 
Cancer  of  Gall- 
Bladder 


STERNUM 


Disease  of  Bone 
Mediastinal  Tumour  or 

Abscess 
Aneurism 

Acute  Aortitis  (rare) 
Disease  of  Stomach 

(common) 

Substernal  soreness 
OF  Bronchitis 


Renal  Colic 
Gravel 
Pyelitis 

Movable  Kidney 
Enlarged 
Spleen  (mala- 
rial, leukemic) 
Perisplenitis 
— -     Gastric  Dys- 
pepsia, 

=  TR0PT08I8, 

Qastrectasia 
Impacted  Colon 
Subphrenic  Abscess 
Aneurism  of  Abdominal 
Aorta 


Fig.  13 


rare  cases  acute  aortitis  is  responsible  for  breast  pain.  Abdominal  aneurism 
may  produce  general  abdominal  pain,  sometimes  acute,  as  well  as  pain  in  the 
lumbar  back  and  between  the  lower  angles  of  the  scapulfe.  Sharp  abdominal 
pain  may  be  due  to  embolism  of  the  superior  mesenteric  artery. 


PAIN 


49 


Lungs  and  Pleura. — Practically  the  pain  in  diseases  of  the  lung  is  due  to 
involvement  of  the  pleura,  the  lungs  themselves  possessing  a  very  low  grade  of 
pain  sensibility.  Leaving  out  of  consideration  the  substernal  soreness  of 
bronchitis  and  the  ordinary  pleuritic  pain  in  the  lateral  portions  of  the  chest, 
one  may  note  the  epigastric  pain  of  diaphragmatic  pleurisy  (sometimes  felt  also 
in  the  left  shoulder  and  above  the  clavicle),  and  the  upper  abdominal  pain  so 
often  complained  of  by  the  child  suffering  from  pneumonia. 


Loaded  Colon 

Ulcer  of  Stomach 

(Tender  Point  over  Spines  of 

Eleventh  and  Twelfth 

Vertebr>e) 


Disease  of  Stomach 

Neuroses 

Ulcer 

Cancer 

Aneurism  of  Thoracic  Aorta 


PAIN 


Girdle  Sensation 

Disease  or  Injury  of  Cord 


Disease  of  Liver 


Fig.  14. 


Stomach. — The  painful  diseases  of  the  stomach  are  ulcer  and  erosions  in 
particular,  less  frequently  cancer;  and  with  varying  incidence  gastritis,  gas- 
troptosis,  gastrectasia,  and  various  neuroses.  The  pain  of  gastralgia  (cardi- 
algia)  is  excessive.  The  pain  of  a  diseased  stomach  is  felt  in  most  cases 
primarily  in  the  epigastrium,  very  frequently  behind  the  lower  sternum  and 
between  the  shoulders;  often  in  the  right  or  left  hypochondrium  or  pos- 
terior lumbar  region ;  and  gastralgic  attacks  may  involve  almost  the  entire 
abdomen. 

Intestines.— lm\)iiCi\on  of  the  colon,  according  to  its  seat,  may  cause  pain  in 
the  right  or  left  hypochondrium,  or  in  the  anterior,  lateral,  and  posterior  aspects 
of  the  thigh ;  mucous  colic  and  inguinal  hernia,  in  the  groin ;  obturator  hernia, 
in  the  knee ;  cancer  or  ulcer  of  the  rectum,  and  hemorrhoids,  in  the  sacral  and 
coccygeal  regions.  The  localized  pain  and  tenderness  of  appendicitis  is  well 
known.  Flatus  in  the  splenic  flexure  of  the  colon  may  cause  prsecordial  pain. 
A  duodenal  ulcer  may  or  may  not  be  painful  until  perforation  occurs,  and  even 
then  pain  may  be  absent.  Flatulence,  poisoning  by  lead,  mercury,  and  arsenic, 
as  well  as  acute  enteritis  and  intestinal  obstruction  or  perforation,  may  initiate 
more  or  less  general  and  severe  abdominal  pain. 


50 


THE  EVIDENCES  OP  DISEASE 


Liver  and  Gall  Bladder. — The  pain-producing  diseases  of  the  liver  are  the 
functional  disorders  and  cirrhosis,  which  may  be  moderately  painful ;  inflamma- 
tion, abscess,  and  cancer,  which  may  give  rise  to  severe  suffering. 

It  is  from  the  gall  bladder  and  its  associated  ducts  that  the  severest  form 
of  liver  pain  originates — viz.,  hepatic  colic.  A  particularly  tender  point,  which 
is  of  much  diagnostic  importance,  is  found  at  the  ninth  right  costal  cartilage  as 
an  evidence  of  an  inflamed,  impacted,  or  cancerous  gall  bladder,  or  a  gallstone 
lodged  in  the  common  duct. 


PAIN  OR  TENDERNESS 
AT  VARIOUS  POINTS 
ALONG  THE  SPINE 


Hysteria  or  Neurasthenia, 

especially  traumatic 
Anaemia 

Spinal  Curvature 
Disease  of  Vertebrae 
Arthritis  Deformans 
Lumbago 
Influenza    i 
Tonsillitis 
Variola 
Dengue 
Rachitis 
Scurvy 

Locomotor  Ataxia 
Febrile  Diseases  frequently 


Pelvic  Disease 


Renal  Colic 
Perirenal  Abscess 
Lumbo-Abdominal  Neuralgia 


PAIN 


LUMBAR  REGION 


Lumbago 

Traumatic 

Gouty 

Rheumatic 
Lumbar  Neuralgia 
Debility 
Fatigue 
Abdominal  Aneurism 


SACRAL  REGION 


Disease  of  Ovaries, 

Uterus,  Pelvic  Inflam. 
Disease  of  Testicles 
Excessive  Venery 
Ulcer  or  Cancer  of  Rectum 
Haemorrhoids 

Disease  of  Sacro-Iliac  Joint 
Disease  of  Hip  Joint 
Sacral  Neuralgia 
Sciatica 
Coccygooynia 


Fto.  15. 


Pancreas. — Acute  inflammation  of  the  pancreas  is  usually  attended  with  epi- 
gastric pain,  so  also  with  cancer  of  the  same  viscus. 

Kidney. — The  typical  painful  disorder  of  the  kidney  is  renal  colic.  Pyelitis 
may  cause  pain,  not  only  in  the  lumbar  region  but  also,  as  the  only  algetic 
symptom,  above  the  pubes.  A  movable  or  floating  kidney,  under  circum- 
stances not  as  yet  definitely  ascertained,  is  the  source  of  much  pain,  which  may 
become  excessive  if  the  ureter  is  twisted  or  kinked  (Dietl's  crisis).     A  peri- 


PAIN 


51 


renal  abscess  may  be  responsible  for  pain  and  swelling  in  one  posterior  lumbar 
region. 

Spleen. — Some  enlargements  of  the  spleen  are  painful  because  of  the  drag- 
ging weight  of  the  organ,  as  in  the  malarial  and  leucaemic  forms ;  others  give 


JOINTS  IN  GENERAL 


Acute  Rheumatism 
Chronic  Rheumatism 
gonorrhoeal  rheumatism 
Gout 
Hysteria 

Arthritis  Deformans 
Synovitis 
Pyaemia 
Post-febrile 
Arthritis 
Rachitis 
Syphilis 
Tuberculosis 


DIFFUSE   PAIN   IN 
EXTREMITIES 


Neuritis 

Muscular  Rheumatism 

Locomotor  Ataxia 

Spinal  Meningitis 

Scurvy 

Lead  Poisoning 


KNEE 


Hip-Joint  Disease 
Obturator  Hernia 


Below  knee,  Unilateral,  Non- 
inflammatory— Premonitory 
OF  Cerebral  Haemorrhage 


Fig.  16. 


PAIN 


PUBIC  REGION 


Cystitis 

Pyelitis 

Uterine  or  Ovarian  Disease 

Pelvic  Inflammations 

Ectopic  Pregnancy 


ANTERIOR  ASPECT 
OF    THIGH     (MAY 

RADIATE     DOWN     TO 
FOOT) 


Crural  Neuralgia 
Disease  of  Ovary  and 

Uterus 
Pregnant  Uterus 
Displaced  Uterus 
Dysmenorrhoea 
Impacted  Faeces 
Aneurism  or  other  Abdominal 

Tumour 
Renal  Couc 
Psoas  Abscess 
Sarcoma  (or  other  growth) 

OF  Femur 
Appendicitis  (right  thigh) 


pain  because  of  the  rapid  swelling  which  overstretches  its  fibro-elastic  frame- 
work, as  in  the  acute  enlargement  of  certain  febrile  diseases.  Pain  is  also 
present  as  an  evidence  of  inflammation  of  its  peritoneal  investment  (perisple- 
nitis). Splenic  pain  is  felt  in  the  left  hypochondrium  and  the  left  side  of  the 
chest  posteriorly. 


52  THE  EVIDENCES  OF  DISEASE 

Genitalia  and  Bladder. — Pain,  more  or  less  acute,  is  felt  as  a  symptom  of 
diseases  or  displacements  of  the  uterus  and  ovaries,  pelvic  inflammations,  the 
pregnant  uterus,  ectopic  gestation,  and  dysmenorrhoea.  According  to  the 
nature  and  severity  of  the  lesion,  the  pain  is  referred  to  the  sacral  and  pubic 
regions  (most  frequently  the  former),  the  mammary  gland,  the  anterior  aspect 
of  the  thigh,  and  the  external  and  posterior  surfaces  of  the  hip.  Rarely  pain  in 
the  heel  and  the  wrist  is  due  to  ovarian  disease,  and  in  the  hand  to  uterine  dis- 
orders. 

Prostatic  disease  may  be  responsible  for  pain  in  the  sole  of  the  foot ;  dis- 
ease of  the  testicle  and  excessive  venery,  for  sacral  pain ;  varicocele,  for  pain  in 
the  groin;  and  cystitis  and  pyelitis,  for  pain  in  the  pubic  region. 

Bones  and  Muscles. — The  painful  diseases  of  bone  which  give  rise  to  some 
confusion  in  the  practice  of  internal  medicine  are  spinal  caries,  rachitis,  or 
arthritis  deformans,  causing  pain  in  the  back,  the  lateral  walls  of  the  chest,  the 
epigastric  region,  or  generally  diffused  over  the  abdomen.  A  psoas  abscess  or 
malignant  disease  of  the  femur  makes  a  painful  thigh;  a  diseased  sternum 
causes  breast  pain;  disease  of  the  hip  joint,  a  painful  knee;  diseased  ribs, 
lateral  chest  pain ;  and  disease  of  a  sacro-iliac  joint,  sacral  backache. 

The  painful  diseases  of  the  joints  are  sufficiently  catalogued  in  the  diagram 
(Fig.  16). 

The  muscles  are  painful  in  pleurodynia  (intercostal  muscles),  lumbago  (lum- 
bar region),  and  other  varieties  of  muscular  rheumatism ;  as  a  result  of  over- 
exertion or  debility,  and  in  trichinosis.  Cramps  in  the  calves  may  be  explained 
by  too  much  walking  or  by  the  presence  of  chronic  nephritis,  and  congestion 
or  toxic  irritation  of  the  nerves  supplying  the  calf  muscles. 

Miscellaneous  Causes  of  Pain. — Mediastinal  tumour  or  abscess,  or  enlarged 
bronchial  glands  may  produce  pain  in  the  right  hypochondriac  region  and 
either  lateral  wall  of  the  chest ;  subphrenic  abscess,  in  either  hypochondrium. 
The  sharp  pain  under  either  costal  margin  after  some  violent  exercise,  espe- 
cially running,  is  probably  familiar ;  so  also  the  epigastric  and  costal  arch  pain 
after  violent  coughing  or  vomiting.  Anjemia  and  debility  are  frequently 
attended  by  a  more  or  less  severe  aching  pain  along  the  spine  and  the  left  lat- 
eral wall  of  the  chest,  extending  into  the  left  hypochondriac  region.  A  general 
backache  is  common  in  acute  febrile  diseases,  and  is  of  diagnostic  severity  in 
epidemic  influenza,  tonsilitis,  smallpox,  and  dengue.  Diffuse  soreness  of  the 
whole  body  in  rickets,  and  of  the  back  and  lower  extremities  in  infantile 
scurvy,  upon  voluntary  or  assisted  movement,  is  in  either  case  a  very  character- 
istic symptom.  As  in  locomotor  ataxia,  so  in  diabetes,  Raynaud's  disease,  and, 
more  rarely,  in  abdominal  aneurism,  there  may  be  sudden,  perhaps  violent, 
attacks  of  general  abdominal  pain. 

II.    TENDERNESS 

Tenderness  is  pain  or  soreness  produced  by  pressure.  The  greater 
portion  of  diseases  attended  by  spontaneous  pain  will  manifest  ten- 
derness on  pressure  over  the  seat  of  pain ;  but  this  is  not  an  invari- 
able rule,  as  either  pain  or  tenderness  may  exist  separately.  More 
or  less  tenderness  exists  over  the  seat  of  all  inflammations.     Pro- 


TENDERNESS  53 

longed  or  repeated  attacks  of  neuralgia  may  be  attended  by  tender 
points  corresponding  to  the  exit  of  the  affected  nerve  through  bone 
or  fascia. 

The  diagnostic  indications  to  be  derived  from  the  localization  of 
tenderness  are  as  follows : 

Head  and  Scalp. — Neuralgia  of  the  cervico-occipital  nerves,  hemicrania,  and 
periostitis  (the  latter  usually  syphilitic),  or  hysteria  may  be  suspected  if  tender- 
ness of  the  scalp  is  found  to  exist.  After  or  during  any  severe  headache  there 
may  be  a  temporary  hypersesthesia  of  the  scalp,  so  that  combing  or  brushing 
the  hair  is  painful. 

Mastoid  Process. — Suppurative  mastoiditis. 

Malar  Bane. — Tenderness  below  the  inner  part  of  the  malar  bone  over  the 
superior  maxilla  is  found  in  suppurative  or  malignant  disease  of  the  antrum  or 
maxilla. 

I^eck. — Swollen  or  inflamed  lymphatic  glands  from  any  cause,  cervico- 
occipital  neuralgia,  cervical  myalgia,  and  cervical  caries  are  the  most  frequent 
causes  of  tenderness  in  the  neck. 

Back. — 1.  Tenderness  along  the  wfiole  length  of  the  spine,  either  continuous 
or  in  a  series  of  points,  may  be  due  to 
Arthritis  deformans.  Periostitis  (spinal), 

Cerebro-spinal  meningitis.  Spinal  irritation. 

Hysteria,  Spinal  meningitis, 

Myelitis,  Rheumatism. 

Neurasthenia, 

2.  Tenderness  over  the  dorsal  spine  may  be  caused  by  thoracic  aneurism,  tuber- 
culous disease  of  the  spine,  enlarged  bronchial  glands,  or  tumour  in  the  pos- 
terior mediastinum. 

3.  Tenderness  over  lumbar  spine,  by  abdominal  aneurism,  subphrenic  ab- 
scess, perinephritic  abscess,  suppurative  and  acute  nephritis,  lumbar  abscess, 
and  tuberculous  disease  of  the  spine. 

Thorax  (in  front). — Tenderness  may  be  due  to  ostitis  or  periostitis  of  sternum 
or  ribs,  or  inflammation  of  the  costal  cartilages;  tender  breast,  to  hysteria  or 
tumour;  tender  points,  to  intercostal  neuralgia,  projecting  or  eroding  aneurism, 
abscess  of  chest  wall,  and  perforating  empyema.  The  infraclavicular  spaces 
are  often  tender  on  percussion  in  advanced  phthisis. 

Pain  from  pressure  on  the  prsecordial  area  may  arise  from  pericarditis. 

Abdomen. — 1,  General  tenderness  of  the  abdomen  may  be  caused  by 
Dysentery,  Simple  peritonitis, 

Dysmenorrhoea,  Suppurative  peritonitis. 

Strangulated  hernia.  Tuberculous  peritonitis, 

Hysteria,  Diaphragmatic  pleuritis, 

Cancer  of  intestine,  Irritant  poisons, 

Ulceration  of  intestine,  Rheumatism  of  abdominal  walls. 

2.  Hypochondrium. — Tenderness  in  the  right  hypochondrium  may  be  due  to 
Empyema  of  gall  bladder.  Influenza  (epidemic). 

Gallstones,  Abscess  of  liver, 

6 


54  THE   EVIDENCES  OF   DISEASE 

Acute  inflammation  of  liver,  Syphilis  of  liver, 

Acute  yellow  atrophy  of  liver,  Malarial  fever  (both  sides), 

Cancer  of  liver,  Perihepatitis, 

Inflamed  hydatids  of  liver.  Relapsing  fever. 

3.  Epigastrium. — Tenderness  in  the  epigastrium  may  be  indicative  of 
Addison's  disease,  Acute  yellow  atrophy  of  liver, 
Gallstones,  Pancreatitis, 

Acute  gastritis.  Acute  pericarditis. 

Chronic  gastritis,  Diaphragmatic  pleurisy, 

Hypochondriasis,  Irritant  poisons. 

Hysteria,  Ulcer  of  stomach. 

4.  Iliac  Region. — Tenderness  in  one  or  both  iliac  regions  may  arise  from 
pelvic  peritonitis  and  pelvic  inflammations  in  general,  hysteria,  fecal  impac- 
tion, and  membranous  enteritis  (usually  in  left  side).  Tenderness  in  the  right 
iliac  region  occurs  with  typhoid  fever  and  appendicitis. 

5.  Hypogastrium. — Tenderness  in  the  hypogastric  region  may  originate 
from  cystitis,  pelvic  inflammations,  or  congestion,  hysteria,  and  dysmenorrhoea. 

Extremities. — Tenderness  found  in  the  extremities  may  be  due  to  neuritis, 
in  which  case  it  will  be  found  along  the  course  of  the  nerve ;  to  phlebitis,  the 
tender  vein  being  felt  as  a  hard  cord ;  to  ostitis  or  periostitis,  or  malignant  dis- 
ease of  the  bone ;  to  myalgia,  rachitis,  scurvy,  trichinosis,  or  tetanus ;  to  disease 
of  the  joints.  Tender  joints  are  usually  due  to  rheumatism,  acute,  chronic,  or 
gonorrhoeal;  to  arthritis  deformans,  synovitis,  sprain,  gout,  tuberculosis,  pyae- 
mia, or  hysteria. 

III.  PAR/ESTHESIAS 

The  word  paraesthesia  is  here  used  as  embracing  a  number  of 
subjective  sensations,  largely  of  cutaneous  origin.  Among  the  pares- 
thesias are  :  Sensations  of  bearing  down,  of  coldness,  faintness,  formi- 
cation, itching,  fulness,  the  girdle  sensation,  sensation  of  heat,  numb- 
ness, tingling,  burning,  oppression  or  weight,  praecordial  constriction 
and  sinking,  throbbing,  tightness,  and  weakness  or  debility. 

Diagnostic  Significance  of  Paraesthesias  in  General. — Leaving  out 
of  account  the  hyperaesthesias  and  anaesthesias,  there  is  a  large  class 
of  cases  in  which  some  of  the  peculiar  and  annoying  sensations  just 
mentioned  are  the  only  symptoms  of  which  complaint  is  made. 
Such  cases,  mainly  in  women,  form  a  considerable  proportion  of  the 
office  practice  of  the  physician,  especially  among  those  in  the  better 
grades  of  society.  The  sensations  of  most  frequent  occurrence  in 
these  patients  are  weakness,  numbness,  flashes  of  heat  or  cold,  throb- 
bing, general  or  localized,  tingling,  burning,  and  sudden  perspira- 
tions, as  well  as  other  sensations  which  are  described  in  the  most 
bizarre  manner,  or,  possibly,  said  to  be  indescribable.  A  careful 
examination  in  such  cases  will  reveal,  as  a  rule,  nothing  beyond  a 
moderate  anaemia,  slight  digestive  disturbance,  constipation,  irregular 


PARiESTHESIAS  55 

innervation,  and  poor  nutrition.  The  previous  history  will  tell  of 
overwork  of  some  kind,  grief,  worry,  anxiety,  or  a  congenital  defi- 
ciency in  what,  for  lack  of  a  better  term,  is  called  "  vitality."  Such 
cases  must  be  classified  as  examples  of  a  slight  degree  of  neuras- 
thenia. 

If,  however,  certain  of  these  paraesthesias,  such  as  numbness,  prick- 
ling, formication,  tingling,  or  burning,  become  localized  in  a  certain 
nerve  or  a  definite  part  of  the  body,  they  become  comparable  to  a 
definite  disease  (Dana).  In  the  majority  of  cases  such  localized  subjec- 
tive sensations  are  due  to  the  same  kind  of  irritation  as  that  which 
gives  rise  to  a  neuralgia,  except  that  it  is  of  lesser  intensity  and  the 
sensation  is  not  sufficiently  severe  to  conform  to  the  usual  conception 
of  pain.  The  most  frequent  perversion  of  sensation  is  that  of  a  prick- 
ling numbness,  less  frequently  a  sensation  of  burning.  When  such 
paresthesias  affect  the  head,  there  are  sensations  of  pressure,  burn- 
ing, or  constriction — incomplete  headaches — and  their  most  common 
cause  will  be  found  in  the  presence  of  neurasthenia  or  lithaemia.  If 
situated  in  individual  nerves,  occurring  especially  in  the  brachial, 
ulnar,  crural,  and  plantar,  they  may  be  regarded  as  incomplete  neu- 
ralgias. If  the  feet  or  hands,  or  both,  are  generally  involved,  it  con- 
stitutes acro-pargesthesia. 

Diagnostic  Significance  of  Special  Paraesthesias. — 

1.  Bearing  Down. — The  sensation  of  bearing  down  is  felt  chiefly  in  the 
pelvis.  The  causes  of  this  sensation  are  for  the  most  part  diseases  or  condi- 
tions affecting  the  uterus,  especially  membranous  dysmenorrhoea.  Hemor- 
rhoids, undue  fulness  of  the  bladder,  and  sometimes  prolonged  standing  may 
also  be  responsible. 

2.  Coldness  or  Chilliness. — Subjective  sensations  of  coldness,  existing  with 
a  normal  or  subnormal  temperature,  may  be  due  to  hysteria,  lateral  sclerosis, 
myxcfidema,  neurasthenia  or  syringomyelia ;  and  chilliness  may  be  present  as  one 
of  the  prodromal  symptoms  of  an  attack  of  migraine. 

Cold  sensations  (psychro-aesthesias)  may  implicate  a  whole  extremity,  or  all 
four  extremities,  without  being  limited  to  certain  areas  or  the  distribution  of 
a  nerve  (Dana).  Not  infrequently  these  are  associated  with  other  paraesthesias 
(jirickling  and  numbness),  with  pain,  and  with  local  disturbances  of  the  circu- 
lation. This  form  of  cold  sensation  is  usually  indicative  of  a  mild  neuritis  due 
to  the  abuse  of  alcohol,  or  to  a  rheumatic  diathesis,  exposure,  and  toxaemias.  It 
may  also  occur  in  locomotor  ataxia  and  in  the  early  stage  of  syringomyelia. 

On  the  other  hand,  the  cold  sensation  may  be  limited  to  some  special  area, 
usually  upon  the  buttock  or  thigh,  sometimes  the  calf,  corresponding  pretty  ac- 
curately to  the  distribution  of  a  nerve.  The  feeling  is  as  though  something 
tangible  and  cold  were  in  contact  with  the  part.  The  sensation  may  be  so  dis- 
tressing that  it  is  very  properly  termed  a  cold  pain  (psychro-algia).  These 
circumscribed  areas  of  coldness  are  found,  as  a  rule,  in  patients  over  40,  more 
commonly  in  men.     The  causes  may  be  found  in  pressure  upon  the  nerves  due 


56  THE  EVIDENCES  OF  DISEASE 

to  occupation,  rheumatism,  or  exposure,  and  in  many  cases  a  neuropathic  diath- 
esis is  an  underlying  agency.  If  obstinate,  syringomyelia  or,  rarely,  loco- 
motor ataxia  may  be  responsible  for  this  symptom. 

3.  Faintness. — A  sensation  of  weakness  with  a  tendency  to  syncope,  persistent, 
recurrent,  or  acute,  may  be  present  as  an  accompaniment  of  the  various  forms 
of  anaemia,  angina  pectoris,  fatty  heart,  thrombosis  of  the  pulmonary  artery, 
pneumothorax,  thoracic  aneurism,  ascites  (especially  during  tapping),  and 
tympanites.  It  may  be  present  as  a  result  of  emotion,  fatigue,  excessive  heat, 
painful  affections,  depressing  poisons,  and  as  an  evidence  of  shock  after  injuries. 
As  an  idiosyncrasy  it  attends  the  act  of  defecation  in  certain  persons,  and  is 
a  frequent  event  in  M6nidre's  disease. 

4.  Formication,  ItcTiing. — Formication  is  a  sensation  as  of  ants  or  other 
insects  crawling  over  the  skin.  It  is  a  variety  of  itching  or  pruritus,  and  in 
varying  degrees  and  in  different  parts  of  the  body  may  result  from  many  dis- 
eases of  the  skin,  including  the  exanthemata.  Affecting  the  external  genitals, 
it  may  be  due  to  diabetes,  leucorrhcea,  or  neuroses ;  the  anus,  to  seat  worms  or 
hemorrhoids.  It  is  an  occasional  premonitory  symptom  of  apoplexy,  and  may 
be  present  as  a  consequence  of  a  tumour  of  the  brain,  in  the  part  supplied  from 
the  seat  of  the  lesion.  More  or  less  general  pruritus  frequently  occurs  in  hys- 
teria and  neurasthenia,  also  in  locomotor  ataxia,  chronic  spinal  meningitis, 
chronic  myelitis,  disseminated  sclerosis,  chronic  lead  poisoning,  and  tetany.  It 
is  general  and  frequent  in  jaundice,  less  often  it  is  found  in  gout  and  cases  of 
granular  kidney.  It  is  an  occasional  result  of  the  administration  of  morphine 
(especially  affecting  the  nose),  copaiba,  and  ergot. 

General  itching  or  pruritus,  if  persistent,  should  lead  to  an  examination  for 
the  existence  of  gout,  lead  poisoning,  chronic  interstitial  nephritis,  or  diabetes 
mellitus. 

5.  Fulness. — A  sensation  of  fulness  in  the  chest  or  epigastrium  is  caused  by 
chronic  gastritis,  nervous  dyspepsia,  or  dilatation  of  the  stomach,  as  well  as  by 
cardiac  hypertrophy,  pulmonary  emphysema,  chronic  peritonitis,  tympanites, 
or  malarial  fevers. 

6.  Girdle  Sensation. — A  subjective  sensation  as  of  a  constricting  band 
around  the  trunk  is  found  in  connection  with  locomotor  ataxia,  chronic  mye- 
litis, injury  or  tumour  of  the  spinal  cord,  and  inflammation  or  tumour  of  the 
spinal  meninges.  After  prolonged  vomiting  or  repeated  paroxysms  of  violent 
cough,  a  similar  sensation  may  be  felt,  corresponding  to  the  insertion  of  the 
diaphragm,  and  due  to  a  strain  of  that  muscle. 

7.  iJsa^.— Subjective  sensations  of  heat  may  be  felt  in  the  epigastrium  and 
beneath  the  sternum  in  pyrosis  and  irritant  poisoning,  and  to  a  less  degree  in 
acute  bronchitis ;  in  the  back,  in  spinal  irritation  or  neurasthenia.  Flashes  of 
heat,  with  or  without  flushing  of  the  face  and  sudden  perspirations,  are  com- 
mon attendants  of  the  menopause,  as  well  as  disease  of  the  pelvic  viscera  and 
conditions  of  debility  and  nerve  tire.  Subjective  sensations  of  heat  may  be 
felt  in  the  back  and  epigastrium  in  paralysis  agitans. 

8.  Numbness,  Tingling,  Burning. — These  are  of  rather  common  occurrence, 
and  may  possess  diagnostic  value.  Particularly  in  the  feet,  they  are  in  some 
cases  the  first  symptoms  of  locomotor  ataxia,  myelitis,  or  chronic  spinal  men- 
ingitis, and  are  very  frequent  in  neurasthenia  and  hysteria,  and  (in  the  fingers 


PARESTHESIAS  57 

and  toesj  are  not  infrequent  in  arthritis  deformans.  Numbness  (fingers,  occa- 
sionally scalp  and  feet)  on  waking  in  the  morning,  which  at  first  passes  away,  but 
later  remains  during  the  day,  is  acro-paraesthesia  or  waking  numbness.  Localized 
numbness  is  sometimes  caused  by  a  tumour  of  that  portion  of  the  brain  which 
supplies  the  area  of  abnormal  sensation.  In  tetany  there  is  numbness  of  the 
fingers  and  toes,  and  tingling  or  biu-ning  is  an  occasional  premonitory  symp- 
tom of  neuralgia  or  herpes  zoster.     Certain  poisons  also  may  cause  numbness. 

The  diseases  or  poisons  of  which  numbness,  tingling,  or  burning  may  be 
indications  are  as  follows: 
Aconite    poisoning    (general    numb-        Epilepsy   (occasionally  as  a  part   of 

ness),  the  aura), 

Apoplexy  (an  occasional  premonitory        Herpes    zoster    (peripheral    termina- 

symptom),  tions  of  affected  nerve). 

Appendicitis    (occasionally  in    right        Hysteria  (a  frequent  symptom), 

leg).  Injuries  of  nerves, 

Artluitis  deformans  (hands  and  feet),         Locomotor  ataxia  (feet  and  legs), 
Beri-beri  (multiple  neuritis).  Myelitis  (early  stage), 

Brain    tumour    (jiart   supplied   from        Myxoedema, 

seat  of  lesion).  Neuralgia  (premonitory), 

Bromism,  Neurasthenia  (frequent), 

Carbolic  acid  (local  contact  of).  Neuritis, 

Chronic  spinal  meningitis,  Sciatica, 

Tetany  (fingers  and  toes). 

9.  Oppression  or  Weight. — When  felt  in  the  chest,  is  most  frequently  found 
in  hemoptysis,  hysteria,  spasmodic  asthma,  angina  pectoris,  nervous  dyspepsia, 
and  chronic  gastritis;  less  commonly  in  cardiac  or  pericardial  disease,  Basedow's 
disease,  exophthalmic  goitre,  and  tumour  of  the  mediastinum.  When  felt  in 
the  epigastrivm,  is  usually  caused  by  neurasthenia,  chronic  gastritis,  nervous 
dyspepsia,  or,  rarely,  as  a  premonition  of  gastric  hemorrhage.  A  feeling  of 
pressure  or  weight  in  the  Tiead  is  common  in  neurasthenia  and  hypochondriasis, 
and  is  occasionally  premonitory  of  apoplexy  or  is  a  part  of  the  epileptic  aura. 
A  similar  sensation  in  the  abdomen  or  pelvis  attends  the  presence  of  abdominal 
or  pelvic  tumours. 

10.  Precordial  Constriction  and  Sinking.  — A  typical  example  of  this  distress- 
ing symptom,  associated  with  agonizing  pain,  is  seen  in  angina  pectoris,  and 
to-  a  lesser  degree  in  pseudo-angina.  A  sensation  of  cardiac  weakness  and 
sinking  may  be  indicative  of  dyspepsia  or  gastritis,  especially  the  acute  forms. 
Severe  acute  diarrhoea,  and  especially  cholera  (sporadic  or  Asiatic),  will  rapidly 
exhibit  this  symptom.  It  is  not  infrequently  a  concomitant  of  tympanites,  car- 
diac dilatation,  or  pericarditis,  and,  finally,  it  may  be  a  subject  of  complaint  in 
hysteria,  neurasthenia,  and  hj-^pochondriasis. 

11.  Throbbing. — This,  as  a  subjective  sensation,  felt  over  the  entire  body  or 
in  the  head  and  extremities,  is  not  infrequent  in  hysteria,  neurasthenia,  vaso- 
motor ataxia,  the  anaemias,  and  aortic  regurgitation.  Locally  it  is  felt  in 
phlegmonous  inflammations  and  over  the  seat  of  an  aneurism ;  in  the  neck  and 
head,  in  cases  of  exophthalmic  goitre ;  in  tlie  head,  in  migrainous  headaches ; 
in  the  precordial  area,  in  cardiac  hypertrophy  or  palpitation;  and  the  "throb- 
bing aorta  "  is  very  common  in  gastritis  and  neurasthenia. 


58  THE  EVIDENCES  OP   DISEASE 

12.  Tightness. — This,  when  substernal,  is  usually  associated  with  the  dry 
stage  of  an  acute  tracheitis  and  bronchitis  of  the  larger  tubes.  The  term  is 
also  applied  to  the  character  of  the  cough  in  the  same  stage. 

13.  Weahness  or  Debility. — A  feeling  of  muscular  weakness,  debility,  or 
lassitude  attends  the  prodromal  stage  of  fevers,  and  is  a  sequel,  more  or  less 
prolonged,  of  all  febrile  and  exhausting  diseases.  It  may  also  be  a  concomitant 
of  tlie  dyspepsias;  the  overuse  of  tea,  coffee,  alcohol,  and  tobacco;  and  rheu- 
matism, gout,  and  lithsemia. 

This  symptom,  when  persistent,  has  a  distinct  clinical  value  in  suggesting 
the  presence  of  neurasthenia  (most  frequent),  pulmonary  tuberculosis  (even 
without  physical  signs),  diabetes,  anaemia,  influenza  (obstinate),  latent  pleurisy, 
and  exophthalmic  goitre. 


SECTION  YI 
VERTIGO 

Vertigo  or  dizziness  is  a  subjective  sensation  of  loss  of  equi- 
librium. The  patient  feels  as  if  he  himself  were  whirling,  sinking,  or 
rising  (subjective  vertigo),  or  surrounding  objects  may  appear  to  be 
rapidly  revolving,  sinking,  or  rising  {objective  vertigo).  Horizontal 
vertigo  is  felt  when  reclining  and  disappears  on  rising.  In  a  severe 
case  the  sensation  may  be  so  sudden  and  profound  as  to  be  likened 
to  a  blow  ;  in  the  slighter  degrees  there  is  a  swimming  lightness  in 
the  head.  The  severe  and  acute  forms  are  usually  of  brief  duration, 
but  in  its  lighter  forms  it  may  last  for  weeks  and  months  (status 
vertiginosus).  The  gait  is  reeling  or  staggering,  like  that  of  a 
drunken  man.  Slight  nausea  often  co-exists,  and  vomiting  may 
follow  a  sharp  attack.  Loss  of  consciousness,  if  occurring,  is  only 
momentary. 

Vertigo  is  a  cause  of  so  much  alarm  to  the  patient  that  the  deter- 
mination of  its  origin  in  a  given  case  is  of  great  importance.  In  by 
far  the  larger  proportion  of  cases  it  is  due  to  neurasthenia,  especially 
the  lithfemic  form,  gastric  disorders,  arteriosclerosis,  aural  disease, 
or  eye  strain,  these  causes  being  arranged  approximately  in  the 
order  of  relative  frequency.  Very  rarely  the  vertigo  is  essential, 
without  discoverable  cause. 

In  all  cases  a  careful  examination  should  be  instituted  for  the 
discovery  of  diseases  or  conditions  which  may  be  responsible  for  this 
symptom,  as  follows : 

Neurasthenia  and  Lithmnia. — (a)  If  a  patient  with  a  history  of  overstrain, 
or  congenital  deficiency  in  nerve  force,  complains  of  constant  weariness,  feel- 
ings of  pressure  in  the  head,  and  other  characteristic  symptoms,  with  vertigo  of 


VERTIGO  59 

brief  duration  and  moderate  severity,  but  of  frequent  occurrence,  the  vertigo  is 
due  to  neurasthenia  (q.  v.). 

(b)  If  in  addition  the  urine  is  high  coloured,  strongly  acid,  and  with  a  high 
specific  gravity  (1.028  to  1.032),  the  cause  of  the  vertigo  is  neurasthenia  ^>?>/« 
lithsemia.     The  latter  alone  may  be  a  cause  of  vertigo. 

Gastric  Disorders. — (a)  If  a  patient  of  middle  age  complains  of  a  sudden 
vertigo  with  headache  after  too  free  indulgence  in  the  pleasures  of  the  table, 
and  the  symptoms  slowly  disappear  after  vomiting  or  the  administration  of  a 
purgative,  the  vertigo  is  due  to  acute  indigestion. 

{h)  If  there  is  sudden  headache,  dimness  of  vision  (blind  headache),  marked 
vertigo  causing  a  reeling  gait,  temporary  mental  confusion,  and  possibly  vomit- 
ing of  an  extremely  sour  fluid,  the  vertigo  is  due  to  hyperacidity  of  the  stomach 
contents  {q.  v.). 

{c)  If  there  is  a  history,  extending  over  months  or  years,  of  oppression  or 
distress  after  eating,  epigastric  tenderness,  etc.,  with  a  rather  constant  but 
slight  vertigo,  it  is  due  to  chronic  gastritis  {q.  v.). 

Arteriosclerosis;  Valvular  Disease  of  Heart;  Aneurism. — (a)  If  a  man  or 
woman,  past  middle  age,  complaining  of  constant  slight  vertigo,  intensified  on 
excitement  or  exertion,  presents  sclerosed  arteries,  areas  senilis,  and  ringing 
aortic  closure,  with  or  without  moderate  cardiac  hypertrophy,  the  vertigo  is 
due  to  arteriosclerosis. 

(b)  A  similar  complaint  in  a  patient  with  water-hammer  pulse,  marked 
cardiac  hypertrophy,  and  a  diastolic  murmur,  most  intense  over  the  aortic 
cartilage,  is  due  to  aortic  regurgitation. 

(c)  Vertigo  may  attend  an  aneurism  of  the  thoracic  aorta,  because  of  the 
disturbed  intracranial  circulation. 

Meniere's  Disease. — If  a  patient,  generally  a  man  past  40,  has  sudden 
attacks  of  vertigo,  with  tinnitus  or  incomplete  deafness  in  one  or  both  ears,  the 
combination  is  sufficient  to  warrant  the  diagnosis  of  Meniere's  disease  (aural 
vertigo,  labyrinthine  vertigo). 

Vertigo  accompanying  other  diseases  or  conditions  is  rarely  associated  with 
tinnitus  or  deafness.  The  vertigo  of  Meniere's  disease  is  abrupt  in  its  onset, 
and  the  patient  may  fall  before  he  has  time  to  grasp  some  near-by  object.  There 
may  be  a  momentary  loss  of  consciousness.  He  becomes  pale,  and  the  face  is 
covered  with  perspiration.  Nausea  follows,  and  vomiting  may  take  place.  The 
tinnitus  may  consist  of  hissing,  buzzing,  roaring,  or  throbbing  noises,  more 
rarely  sudden  and  loud  reports  like  pistol  shots.  The  attacks  may  recur  several 
times  in  a  day,  or  may  be  months  apart.  In  the  intervals  there  may  be  a  more 
or  less  continuous  giddiness.  Rare  symptoms  during  the  attack  are  diplopia 
and  nystagmus,  double  vision,  or  oscillatory  movements  of  the  eyeballs.  The 
deafness  is  usually  progressive  but  incomplete,  affecting  one  or  both  ears. 

The  causes  of  Meniere's  disease  are  variously  stated.  It  has  been  attributed 
to  disease  of  the  labyrinth  in  particular,  hemorrhagic  or  degenerative;  to  sup- 
purative or  other  disease  of  the  middle  ear;  to  disease  of  the  external  ear 
(furuncle,  inspissated  cerumen) :  to  a  vasomotor  neurosis  of  the  vessels  of  the 
semicircular  canals ;  to  disease  of  the  centres  of  hearing  and  equilibration. 

Eye  Strain. — In  a  patient  presenting  symptoms  of  eye  strain,  viz.,  indis- 
tinctness or  blurring  of  sight,  brow  pain  or  occipital  headache,  reddening  or 


60  THE  EVIDENCES  OF  DISEASE 

watering  of  the  eyes,  these  following  use  of  the  eyes  upon  near  work,  as  read- 
ing, writing,  or  sewing,  together  with  vertigo  which  is  not  severe  but  rather 
persistent,  and  examination  of  the  eye  reveals  errors  of  refraction,  strabismus, 
or  exophoria,  the  vertigo  may  be  due  to  the  ocular  defect.  The  diagnosis  can 
be  made  positively  only  by  the  disappearance  of  the  vertigo  after  the  necessary 
corrections,  optical  or  operative,  have  been  made. 

Among  the  less  common  causes  of  vertigo  {q.  v.)  are:  epilepsy,  in  which 
vertigo  may  be  a  part  of  the  aura  preceding  the  convulsion  or,  alone,  usually 
with  a  momentary  loss  of  consciousness,  constitute  an  attack  of  petit  mal,  and 
is  discriminated  from  Meniere's  disease  by  the  absence  of  tinnitus;  anaemia, 
especially  upon  exertion ;  brain  tumours ;  the  abuse  of  tea,  coffee,  alcohol,  and 
tobacco;  auto-intoxication  from  absorption  of  decomposing  substances;  and 
chronic  interstitial  nephritis.  Vertigo  may  also  be  a  symptom  of  locomotor 
ataxia ;  disseminated  sclerosis  (rarely) ;  great  mental  overwork  or  excitement  in 
neurotic  persons  (sudden,  with  faintness  and  nausea,  lasting  several  hours) ;  or 
mechanical  (sea-sickness,  railway  and  elevator  sickness).  It  may  be  transitory 
and  caused  by  looking  at  a  rapidly  rotating  body;  vertical,  by  looking  up 
toward  or  down  from  a  height ;  lateral,  occurring  while  the  patient  is  walking 
alongside  of  some  construction  made  up  of  similar  parts,  like  a  wall  or  fence; 
or  nocturnal,  felt  in  the  act  of  going  to  sleep. 

Laryngeal  Vertigo  (L.  syncope,  L.  epilepsy). — This  rare  disease  is  either  a 
true  epilepsy  or  a  reflex  neurosis,  probably  the  latter.  It  usually  manifests 
itself  in  middle-aged  neurotic  men,  who  are  suffering  from  laryngitis,  bron- 
chitis, bronchial  asthma,  or  phthisis  pulmonalis.  The  attack  begins  with 
laryngeal  tickling  or  irritation,  followed  by  a  short  cough,  spasm  of  the  larynx, 
dyspnoea,  transitory  syncope,  and  slight  convulsive  movements.  Such  attacks 
may  recur  every  day  or  at  intervals  of  a  month  or  more.  As  a  rule,  the  removal 
of  the  local  lesions,  when  possible,  will  put  a  stop  to  the  paroxysms. 


SECTION   VII 

TEMPERAMENT— PSYCHICAL    CONDITION— EXPRESSIO?^ 
OF  FACE— DELIRIUM 

DuRiKG  the  general  examination  the  physician  should  endeavour 
to  form  some  conception  of  the  mental  characteristics  of  the  indi- 
vidual, in  health  and  as  modified  by  disease.  As  a  rule,  the  more 
highly  trained  the  mind  and  the  more  elaborate  and  complex  the 
social  environment,  the  greater  is  the  necessity  for  an  appreciation 
of  the  personal  traits  of  the  individual.  Influences  which  produce 
no  apparent  effect  upon  the  labourer,  toughened  by  hard  life,  will 
cause  profound  perturbation  in  the  somewhat  hyperaesthetic  woman 
whose  nervous  system  is  in  a  state  of  tension  from  the  demands  of 
society,  art,  or  literature.  Delirium,  for  instance,  is  a  much  less 
significant  symptom  when  encountered  in  a  person  possessing  a  sen- 


TEMPERAMENT  61 

sitive  nervous  organization  than  when  it  is  present  in  one  of  a 
phlegmatic  and  sturdy  temperament. 

If  necessary,  information  may  be  obtained  from  friends  or  relatives 
concerning  the  mental  traits  of  the  patient  in  health.  One  should 
inquire  especially  as  to  the  existence  of  extreme  susceptibility  to 
pain  and  exaggeration  in  the  manner  of  expression ;  as  to  whether 
the  patient  is  or  is  not  easily  elated  or  depressed,  or  given  to  undue 
solicitude  about  personal  health ;  and  other  points  which  may  be 
serviceable  in  estimating  the  value  of  the  statements  made  by  the 
patient,  or  the  present  deviation  from  the  normal  mental  condition. 
Such  inquiries  should  be  made  with  circumspection  and  tact  in  order 
to  avoid  misconception  of  motives  and  the  charge  of  making  imputa- 
tions uncomplimentary  to  the  patient. 

I.  Temperament. — In  this  connection  a  word  may  be  said  in 
regard  to  the  old  classification  of  temperaments,  into  sanguine, 
bilious,  nervous,  strumous,  and  lymphatic.  Considered  as  large  groups, 
there  is  doubtless  a  partial  justification  for  such  divisions,  but  the 
attempt  to  place  an  individual  patient  in  one  of  these  is  almost  hope- 
less, as  is  clearly  proved  by  the  frequent  necessity  felt  by  the  older 
writers  for  word  combinations,  of  which  Mlio-sanguine,  lymphatico- 
sanguine,  are  examples.  As  a  matter  of  fact,  the  majority  of  men 
exhibit  the  characteristics  belonging  to  more  than  one  of  the  tem- 
peramental classes. 

Xevertheless,  it  is  often  convenient  to  use  the  names  given  to 
the  temperaments  as  descriptive  terms,  without  the  broad  meaning 
which  was  formerly  implied  by  their  use.  Thus  it  may  be  a  mate- 
rial aid  in  the  description  of  a  particular  case  to  say  that  the  patient 
is  of  a  nervous  temperament,  meaning  thereby  that  his  nervous 
system  is  sensitive,  and  that  he  has  a  gouty  diathesis.  Practically, 
the  tendency  of  modern  writers  is  to  retain  some  of  the  names  of 
temperaments  for  the  characterization  mainly  of  mental  qualities, 
while  physical  characteristics  and  predispositions  toward  disease  are 
spoken  of  as  diatheses  {q.  v.),  a  suitable  qualifying  adjective  being 
prefixed. 

Choleric  Temperament. — Exhibits  great  irritability  and  strong 
passions,  with  very  active  voluntary  muscles. 

Phlegmatic  or  Lymphatic  Temperament. — Characterized  by  a  want 
of  energy,  small  or  slow  reaction  to  psychic  excitations,  slightly  de- 
veloped passions,  and  little  sensibility  to  bodily  suffering. 

Melancholic  (Atrabiliary)  Temperament. — Marked  by  slight  irri- 
tability, united  with  strong  capacity  for  reacting  to  sensory  excita- 
tions, and  by  great  persistence  of  the  frame  of  mind,  especially  that 
of  sullenness  or  dulness. 


62  THE  EVIDENCES  OF   DISEASE 

Nervous  Temperament. — Characterized  by  marked  sensitiveness 
of  the  nervous  system  to  slight  impressions. 

Sanguine  Temperament. — Characterized  by  marked  irritability, 
great  liability  of  the  nervous  system  to  exhaustion,  and  sudden 
changes  in  humour. 

II.  Psychical  Condition. — In  determining  the  present  psy- 
chical condition  of  the  patient  it  is  necessary  to  test  the  m,emory,  not 
only  in  regard  to  recent  but  also  in  regard  to  long  past  occurrences, 
as  one  of  the  first  faculties  of  the  mind  to  give  way  in  conditions  of 
weakness  or  disease  is  the  power  of  recollection.  It  is  also  requisite  to 
determine  the  power  of  judgment,  the  ability  to  follow  a  logical  train 
of  thought  and  to  appreciate  the  relative  value  of  facts.  An  abnor- 
mal increase  in  mental  activity,  with  a  rapid  flow  of  ideas  and  a  cer- 
tain exaltation  of  the  frame  of  mind,  may  be  encountered,  as  well 
as  its  opposite,  a  depressed,  sluggish,  and  melancholy  humour.  It  is, 
of  course,  necessary  to  make  due  allowance  for  the  degree  of  educa- 
tion and  the  age  of  the  patient.  The  emotional  state  of  the  patient 
is  a  part  of  the  psychical  condition ;  and,  as  an  index  to  the  mental 
status,  the  expression  of  the  face  may  give  valuable  information.  The 
occurrence  of  delirium  and  more  or  less  complete  unconsciousness 
may  also  be  conveniently  included  in  this  part  of  the  general 
examination. 

The  class  of  symptoms  here  considered  may  occur  in  connection 
with  either  acute  or  chronic  disease,  and  the  disease  may  be  one 
which  affects  the  brain  and  nervous  system  alone  or  may  be  a  general 
morbid  condition  of  which  the  symptoms  referable  to  the  nervous 
system  are  merely  indications  or  effects,  as  follows : 

(1)  Facial  Expression. — {a)  An  anxious  expression  is  observed  in 
diseases  attended  with  pain,  as  angina  pectoris,  aneurism  pressing  on 
nerve  branches  or  causing  erosion  of  the  vertebrae,  simple  intestinal 
or  lead  colic,  pleurisy  and  pneumonia,  intestinal  obstruction  from 
any  cause,  and  especially  in  peritonitis.  A  peculiarly  worried  and 
anxious  look  is  especially  important  if  occurring  in  patients  with  the 
symptoms  of  appendicitis,  as  it  is  significant  of  peritoneal  involve- 
ment. It  also  attends  diseases  which  cause  dyspnoea,  as  asthma, 
pneumothorax  or  large  pleural  effusions,  and  laryngeal  stenosis  from 
any  cause.  It  is  a  frequent  accompaniment  of  general  septic  condi- 
tions (septicaemia,  pyaemia)  and  the  beginning  of  many  infectious 
fevers,  as  well  as  of  pericardial  and  endocardial  inflammations. 

{h)  An  expression  of  fright  and  alarm  is  usual  in  connection  with 
large  hemorrhages,  and  is  frequently  seen  in  nervous  and  hypo- 
chondriacal individuals. 

(c)  A  face  devoid  of  expression,  vacant  and  unmeaning  in  aspect, 


PSYCHICAL  CONDITION  63 

may  be  witnessed  in  varying  degrees  in  facial  paralysis,  idiocy, 
dementia,  and  hydrocephalus.  Its  most  frequent  occurrence  is  in 
typhoid  fever  (hebetude)  and  the  typhoid  condition  which  attends 
so  many  low  fevers  and  septic  processes. 

(d)  There  are  certain  contortions  or  spasms  of  the  facial  muscles 
which  give  a  peculiar  expression  to  the  face,  as  in  chorea,  hysteria,  or 
insanity.  Here,  too,  may  be  classed  the  risus  sardonicus,  due  to 
contraction  of  the  depressors  of  the  angles  of  the  mouth,  which  may 
be  seen  in  tetanus  and  strychnine  poisoning,  and  which  has  been 
observed  also  in  inflammation  of  the  diaphragmatic  pleura  and  gen- 
eral peritonitis. 

For  further  information  concerning  the  fades  of  disease,  consult 
index. 

2.  Emotional  State. — («)  Mental  Depression. — A  melancholy 
humour  is  characteristic  of  hypochondriasis,  melancholia,  jaundice 
and  other  derangements  of  the  digestive  system ;  and  an  alternation 
of  high  and  low  spirits  not  infrequently  attends  neurasthenia,  hys- 
teria, chloro-anasmia,  embolic  or  thrombotic  cerebral  softening,  and 
the  menopause. 

(b)  Mental  Excitement. — A  condition  of  emotional  excitement  is 
present  in  certain  forms  of  mania,  delirium,  and  the  first  stage  of 
acute  alcoholism.  It  may  be  seen  also  during  the  administration  of 
chloroform,  ether,  or  nitrous  oxide. 

(c)  Irritability  of  temper,  manifested  by  outbursts  of  anger,  or,  in 
a  lesser  degree,  by  querulousness,  may  be  present  in  connection  with 
gout,  rheumatism,  jaundice,  neurasthenia,  and  chronic  invalidism. 

{d)  A  noticeable  change  of  the  habitual  temper,  usually  fr^m 
placid  to  fretful,  less  frequently  the  opposite,  is  witnessed  in  preg- 
nancy, melancholia,  typhoid  fever  in  its  middle  course,  in  the  aura 
of  epilepsy,  and  occasionally  in  the  early  stage  of  exophthalmic 
goitre. 

(3)  Intellection.— The  disorders  of  intellection  embrace  dul- 
ness  or  confusion  of  the  mental  processes,  loss  of  memory,  delusions, 
illusions,  hallucinations,  and  delirium.  Disorders  of  consciousness 
will  be  considered  under  a  separate  heading. 

{a)  Dulness  or  confusion  of  mind  may  be  observed  in  patients 
who  are  quite  conscious,  and  is  manifested  by  difi&culty  or  slowness 
in  apprehending  the  meaning  of  questions  which  may  be  put  to 
them,  and  a  corresponding  difficulty  in  framing  the  proper  answers. 
In  the  extreme  degrees  it  is  impossible  to  overcome  the  mental 
apathy  sufficiently  to  obtain  intelligible  replies.  The  patient  makes 
an  evident  effort  to  grasp  the  significance  of  the  spoken  words,  but 
the   endeavour  is  fruitless  (see  also  Aphasia).     The  hebetude   of 


64  THE  EVIDENCES  OF  DISEASE 

typhoid  fever  has  been  mentioned.  Mental  dulness  is  seen  in  cere- 
bral inflammations  at  certain  stages  of  their  progress,  in  some  of  the 
scleroses  of  the  brain,  in  cerebral  thrombosis  and  embolism,  myxce- 
dema,  typhus  and  other  low  fevers,  and  in  some  of  the  psychoses  or 
insanities.  Confusion  of  thought  may  be  incidental  to  neurasthenia, 
anaemia,  brain  tumour,  and  old  age. 

(b)  Loss  of  memory  usually  accompanies  dulness  or  confusion  of 
mind,  but  is  especially  characteristic  of  neurasthenia,  epilepsy,  over- 
use of  the  bromides,  and  beginning  insanities. 

(c)  Delusions^  Hallucinations,  and  Illusions. — A  delusion  is  an 
absurd  and  unfounded  belief,  and  if  it  occurs  in  an  insane  person  it 
is  an  insane  delusion.  The  truth  of  the  belief  and  the  insanity  of 
the  believer  are  matters  of  judgment.  A  belief  which  is  false  and 
ridiculous  to  one  may  be  an  article  of  faith  with  another.  In 
ordinary  medical  diagnosis  it  is  usually  easy  to  distinguish  between 
true  and  false  beliefs  without  splitting  hairs. 

An  halluciiiation  is  a  sense  perception  without  a  physical  basis. 
If  one  imagines  that  he  hears  a  sound  or  smells  an  odour,  when  the 
sound  or  odour  does  not  exist,  he  is  the  subject  of  an  hallucination. 
Any  one  of  the  senses  may  be  the  agent  of  an  hallucination. 

An  illusion  is  a  false  interpretation  of  objects  which  really  exist. 
If  one  sees  a  chair  and  imagines  it  to  be  a  man,  or  hears  a  gentle  rap 
upon  the  door  and  insists  that  it  is  an  explosion,  he  is  the  subject  of 
an  illusion. 

If  the  patient  is  unaware  of  the  falsity  of  his  hallucinations  or 
illusions,  they  are  said  to  be  delusive ;  if  he  knows  their  falsity,  they 
are  non-delusive. 

Delusions,  hallucinations,  and  illusions  are  characteristic  of  the 
insanities.  They  are  occasionally  seen  in  hysteria,  and  to  some 
degree  in  every  case  of  hypochondriasis,  both  of  which  are  consid- 
ered on  good  authority  to  be  forms  of  insanity.  False  beliefs  and 
false  or  perverted  sense  perceptions  also  constitute  a  part  of  the 
mental  condition  known  as  delirium. 

{d)  Delirium. — This  is  a  state  of  mental  agitation  characterized 
by  restlessness,  incoherence  of  speech,  delusions,  and  sensory  perver- 
sions. Two  varieties  of  delirium  are  recognised,  although  transition 
forms  are  common.  The  first  form  is  termed  active  or  wild  delirium, 
in  which  the  patient  tries  to  escape  from  bed,  shouts,  struggles  with 
imaginary  enemies,  and  requires  forcible  restraint.  The  other  is  a 
low  or  muttering  delirium,  the  patient  lying  with  comparative  quiet- 
ness, but  incessantly  engaged  in  incoherent  and  disjointed  converse 
with  imaginary  personages,  or  communing  with  his  own  disordered 
brain.     The  onset  of  delirium  may  be  sudden  or  slow.     If  coming 


INSOMNIA,   AND  STARTING  DURING   SLEEP  65 

slowly,  the  first  indication  of  its  presence  may  be  a  certain  confusion 
and  difficulty  in  realizing  his  surroundings  after  waking  from  sleep, 
the  mental  confusion  lasting  for  a  longer  period  on  each  occasion, 
and  finally  developing  into  well-marked  delirium. 

Active  or  wild  delirium  is  typically  seen  in  delirium  tremens ; 
low  or  muttering  delirium  in  the  2d  and  3d  weeks  of  typhoid  fever. 
A  practical  point  to  bear  in  mind  is  that  a  quiet  delirium  may  shift 
very  suddenly  into  the  active  form. 

Aside  from  the  insanities,  delirium  may  be  present  in  the  acute 
infectious  diseases.  Any  febrile  disease  in  children  may  manifest 
it  to  a  greater  or  less  degree.  I  have  seen  several  cases  of  dysmen- 
orrhoea  in  young  women,  attended  with  a  rather  active  delirium  last- 
ing from  12  to  24  hours.  It  attends  the  typhoid  state  without  refer- 
ence to  the  cause,  and  may  be  present  toward  the  close  of  life  in 
either  acute  or  chronic  disease.  It  is  associated  also  with  inflamma- 
tory cerebral  disease,  and  may  be  present  in  connection  with  uraemia 
and  with  poisoning  by  certain  drugs,  such  as  alcohol,  belladonna,  or 
opium.  Nocturnal  delirium  frequently  persists  after  convalescence 
has  been  well  established,  especially  in  pneumonia  and  typhoid  fever. 
Under  these  circumstances  it  is  doubtless  akin  to  the  delirium  of 
inanition.  The  latter,  as  its  name  indicates,  is  usually  associated  with 
acute  wasting  diseases,  either  febrile  or  angemic.  Its  onset  is  sudden, 
in  the  early  morning,  and  the  patient  is  found  to  be  extremely  weak 
and  collapsed.  It  may  continue  from  a  few  hours  to  2  days.  Brief 
delirium  may  follow,  and  in  some  instances  may  replace,  an  epileptic 
convulsion.    Delirium  is  also  one  of  the  manifestations  of  hysteria. 

III.  Insomnia,  and  Starting  during  Sleep. — Sleepless- 
ness possesses  slight  diagnostic  value.  Disturbed  sleep  is  present  in 
the  majority  of  febrile  diseases.  Prolonged  or  persistent  wakeful- 
ness is  a  prominent  symptom  in  delirium  tremens,  pneumonia, 
melancholia,  gout,  meningitis,  and  cerebral  syphilis,  and  it  may  also 
be  caused  by  the  over-free  use  of  tea,  coffee,  and  tobacco. 

Sudden  twitching  or  starting  of  the  body  during  sleep  may  be  due 
to  mental  or  physical  fatigue,  especially  if  the  person  be  already 
neurasthenic.  It  is  not  at  all  uncommon  in  connection  with  dys- 
pepsia or  acute  indigestion,  as  well  as  with  delirium  tremens,  menin- 
gitis, and  cerebral  embolism.  In  children  it  may  be  due  to  fever, 
dentition,  or  worms,  and  may  be  indicative  of  disease  of  the  joints. 
It  is  a  very  unpleasant  symptom,  occurring  just  as  the  patient  is 
falling  asleep,  when  the  compensation  is  broken  in  valvular  disease  of 
the  heart.  In  meningitis  and  joint  diseases  it  is  usually  accompanied 
by  a  cry.  The  most  frequent  causes  are  dyspepsia,  fatigue,  fever,  and 
dentition. 


QQ  THE  EVIDENCES  OF  DISEASE 

SECTION  YIII 
DISTURBANCES   OF   COXSCIOUSNESS 

IifABiLiTY  to  cognize  impressions,  from  within  or  without,  which 
are  ordinarily  capable  of  producing  physical  or  mental  sensations, 
constitutes  unconsciousness,  which  as  a  symptom  is  of  much  diagnostic 
importance.  It  is  also,  as  a  symptom,  the  cause  of  frequent  diag- 
nostic perplexity. 

Loss  of  consciousness  may  be  gradual  or  sudden,  and  may  present 
various  degrees  of  completeness.  With  reference  to  its  complete- 
ness, three  degrees  are  clinically  recognised :  somnoloice,  stupor,  and 
coma.  Coma  vigil  is  a  fourth  acknowledged  variety  or  form  of  uncon- 
sciousness. 

Somnolence,  or  lethargy,  is  the  lightest  degree  of  disordered  con- 
sciousness, and  is  manifested  by  a  persistent  sleepiness,  from  which, 
however,  the  patient  can  be  easily  aroused. 

Stupor  is  a  more  decided,  but  partial,  loss  of  consciousness,  a  pro- 
found slumber  from  which  it  is  possible  to  awaken  the  patient,  but 
only  with  great  difficulty  and  by  importunate  solicitations. 

Coma  is  a  condition  of  insensibility  from  which  it  is  impossible  ta 
arouse  the  patient.  The  face  is  expressionless,  the  respiration  may 
be  stertorous,  the  mouth  is  usually  open,  and  the  tongue  dry. 

Cotna  Vigil. — In  coma  vigil  the  patient  lies  with  his  eyes  open,  but 
absolutely  unconscious  of  his  suriH)undings,  and  there  is  usually  a 
muttering  delirium,  with  aimless  movements  of  the  hands.  It  is  a 
condition  indicative  of  extreme  peril. 

(A)  The  Diagnostic  Significance  of  Coma 

Coma  occurring  very  suddenly  is  characteristic  of  apoplexy, 
catalepsy,  and  sunstroke.  More  or  less  complete,  and  making  its. 
appearance  gradually,  it  may  attend  any  of  the  fevers  and  acute 
infectious  diseases,  as  typhoid,  typhus,  and  pernicious  malarial 
fevers.  It  is  also  a  symptom  of  narcotic  poisoning,  as  from  alcohol,, 
chloral,  opium,  ether,  chloroform,  nitrous-oxide  gas,  and  coal  gas. 
In  addition  to  the  poisons  of  the  specific  infectious  diseases,  coma  is 
caused  by  uraemia,  and,  late  in  the  disease,  by  diabetes.  Other  poi- 
soned states  of  the  blood  which  may  produce  it  are  those  of  septi- 
caemia, pyaemia,  carcinomatous  growths,  and  the  very  rare  acute 
yellow  atrophy  of  the  liver.  Asphyxia  is  attended  with  drowsiness 
or  perhaps  actual  coma.  Injuries  to  the  head  which  involve  concus- 
sion or  laceration,  and  pressure  upon  the  brain,  as  from  a  depressed 


THE  DIAGNOSIS  OP  THE   VARIETIES  OF  COMA  67 

fracture,  may  produce  total  unconsciousness.  Hysterical  coma  is  not 
infrequent.  The  convulsions  of  epilepsy  and  infantile  eclampsia  are 
followed  by  a  period  of  unconsciousness.  A  momentary  loss  of  con- 
sciousness may  be  almost  the  only  symptom  of  minor  epilepsy  {petit 
mal).  Coma  may  attend  any  organic,  hemorrhagic,  or  inflammatory 
disease  of  the  brain,  as  in  the  various  forms  of  cerebral  meningitis, 
in  which  it  makes  its  appearance  late  in  the  disease  and  is  due  to 
pressure  from  the  exudate.  It  may  be  associated  also  with  disease  of 
the  cranial  bones,  meningeal  hemorrhage  or  tumour,  abscess  or 
tumour  of  the  brain,  acute  encephalitis,  cerebral  syphilis,  cerebral 
hemorrhage,  embolism  or  thrombosis,  and  softening,  thrombosis  of 
the  cerebral  sinuses,  general  paresis,  and  multiple  sclerosis. 

Syncope  is  a  sudden  loss  of  consciousness  due  to  acute  anaemia  of 
the  brain.  A  rather  sudden  coma  may  occur  as  the  result  of  severe 
muscular  exertion,  independent  of  sunstroke.  Finally,  coma,  begin- 
ning from  a  few  hours  to  several  days  before  death,  may  herald  the 
end  of  many  acute  and  chronic  diseases. 

Coma  vigil  may  be  present  in  connection  with  typhoid  and  typhus 
fevers,  and  with  the  typhoid  state,  especially  when  it  supervenes  in 
septicaemia,  pyaemia,  and  delirium  tremens. 

(B)  The  Diagnosis  of  the  Varieties  of  Coma 

In  General. — In  all  cases  of  more  or  less  sudden  unconsciousness 
the  following  points  are  of  value  : 

1.  Skin. — During  extremely  warm  weather  it  is  important  to 
observe  the  temperature  of  the  skin.  If  it  is  excessively  hot  and  dry, 
one  may  infer  the  presence  of  sunstroke  (insolation). 

2.  Head. — Examine  for  evidence — bruises,  cuts,  or  depressions — 
which  may  point  toward  injury  of  the  brain. 

3.  Face. — Determine  the  presence  of  unilateral  facial  paralysis 
(one  side  of  face  expressionless  and  smooth),  which  is  usually  asso- 
ciated with  hemiplegia  and  indicates  a  unilateral  brain  lesion — e.  g., 
hemorrhage,  embolism,  thrombosis,  or  other  cause  of  interference 
with  intracranial  function  ;  or  hysteria. 

4.  Eyes. — If  both  pupils  are  contracted  and  do  not  dilate  when 
covered,  suspect  narcotic  poisoning  (especially  by  opium)  or  a  cere- 
bral lesion.  If  the  pupils  are  unequal  (anisocoria),  it  is  pretty  certain 
under  such  circumstances  to  be  caused  by  a  cerebral  lesion.  If  upon 
attempting  to  raise  the  eyelids  there  is  a  quivering  resistance  and 
the  eyeballs  are  kept  continuously  turned  upward,  hysteria  is  the 
probable  cause  of  the  coma.  In  other  forms  of  unconsciousness 
there  is  never,  or  but  very  rarely,  the  slightest  difficulty  in  raising 
the  lids,  and  the  eyes  are  not  necessarily  upturned. 


08  THE  EVIDENCES  OF  DISEASE 

5.  Mouth  and  Tongue. — If  the  lips  or  tongue  are  bitten  and  there 
is  froth  upon  the  lips,  one  may  correctly  suspect  epilepsy,  although 
the  injuries  may  have  been  inflicted  accidentally  by  the  teeth  when 
the  patient  fell  unconscious. 

6.  Extremities. — These  are  to  be  examined  for  paralysis,  especially 
hemiplegia,  in  which  the  arm  and  leg  of  the  same  side  fall  limp  and 
helpless  when  raised  and  dropped.  If  the  unconsciousness  is  abso- 
lute, all  four  extremities  may  be  apparently  paralyzed,  but  a  greater 
degree  of  relaxation  may  be  manifest  on  one  side  than  on  the  other. 
At  the  very  onset  of  an  apoplexy  there  may  be  an  "  initial  "  rigidity 
of  the  paralyzed  side.     See  also  3,  preceding. 

It  should  be  borne  in  mind  as  a  diagnostic  aid  that  there  are  cer- 
tain comatose  conditions  which  may  be  preceded  or  followed  by  gen- 
eral convulsions.  These  are :  the  primary  convulsion  and  subse- 
quent extreme  drowsiness  caused  by  the  exanthemata  and  other  acute 
specific  infections  in  children;  the  coma  which  follows  convulsions  due 
to  dentition  or  digestive  disorders  in  children ;  the  coma  sequent  to 
the  epileptiform  seizures  of  cerebral  syphilis,  general  paralysis  of  the 
insane  and,  more  rarely,  of  alcoholism ;  the  coma  subsequent  to  the 
convulsions  of  epilepsy  and  hysteria ;  and  the  coma  following  the 
uraemic  convulsion.  The  coma  of  sunstroke,  cerebral  hemorrhage, 
and  some  other  ailments  of  less  frequency  and  importance  may  be 
preceded  by  a  general  convulsion. 

In  Special. — Certain  special  varieties  of  coma  (with  or  without 
convulsions)  are  of  suflBcient  frequency  and  consequence  to  be 
grouped  and  described  with  enough  detail  to  enable  at  least  a  pre- 
sumptive differential  diagnosis  to  be  made.  The  discrimination  is 
of  great  importance  because  of  the  liability  and  the  danger  of  con- 
founding one  with  another,  especially  the  first  four  which  will  be 
considered — viz.,  coma  from  opium,  alcohol,  apoplexy,  and  uraemia. 

1.  Opium  Coma. — The  patient  is  deeply  comatose ;  the  face  is 
dusky  and  cyanotic ;  the  respirations  are  slow  (12  to  4  or  even  less  per 
minute) ;  the  pulse  is  also  infrequent  and  full  until  the  terminal 
stage ;  the  pupils  are  equal,  and  contracted  to  pin  points.  The  tem- 
perature of  the  body  is  normal,  and,  except  toward  the  end,  the  skin 
is  dry  and  moderately  warm. 

2.  Alcoholic  Coma. — It  may  or  may  not  be  possible  to  arouse  the 
patient.  If  he  can  be  awakened,  he  may  protest  by  words  or  blows. 
The  face  is  usually  flushed,  often  somewhat  cyanotic,  more  rarely 
pallid.  The  respirations  are  of  normal  frequency,  deep,  and  some- 
times stertorous.  The  odour  of  alcoholic  liquor  can  be  detected  in 
the  breath;  and  there  is  usually  the  peculiar  sour,  mawkish  smell 
which  results  from  the  disturbing  effect  of  alcohol  upon  the  buccal 


FORMS  OF  COMA  69 

and  gastric  mucosa — the  odour  of  "drunkard's  stomach."  This 
odour  is  of  no  value  as  a  diagnostic  symptom ;  its  absenee  is  of 
importance  as  a  negation  of  alcoholism.  The  pulse  is  rather  rapid, 
full,  and  strong,  finally  becoming  small  and  feeble.  The  pupils  are 
equal,  and  either  of  normal  size  or  dilated.  Very  commonly  the  skin 
is  cool  and  moist,  and  the  bodily  temperature  below  the  normal 
point.  Convulsions  are  infrequent,  but  there  may  be  some  local 
muscular  spasm  or  twitching. 

Two  points  should  be  remembered  before  making  a  diagnosis  of 
alcoholic  coma:  one,  that  it  maybe  closely  simulated  by  apoplexy; 
the  other,  that  apoplexy  may  occur  in  a  drunken  person  and  the 
symptoms  of  a  cerebral  lesion  be  added  to  those  of  acute  alcoholism. 
Further,  it  should  be  borne  in  mind  that  the  patient  may  have  had 
administered  by  mouth  a  dose  of  liquor  from  the  hands  of  some  well- 
meaning  person  after  the  onset  of  the  attack.  Consequently,  in 
cases  simulating  drunkenness,  the  signs  of  apoplexy,  to  be  described 
in  the  next  paragraph,  especially  paralysis,  should  be  most  carefully 
looked  for. 

3.  Coma  from  Apoplexy. — The  coma  is  usually  profound,  and  the 
patient  can  not  be  aroused.  The  face  is  flushed  or  pale  and  cyanotic. 
The  respirations  are  slow,  stertorous,  and  sometimes  of  the  Cheyne- 
Stokes  type.  The  lips  are  blown  out,  and  one  cheek  flaps  more  than 
the  other  during  respiration.  The  pulse,  as  a  rule,  is  full,  strong, 
and  infrequent,  and  the  arteries  are  hard.  The  pupils  do  not  react  to 
light,  are  dilated,  and  often  unequal.  There  may  be  conjugate 
deviation  of  the  head  and  eyes — i.  e.,  they  are  turned  persistently  to 
one  side.  One  side  of  the  face  is  usually  paralyzed,  as  indicated  by 
the  smoothing  out  of  its  wrinkles,  the  flapping  cheek,  and  the  droop  of 
one  angle  of  the  mouth.  By  lifting  the  limbs  and  finding  those  of 
one  side  to  fall  more  flaccidly  than  those  of  the  other  side,  the  pres- 
ence of  hemiplegia  may  be  demonstrated.  The  skin  is  dry  and  the 
temperature  of  the  body  above  the  normal. 

4.  Uremic  Coma. — Convulsions  often  initiate  an  attack  of  ursemic 
coma,  but  the  unconsciousness  may  develop  gradually  and  without 
spasm.  The  face  may  present  the  swollen  pallor  of  renal  disease. 
The  pulse  is  generally  infrequent  and  is  apt  to  be  of  high  tension. 
The  pupils  are  equal,  either  dilated  or  of  normal  size.  There  may  be 
muscular  twitchings  and  rigidity  affecting  the  hands  and  feet.  The 
temperature  may  be  normal,  in  severe  cases  subnormal,  and  in  those 
attended  by  several  convulsions  it  may  be  greatly  elevated.  The 
breath  and  bodily  exhalations  may  have  a  urinous  and  ammoniacal 
odour.  In  suspected  uraemic  coma  the  urine  should  be  promptly 
examined  for  albumin  and  casts,  the  heart  and  vessels  for  hyper- 

7 


70  THE   EVIDENCES  OP   DISEASE 

trophy  and  sclerosis,  the  eye  grounds  for  retinitis,  and  various  portions 
of  the  body  for  oedema.  It  is  not  to  be  forgotten  that  there  are 
occasional  instances  of  uraemic  hemiplegia,  often  transient  and  with- 
out discoverable  organic  lesions  of  the  brain,  which  resemble  apo- 
plexy 80  closely  that  it  proves  impossible  to  make  a  differential  diag- 
nosis except  at  autopsy. 

5.  Coma  from  Epilepsy. — There  is  usually  little  difficulty  in  the 
diagnosis  of  the  post-convulsive  coma  of  epilepsy.  The  history  of  a 
convulsion,  the  bitten  tongue,  the  foam  on  the  lips,  and,  above  all, 
the  brief  duration  of  the  gradually  lessening  unconsciousness,  are  in 
the  majority  of  cases  sufficient  to  settle  the  question.  The  face  i& 
congested,  the  breathing  stertorous,  the  limbs  are  relaxed,  but  there 
is  no  hemiplegia. 

6.  Hysterical  Coma. — There  is  something  characteristic,  although 
difficult  to  describe,  in  the  appearance  of  a  patient  in  the  coma  of 
hysteria.  The  attack  may  be  preceded  by  laughing,  crying,  delirium, 
or  convulsive  movements ;  or  it  may  come  on  without  premonition. 
The  face  is  somewhat  flushed,  the  pulse  is  usually  of  normal  rapidity, 
the  breathing  may  be  rapid  but  not  stertorous  ;  the  pupils  are  equal, 
of  normal  size,  and  responsive  to  light ;  the  eyelids  resist  opening,  and 
the  eyeballs  are  persistently  upturned.  After  a  little  experience 
with  such  cases  the  facial  expression,  attitude,  and  general  appearance 
of  the  patient  make  an  impression  upon  the  observer  difficult  to  define, 
but  extremely  characteristic — as  of  an  unconsciousness,  in  part  real, 
in  part  intentional.  An  irritant,  such  as  ammonia,  to  the  nostrils 
or  continued  firm  pressure  upon  the  supraorbital  nerve  at  its  point 
of  emergence,  will  at  least  partly  arouse  the  patient. 

In  view  of  the  undoubted  fact  that  serious  organic  disease  of  the 
brain  may  be  ushered  in  by  pseudo-hysterical  symptoms,  it  is  best  to 
be  somewhat  chary  in  announcing  a  positive  diagnosis  of  hysteria, 
unless  there  is  a  total  absence  of  organic  symptoms  and  the  hyster- 
ical characteristics  of  the  attack  are  so  marked  as  to  be  beyond 
question. 

7.  Syncope. — Unconsciousness  from  sudden  anaemia  of  the  brain 
is  rarely  confounded  with  other  forms  of  coma.  The  pallor  of  the 
face  is  absolute,  the  respirations  are  shallow  and  almost  imperceptible, 
the  pulse  is  weak,  perhaps  absent,  and  the  pupils  are  widely  dilated. 
The  eyes  may  remain  open.  If  the  syncope  is  due,  as  it  is  in  the 
majority  of  cases,  to  a  temporary  weakness  of  the  heart  action  from 
emotional  causes  or  the  sudden  assumption  of  the  erect  position  by 
an  enfeebled  person,  consciousness  will  soon  return  under  appro- 
priate treatment. 

It  is  to  be  remembered,  however,  that  if  there  is  ^nWov  plus  cya- 


COMA— GENERAL  CONVULSIONS  71 

nosis  and  some  stertor,  the  attack  may  be  due  to  serious  cardiac  dis- 
ease, or  may  be  one  of  the  slight  apoplectic  seizures  premonitory  of  a 
serious  cerebral  thrombosis. 

8.  Diabetic  Coma. — This  variety  of  coma  may  occur  without  pre- 
monition, may  be  preceded  by  syncope  and  drowsiness,  or  may 
begin  with  vomiting,  headache,  delirium,  and  dyspnoea.  After  coma 
is  established  the  respirations  are  either  normal  or  increased  in  fre- 
quency, the  pulse  normal  and  full,  and  the  bodily  temperature  is  sub- 
normal. The  distinctive  symptoms  which  will  enable  a  recognition 
of  diabetic  coma  are  the  sweetish,  fruity,  or  "  oveiTipe-apple  "  odour 
of  the  breath,  and  the  discovery  of  a  considerable  amount  of  sugar  in 
the  urine. 

9.  Coma  from  Gas  Poisoning. — The  cause  of  this  form  of  uncon- 
sciousness is  almost  invariably  obvious  from  the  circumstances  under 
which  the  patient  is  found.  It  results  from  the  inhalation  of  carbon 
dioxide  (old  wells  or  deep  caves),  carbon  monoxide  (illuminating 
gas,  charcoal  fire),  or  hydrogen  sulphide  (sewers). 

10.  Coma  from  Sunstroke. — The  patient  is  profoundly  uncon- 
scious, the  face  is  flushed,  the  skin  pungently  hot,  the  respiration  is 
laboured,  deep,  and  often  stertorous,  and  the  pulse  frequent  and 
full.  The  excessively  high  temperature  of  the  body,  the  heat  of  the 
weather,  and  the  circumstances  under  which  the  attack  has  occurred 
(e.  g.,  bodily  exertion  under  exposure  to  the  sun),  render  the  diag- 
nosis easy. 


SECTION  IX 
GEXEEAL   CONVULSIONS 

A  convulsion  is  a  series  of  involuntary  contractions,  involving 
mainly  the  major  portion  of  all  the  voluntary  muscles,  and  occur- 
ring with  varying  degrees  of  violence.  It  is  customary  to  apply  the 
term  spasm  to  convulsive  contractions  of  the  muscles  belonging  to 
particular  portions  of  the  body.  It  is  a  distinction  which  can  not  be 
accurately  drawn,  because  the  same  factors  are  often  causative  in 
each,  and  general  convulsions  may  precede,  follow,  or  alternate  with 
local  convulsions  or  spasms. 

Convulsions  may  be  tonic  or  clonic.  A  tonic  convulsion  is  char- 
acterized by  a  continuous  contraction  of  the  affected  muscles,  which 
may  last  for  a  few  seconds,  as  at  the  onset  of  an  epileptic  paroxysm, 
or  for  days,  as  in  tetanus.  A  clonic  convulsion  is  distinguished  by 
rapidly  alternating  contractions  and  relaxations  of  the  muscles  in- 
volved, as  in  hysteria  or  in  the  epileptic  convulsion  immediately  fol- 


72  THE  EVIDENCES  OF   DISEASE 

lowing  the  primary  tonic  contraction.  The  body  and  limbs  in  a 
tonic  convulsion  are  rigid  and  immovable,  contrasting  vividly  with 
the  agitated  and  violent  motions  of  the  clonic  form.  A  clonic  (or 
epileptiform)  convulsion  is  usually  of  cerebral  origin ;  the  tonic  (or 
tetanic)  convulsion  is  more  apt  to  result  from  the  heightened  excita- 
bility of  the  spinal  cord.  Consciousness  may  be  preserved,  as  in 
tetanus,  partly  lost,  as  in  hysterical  convulsions,  or  totally  absent,  as 
in  the  epileptic  convulsion. 

The  diagnostic  associations  of  general  convulsions  are  with  urae- 
mia, puerperal  eclampsia,  epilepsy,  and  hysteria ;  poisoning  from 
alcohol,  lead,  aconite,  prussic  acid,  and  veratrum  viride ;  tetanus, 
strychnine  poisoning,  and  hydrophobia.  In  the  last  three,  conscious- 
ness is  preserved.  Convulsions  may  occur  also  in  connection  with 
profuse  hemorrhages  and,  very  seldom,  with  sunstroke  and  apoplexy. 
They  appear  with  much  frequency  in  the  later  stages  of  organic 
cerebral  disease,  as  in  infantile  hemiplegia;  tumour,  cyst,  or  sclero- 
sis of  the  brain ;  cerebral  syphilis  and  general  paresis,  as  well  as  in 
meningitis,  hematoma  of  the  dura  mater,  and  other  inflammations 
of  the  membranes  of  the  brain  and  spinal  cord. 

Convulsions  occur  in  children,  especially  those  under  2  years 
of  age,  upon  very  slight  provocation.  Digestive  disturbances  from 
an  unsuitable  or  overlarge  food  supply  are  frequent  causes.  Irrita- 
tion from  dentition  and  from  intestinal  parasites  may  give  rise  to 
convulsions,  but  these  causes  are  probably  not  operative  as  frequently 
as  popular  opinion  supposes.  Convulsions  may  attend  the  onset 
of  acute  poliomyelitis  and  the  acute  infectious  diseases,  especially 
scarlet  fever,  measles,  pneumonia,  and  malaria,  a  convulsion  replac- 
ing the  chill  of  the  adult.  In  some  infants  who  are  predisposed  by  a 
congenitally  unstable  nervous  system,  or  by  the  existence  of  rachitis, 
eclampsia  may  initiate  any  slight  febrile  attack. 

Spasm  or  localized  convulsions,  jerking  or  choreic  movements, 
and  tremor  are  considered  in  detail  in  connection  with  the  examina- 
tion of  the  nervous  system  {q.  v.). 

Certain  ailments,  of  which  general  convulsions  constitute  the 
sole,  leading,  or  important  symptom,  may  be  here  considered  as 
follows  : 

(1)  Epilepsy. — The  epileptic  convulsion  is  typically  clonic.  It  is 
in  many  instances  preceded  by  an  aura,  a  peculiar  premonitory  symp- 
tom, usually  subjective  and  sensory,  more  rarely  motor.  The  most 
common  is  epigastric  or  abdominal  distress,  with  or  without  palpita- 
tion of  the  heart.  Less  frequent  are  subjective  sensations  of  taste, 
odour,  noises,  musical  sounds,  voices,  flashes  of  light  or  colour ;  or 
peculiar  mental  states  of  terror  or  perplexity ;  or  rapid  moving  or 


GENERAL  CONVULSIONS  Y3 

turning  after  the  manner  of  a  whirling  dervish.  Immediately  suc- 
ceeding the  aura,  and  in  many  cases  preceded  by  a  scream  or  outcry, 
the  patient  falls  unconscious ;  all  the  skeletal  muscles  become  tonic- 
ally  contracted,  with  the  legs  extended,  hands  tightly  closed,  jaw 
clenched,  and  head  turned  forcibly  to  one  side ;  the  muscles  of  respira- 
tion are  fixed,  and  the  face  in  consequence  is  deeply  cyanosed.  In  less 
than  a  minute  the  clonic  movements  supervene.  The  muscles  of  the 
face,  eyes,  eyelids,  and  jaw  work  convulsively,  and  the  extremities 
jerk  violently  and  rhythmically.  Foam,  blood-stained  if  the  tongue 
and  lips  have  been  bitten,  exudes  from  the  mouth ;  the  cyanosis  less- 
ens ;  the  bladder  and  rectum  may  be  emptied  unconsciously.  After 
two  or  three  minutes  the  movements  cease  and  the  patient  is  left  in 
deep  coma. 

(2)  Hysterical  Convulsions. — In  young  patients  epilepsy  and  hys- 
teria may  bear  so  close  a  resemblance  that  great  difficulty  may  be 
experienced  in  the  discrimination.  The  hysterical  (or  hysteroid) 
convulsion,  however,  is  often  obviously  initiated  by  some  form  of 
emotional  excitement.  It  is  preceded  by  "globus,"  palpitation, 
tingling,  and  numbness  of  both  hands  or  both  feet,  or  all  four  ex- 
tremities, and  the  onset  of  the  attack  is  frequently  gradual.  The 
single  outcry  at  the  beginning  of  the  epileptic  attack  may  be 
replaced  by  a  series  of  screams  during  the  course  of  the  hysterical 
paroxysm.  The  movements  of  the  hysterical  convulsion  are  more 
purposive  and  less  rhythmical ;  there  may  be  rigidity,  opisthotonus, 
and  attitudinizing ;  the  tongue  is  rarely  bitten  or  the  patient  injured ; 
there  are  no  involuntary  evacuations ;  the  attack  lasts  longer  than 
that  of  epilepsy,  and  the  subsequent  coma  is  not  so  profound.  The 
hysterical  facies  is  not  unimportant  evidence. 

(3)  Uraemic  Convulsions  and  Puerperal  Eclampsia.— The  nature  of 
the  epileptoid  convulsions  in  these  cases  is,  as  a  rule,  readily  recog- 
nised by  the  urinalysis  in  both  instances :  by  the  history  in  the  first 
ailment,  and  the  presence  of  jfregnancy  or  the  puerperium  in  the 
second. 

(4)  Infantile  Eclampsia. — Convulsions  in  children  resemble  those 
of  epilepsy,  except  that  the  symptoms  are  usually  not  quite  so  severe 
and  fully  developed.  Such  attacks  are  usually  symptomatic  of  some 
causative  condition,  viz.,  overeating,  especially  of  indigestible  food, 
rachitis,  debility  from  exhausting  diarrhoeal  diseases  (hydrencepha- 
loid  state) ;  high  fever,  especially  at  the  onset  of  the  acute  specific 
infections ;  very  seldom  dentition,  phimosis,  and  acute  middle-ear 
inflammation ;  injuries  to  the  brain  at  birth,  infantile  hemiplegia, 
meningitis,  and  tumour  of  the  brain ;  rarely  of  spinal-cord  disease. 
As  some  disturbance  of  the  digestion  is  probably  the  most  frequent 


74  THE  EVIDENCES  OF  DISEASE 

cause  of  a  single  convulsion,  one  should  always  inquire  with  reference 
to  possible  overfeeding,  improper  food,  or  constipation. 

If  a  convulsion  with  high  fever  and  perhaps  vomiting  occurs  sud- 
denly in  a  previously  healthy  child,  it  is  proper  to  suspect  and  watch 
for  acute  meningitis  or  infantile  hemiplegia,  scarlet  fever,  malaria,  or 
lobar  pneumonia,  although  indigestible  food  may  be  alone  responsible 
for  the  attack.  It  is  also  to  be  borne  in  mind  that  lobar  pneumonia 
in  children  may  be  mistaken  for  meningitis,  as  the  pulmonary  disease 
may  present  convulsions,  delirium,  rigidity  or  retraction  of  the  neck, 
and  other  signs  of  a  meningeal  character.  In  searching  for  the  cause 
of  the  eclampsia  the  urine  should  be  examined  if  practicable.  Kachitis 
and  debility  from  exhausting  disease  are  not  uncommon  causes  of 
spasms  (usually  tonic)  affecting  mainly  the  hands,  feet,  and  larynx 
(carpo-pedal  spasm,  laryngismus  stridulus).  Jacksonian  or  localized 
convulsions  affecting  one  extremity  may  be  an  early  symptom  of 
tumour  of  the  brain  or  infantile  hemiplegia.  Convulsions  recurring 
at  irregular  intervals  during  childhood,  without  obvious  cause,  are  in 
all  probability  true  epilepsy. 

(5)  Tetanus  and  Strychnine  Poisoning.— Tetanus  and  overdoses 
of  strychnine  each  give  rise  to  convulsions  or  spasms  of  the  tonic 
(tetanic  or  spinal)  type.  The  convulsions  due  to  these  two  different 
causes  may  bear  a  close  resemblance.  In  each  case  the  muscles  are 
tetanically  contracted,  the  body  may  be  curved  and  twisted  into 
various  postures  (emprosthotonus,  opisthotonus),  and  the  spasms 
occur  at  irregular  intervals,  with  more  or  less  muscular  rigidity  exist- 
ing between  the  seizures.  The  distinction  is  to  be  made  by  noting 
that  in  strychnine  poisoning  the  jaw  muscles  are  the  last  to  be 
involved  (perhaps  escaping  entirely),  there  is  little  if  any  rigidity 
between  the  paroxysms,  and  there  will  probably  be  a  history  of  the 
ingestion  of  the  poison.  On  the  other  hand,  in  tetanus  lockjaw  is 
the  earliest  well-marked  symptom,  the  muscles  remain  rigid  during 
the  interparoxysmal  periods,  and  fhere  is  a  history  of  an  injury, 
especially  a  punctured  or  lacerated  wound  of  the  hand  or  foot. 

Tetany  {q.  v.)  is  an  entirely  different  disease,  in  which  the  spasm 
and  peculiar  position  of  the  hands  and  feet,  particularly  of  the 
hands,  together  with  the  altogether  different  history,  enable  its 
discrimination  from  tetanus. 


THE  COLOUR  OF  THE  SKIN  75 

SECTION"  X 

CUTANEOUS  SURFACE 

The  cutaneous  surface  is  studied  in  general  with  reference  to  its 
colour,  heat  and  moisture,  the  presence  of  a  rash  or  eruption,  of  cica- 
trices, swellings,  oedema,  and  varicosities.  Abnormal  conditions  of 
the  joints  are  also  included.  It  is  advisable,  in  examining  the  colour 
of  the  skin,  to  inspect  also  the  colour  of  the  mucous  membrane  of  the 
mouth  and  the  conjunctiva. 

I.   THE  COLOUR  OF  THE  SKIN 

The  effects  of  exposure  to  wind  and  weather,  as  seen  in  labourers, 
drivers,  railway  employees,  and  especially  in  seafaring  men,  are  suf- 
ficiently familiar.  The  tanned,  leathery,  fine-wrinkled  skin  will  in 
such  persons  hide  marked  changes  of  colour  unless  other  skin  or 
mucous  surfaces  are  examined.  Habitual  pallor  is  seen  in  persons 
living  an  indoor  life,  or  who  sleep  in  the  daytime  and  work  at  night. 
Allowing  for  the  foregoing  physiological  conditions,  the  colorations 
of  the  skin  which  occur  in  disease  are  as  follows : 

Pallor. — Tliis  may  come  suddenly,  or  may  begin  insidiously  and 
progress  so  slowly  that  only  by  looking  back  over  months  or  years 
can  the  date  of  its  onset  be  determined.  In  general  it  must  be  due 
to  one  or  both  of  two  conditions  :  first,  a  lessened  amount  of  blood 
in  the  cutaneous  capillaries,  caused  either  by  spasm  of  the  arterioles 
or  defective  action  of  the  heart ;  second,  by  blood  alterations — viz.,  a 
decreased  number  of  red  cells,  an  enormous  leucocytosis,  a  deficiency 
in  the  amount  of  haemoglobin,  or  loss  in  the  total  amount  of  the 
blood  by  hemorrhage. 

(1)  Evanescent  pallor  may  be  caused  by  a  temporary  weakness  of 
the  heart's  action,  as  in  syncope,  rigours  or  chills,  nausea,  the  slighter 
degrees  of  shock,  and  the  arterial  spasm  of  certain  vasomotor 
neuroses. 

(2)  Sudden  and  more  or  less  permanent  paleness  is  seen  for  the 
most  part  in  large  and  rapid  hemorrhages,  and  in  cases  where  the 
heart  fails  abruptly.  Leaving  traumatism  out  of  consideration,  the 
first  diagnostic  symptom  of  internal  hemorrhage  {q.  v.)  may  be  a 
sudden  pallor,  to  be  soon  followed  by  associated  symptoms  and 
perhaps,  depending  on  its  source  and  within  a  varying  period,  by  a 
discharge  of  blood  from  an  ori  ice  of  the  body. 

(3)  Slow-coming  a,rd  permanent  pallor  arises  from  a  gradual 
diminution  in  the  niimber  of  red  cells  and  the  amount  of  haemo- 
globin.    Such  alterations  may,  in  a  sense,  constitute  the  disease,  as 


Y6  THE  EVIDENCES  OP   DISEASE 

in  maladies  due  to  defects  in  the  haematopoietic  or  blood-making 
organs,  or  may  be  secondary  to  other  chronic  diseases,  as  in  tuber- 
culosis. The  pallor  is  often  modified  by  tints  which  are  somewhat 
characteristic  of  the  causative  disease,  but  in  themselves  are  of  little 
value  except  as  corroborating  a  diagnosis  made  by  means  of  other 
signs  and  symptoms.  A  list  of  the  principal  diseases  attended  by 
slow  and  permanent  pallor,  either  anaemic  or  circulatory,  is  appended  : 
Cancer  (yellow  tint).  Hemorrhages  (slight  recurring). 

Chloro-anaemia     (yellowish-green     Leucaemia. 

tint).  Malarial  cachexia. 

Chronic  arsenical  poisoning.  Nephritis  (waxy  pallor). 

Chronic  febrile  diseases.  Pernicious  aneemia  (lemon-yellow 

Chronic  gastro-intestinal  disease.         tint). 
Chronic  lead  poisoning.  Pseudo-leucaemia. 

Chronic  mercurial  poisoning.  Syphilis. 

Chronic  suppurations.  Tuberculosis. 

Heart  diseases   (especially  fatty 
heart,  mitral,  and  aortic  steno- 
sis). 
Redness. — Unusual  redness  of  the  skin  depends  upon  the  over- 
filling of  the  cutaneous  capillaries — hyperaemia.     It  may  be  physio- 
logical, as  in  those  of  a  fresh  and  florid  complexion,  in  blushing,  in 
the  general  redness  consequent  upon  a  warm  bath,  friction  of  the 
surface,  and  exercise.     Long  exposure  to  heat,  cold,  and  moisture 
produces  a  purplish  redness  of  the  hands,  which  may  be  seen  typic- 
ally in  common  labourers  and  washerwomen.     The  hands  are  cold, 
and  pressure  with  the  point  of  the  finger  leaves  a  light-coloured  spot 
to  which  the  blood  very  gradually  returns,  showing  a  very  sluggish 
capillary  circulation.     Xevertheless,  this  condition  may  coexist  with 
perfect  health. 

Pathological  redness  may  be  either  diffused  or  localized. 

(1)  Diffused  redness  is  seen  in  many  fevers,  especially  in  children, 
because  of  their  particularly  free  capillary  circulation.  Full  doses 
of  belladonna  or  hyoscyamus  will  produce  general  hyperaemia. 

(2)  Localized  redness  is  sometimes  characteristic,  as  in  the  bilat- 
eral flush  upon  the  cheeks  which  accompanies  excitement  or  fever  in 
the  phthisical,  the  redness  of  one  cheek  in  acute  pneumonia,  and 
the  unilateral  redness  of  the  face  which  attends  some  attacks  of 
migraine.  In  certain  cases  of  anaemia  {clilorosis  rubra)  the  flushing 
of  the  face  is  so  marked  that  at  first  the  existence  of  a  deficiency  of 
haemoglobin  may  be  quite  unsuspected.  The  dusky  redness  of  the 
face  in  chronic  alcoholics  is  familiar,  and  in  obstructed  portal  cir- 
culation there  may  be  limited  red  areas  on  the  nose  and  cheeks. 


CYANOSIS  Y7 

Cyanosis. — A  blue  or  purple  tint  of  the  skin,  dependent  upon 
the  presence  of  dark  venous,  imperfectly  oxygenated  blood  in  the 
capillaries,  is  seen  in  many  diseases  and  conditions.  It  is  best  ob- 
served in  the  finger  nails,  lips,  and  mucous  membranes,  because  of 
the  thinness  and  translucency  of  their  epithelial  covering.  If  the 
cyanosis  becomes  decided,  the  whole  cutaneous  surface  will  assume  a 
dusky,  leaden  tint.  The  causes  of  cyanosis  may  be  enumerated  under 
the  following  heads.  It  will  be  evident  that  more  than  one  cause 
may  be  present  in  a  given  case. 

(1)  Conditions  luhich  Hinder  the  Admission  of  Air  to  the  Lungs. 
— Angina  Ludovici,  phlegmonous  inflammation  of  the  floor  of  the 
mouth  ;  glossitis  ;  pharyngitis,  if  acute  and  severe,  and  retropharyn- 
geal abscess  may  cause  cyanosis  by  producing  oedema  of  the  glottis  ; 
laryngismus  stridulus ;  spasmodic  croup ;  laryngitis  (acute  or  chronic) ; 
tuberculous  or  syphilitic  inflammation  of  larynx ;  diphtheria  of  larynx 
(membranous  croup),  trachea,  and  bronchi ;  traumatism  of  larynx 
and  pharynx,  old  or  recent ;  foreign  bodies  in  the  upper  air  pas- 
sages ;  paralysis  of  dilators  of  larynx ;  compression  of  trachea  or 
bronchi  from  aortic  aneurism,  goitre,  enlarged  bronchial  glands,  or 
tumours  of  mediastinum;  spasmodic  asthma;  fibrinous  or  plastic 
bronchitis;  bulbar  paralysis  and  peripheral  neuritis,  by  causing 
paralysis  of  the  muscles  of  respiration ;  peritonitis,  by  causing  paral- 
ysis of  the  diaphragm ;  epilepsy,  tetanus,  and  strychnine  poisoning  by 
causing  respiratory  spasm ;  pleurisy,  pneumonia,  intercostal  neural- 
gia, diaphragmatic  pleurisy,  pleurodynia,  and  peritonitis,  the  pain 
which  attends  these  diseases  preventing  the  full  and  free  action  of 
the  respiratory  muscles. 

(2)  Conditions  which  Lessen  the  Working  Breathing  Surface  of 
the  Lungs^  either  by  effusion  or  exudation  into  the  air  cells,  by 
alterations  in  the  form  and  structure  of  the  air  cells,  or  by  direct 
compression  from  outside,  as  in  pneumonia  (all  varieties),  collapse 
of  lungs,  pulmonary  oedema,  pulmonary  tuberculosis,  emphysema, 
pleurisy  with  effusion,  hydrothorax,  pneumothorax,  pericarditis  (with 
large  effusion),  thoracic  tumours,  and  large  abdominal  effusions  and 
tympanites,  by  pressing  up  the  diaphragm. 

(3)  Conditions  ivhich  Interfere  tvith  the  Pulmonary  or  Systemic 
Circiilation. — The  interference  may  be  with  one  or  both,  causing  a 
general  cyanosis.  There  may  be  also  a  limited  cyanosis  due  to  local- 
ized obstruction  of  the  venous  trunks  of  an  extremity  or  a  portion  of 
the  body.  The  circulation  through  the  capillaries  of  the  lungs  is 
necessarily  obstructed  by  any  of  the  diseases  or  conditions  previously 
mentioned  (e.  g.,  pleurisy  with  effusion),  which  act  in  such  a  manner 
as  to  compress  the  lung,  because  the  capillaries  also  are  compressed 


^8  THE  EVIDENCES  OF   DISEASE 

and  their  calibre  lessened  to  a  greater  or  less  extent.  In  emphysema 
of  a  high  grade  and  in  pulmonary  tuberculosis  many  capillaries  are 
obliterated.  General  cyanosis  is  also  produced  by  the  large  class  of 
valvular  and  degenerative  diseases  of  the  heart  when  compensation 
fails  and  the  heart  muscle  loses  power,  especially  when  the  right 
ventricle  becomes  dilated  and  is  unable  to  clear  itself.  It  appears  in 
pericarditis  with  large  effusion,  or  when  mediastinal  tumours  press 
upon  the  superior  or  inferior  vena  cavae  at  their  entrances  to  the 
right  auricle. 

Local  cyanosis  is  caused  by  pressure  upon  large  veins  or  venous 
trunks,  thus  damming  the  venous  blood  back  upon  the  part  or  area 
drained  by  them — viz.,  thrombosis  of  the  femoral  or  brachial,  compres- 
sion of  the  inferior  vena  cava  by  ascites,  or  pressure  upon  any  vein 
by  inflammatory  swellings  or  neoplasms. 

(4)  Cyanosis  may  he  Produced  by  Certain  Drugs  or  Poisons. — 
Examples  of  this  condition  occur  with  overdoses  of  the  coal-tar 
preparations  (antipyrine,  acetanilide),  with  drugs  which  depress  the 
respiratory  centres  (opium  and  its  preparations),  or  with  those  which 
cause  chemical  changes  in  the  blood  (hydrocyanic  acid,  chloride  of 
oalcium). 

Jaundice  or  Icterus. — This  is  a  yellowish  coloration  of  the 
«kin,  mucous  membranes,  and  fluids  of  the  body,  varying  in  intensity 
from  a  light  lemon-yellow  to  a  brownish-yellow  or  saffron  tint,  and 
caused  by  the  presence  of  bile  pigment  in  the  blood.  In  exceptional 
cases  it  is  a  dark-brown  or  greenish-black,  the  so-called  "  black  Jaun- 
dice." It  is  observed  first  and  best  in  the  conjunctiva  and  the  oral 
mucous  membrane,  and,  when  slight,  in  the  eyes  and  mouth  only. 
in  order  to  demonstrate  it  in  the  mucous  membranes,  it  may  be  neces- 
•sary  to  render  an  area  of  the  membrane  anemic,  by  pressure  with  the 
fingers  or  by  a  glass  mounting  slide,  which  allows  the  yellow  ground 
tint  to  become  visible.  It  may  be  readily  seen  upon  the  under 
surface  of  the  tongue  and  the  anterior  portion  of  the  floor  of  the 
mouth. 

Sources  of  error  are  the  yellowish  tint  of  chloro-anaemia,  ma- 
lignant tumour,  malarial  cachexia,  renal  cirrhosis,  lead  poisoning, 
and  the  temporary  icterus  of  the  newborn ;  but  mistakes  may  be 
avoided  by  noting  that  the  conjunctiva  retains  a  normal  colour.  In 
examining  the  eye,  the  presence  of  yellow  subconjunctival  fat  will 
not  deceive  the  careful  observer. 

In  studying  jaundice  we  may  consider  it  from  two  aspects — first, 
its  cause  or  origin ;  second,  its  severity. 

A.  Jaundice,  with  Kefekence  to  its  Origin,  may  be  either 
obstructive  or  toxcemic. 


JAUNDICE  79 

(1)  Obstructive  Jaundice. — In  this,  as  its  name  indicates,  there  is 
some  hindrance  to  the  passage  of  bile  from  the  liver  into  the  intes- 
tine, and  in  consequence  it  is  absorbed  into  the  rootlets  of  the 
hepatic  vein  and  carried  into  the  general  circulation. 

In  addition  to  the  yellowish  skin  and  mucous  membranes  previ- 
ously described,  the  symptoms  of  the  obstructive  form  are  as  follows  : 
There  is  a  yellow  coloration  of  the  sweat  (rarely  of  the  saliva,  tears, 
and  milk)  and  of  the  sputum  if  pneumonia  coexists.  The  urine  is 
more  or  less  deeply  coloured  and  may  resemble  dark  beer.  As  no 
bile  enters  the  intestine,  the  stools  are  pasty,  fetid,  and  of  a  drab  or 
clay  colour.  The  clay-coloured  faeces  constitute  an  important  differ- 
ential point  between  obstructive  and  toxaemic  jaundice.  Constipa- 
tion is  usual,  but  diarrhoea  may  be  caused  by  excessive  putrefaction 
in  the  intestine.  Distressing  cutaneous  itching  or  pruritus  is  com- 
mon in  the  more  chronic  cases.  Furuncles,  urticaria,  xanthelasma, 
and  other  diseases  of  the  skin  may  ensue.  In  chronic  cases  there 
may  be  red  patches  up  to  an  inch  in  diameter,  due  to  dilated  vessels, 
on  the  skin  and  mucous  membranes,  and  the  blood  coagulates  very 
slowly,  giving  rise  to  obstinate  and  sometimes  fatal  hemorrhage  fol- 
lowing injury  or  operation.  Large  ecchymoses,  purpuric  spots,  and, 
although  rarely,  spontaneous  bleeding  from  the  mucous  membranes 
may  be  seen  in  chronic  cases.  The  pulse  is  usually  slow  (40  to 
20),  especially  in  catarrhal  jaundice;  and  the  respiration  slow,  10 
or  even  less  per  minute.  The  patient  is  apt  to  be  depressed  and 
melancholy.  In  the  chronic  and  fatal  cases  the  patient  may  pass 
into  the  typhoid  state  {q.  v.),  or  there  may  be  a  sudden  onset  of  con- 
vulsions, delirium,  or  coma — usually,  in  either  case,  followed  by 
death. 

The  causes  of  the  obstructive  form  are  :  Gastro-duodenal  catarrh  ; 
catarrh  of  the  bile  ducts,  common,  large,  or  small,  with  swelling  of 
the  lining  membrane;  lodgment  of  gallstones  or  roundworms  in 
the  common  duct ;  pressure  on  or  closure  of  the  duct  by  tumour  of 
the  liver,  stomach,  kidney,  omentum,  and  especially  of  the  pancreas ; 
and  new  growths  or  cicatricial  tissue  affecting  the  duct  itself  so  as 
to  produce  stricture  or  obliteration  of  its  lumen.  In  rare  instances 
the  pressure  of  a  pregnant  uterus,  an  abdominal  aneurism,  or  a  large 
faecal  accumulation  may  be  responsible  for  the  obstruction. 

(2)  Toxaemic  Jaundice. — The  non-obstructive  form  of  jaundice 
depends  upon  the  presence  in  the  circulation  of  various  poisons 
which  destroy  the  red  cells  of  the  blood,  or  more  rarely  the  hepatic 
cells  as  well. 

The  symptoms  of  toxic  jaundice  may  be  very  slight.  The  yellow 
■colour  may  be  slight  and  is  rarely  so  intense  as  in  obstructive  jaun- 


80  THE  EVIDENCES  OP  DISEASE 

dice.  As  there  is  no  hindrance  to  the  entrance  of  bile  into  the 
intestines,  the  faeces  not  only  retain  their  normal  colour,  but  because 
of  an  increased  flow  of  bile  (polycholia,  due  to  the  destruction  of  the 
red  blood  cells)  may  be  darker  than  usual.  The  urine  may  be  deep- 
ened in  colour,  but  bile  pigment  is  absent  or  small  in  quantity,  and 
the  coloration  is  due  to  an  increase  in  the  amount  of  the  normal 
pigments  of  the  urine.  If  the  toxaemia  is  severe,  there  may  be  grave 
general  symptoms — coffee-ground  vomiting,  hemorrhages  into  the 
skin  and  mucous  membranes,  delirium,  convulsions,  and  high  tem- 
perature. Toxaemic  jaundice  is  never  chronic,  death  or  recovery 
taking  place  within  a  comparatively  short  period. 

The  causes  of  toxaemic  jaundice  are  the  toxines  or  venoms  produced 
by  living  organisms,  or  poisoning  by  certain  chemical  comj)ounds. 
Consequently  this  variety  of  jaundice  is  met  with  as  a  consequence  of 
the  acute  infectious  diseases — viz.,  epidemic  influenza,  malaria  (inter- 
mittent and  remittent),  pneumonia,  typhoid  fever,  typhus  fever,  scarlet 
fever,  yellow  fever,  relapsing  fever,  pyaemia,  ulcerative  endocarditis, 
acute  yellow  atrophy  of  the  liver,  and  Weil's  disease ;  also  poisoning 
by  snake  venom,  antimony,  arsenic,  chloral  hydrate,  chloroform, 
copper,  ether,  mercury,  phosphorus  (especially),  potassium  chlorate, 
and  toluylendiamine. 

B.  Jaundice,  with  Eeferekce  to  its  Severity,  may  be  either 
mild  {icterus  simplex)  or  severe  {icterus  gravis).  It  is  a  matter  of 
much  clinical  importance  to  determine  in  which  of  these  categories 
an  individual  case  belongs. 

(1)  Mild  Jaundice ;  Symptoms  and  Causes.— /f/er?^s  simplex  is  fre- 
quently ushered  in  by  nausea  or  vomiting,  which  may  last  only  for 
a  day  or  two,  with  malaise,  slight  fever,  some  headache,  clay-coloured 
stools,  slow  pulse,  and  slight  or  no  itching  of  the  skin,  although 
the  latter  may  be  much  stained.  This  mild  type  almost  always  arises 
from  a  catarrhal  inflammation  of  the  common  duct,  the  swollen  mu- 
cosa occluding  the  duct  and  preventing  the  bile  from  entering  the 
intestine.  It  is  usually  an  extension  of  a  gastro-duodenitis,  and 
recovery  is  the  rule  within  a  few  weeks.  A  mild  jaundice  may  or 
may  not  be  present  in  the  later  stages  of  certain  diseases  of  the  liver — 
viz.,  cirrhosis,  passive  congestion,  carcinoma,  syphilis,  amyloid  and 
fatty  liver,  and  echinococcus. 

(2)  Severe  Jaundice;  Symptoms  and  Causes. — Icterus  gravis  may 
be  acute,  subacute,  or  chronic.  The  symptoms  are  of  an  ominous 
character  as  compared  with  the  mild  form.  The  jaundice  is  associated 
with  delirium,  vomiting,  hemorrhages,  and  high  fever ;  or  the  dry 
tongue,  mental  confusion,  low  continued  fever,  and  profound  ady- 
namia of  the  typhoid  state.     This  severe  type  of  icterus  may  be  due  to 


THE  HEAT   OF  THE  SKIN  81 

toxaemic  causes  {q.  v.),  or,  if  chronic  and  attended  with  emaciation,  to 
some  of  the  conditions  which  produce  more  or  less  permanent  and 
perhaps  irremediable  obstruction  of  the  bile  ducts— e.  g.,  an  impacted 
gallstone.  Jaundice  plus  hepatic  colic  or  pain  in  the  right  hypo- 
chondrium  may  signify  the  passage  or  lodgment  of  a  gallstone  or  a 
cancer  of  the  duodenum.  Jaundice  with  a  marked  cachexia  may  indi- 
cate carcinoma  of  the  liver ;  with  chills  and  fever,  hepatic  abscess  ; 
with  ascites,  a  cirrhotic  liver  or  a  chronic  peritonitis. 

Bron2d.ng. — Affecting  the  general  cutaneous  surface,  this  is  seen 
in  Addison's  disease  {q.  v.).  It  consists  of  a  brown  or  brownish-black 
discoloration,  not  dispelled  by  pressure,  most  marked  in  the  face 
and  hands  and  in  the  portions  of  the  body  which  normally  contain 
pigment.  It  occurs  also  in  the  mucous  membrane  of  the  mouth  and 
vagina  as  discrete  brown  spots  of  varying  size.  The  nails,  cornea, 
and  conjunctiva  usually  escape.  The  bronzing  is  due  to  the  deposi- 
tion of  pigment  in  the  deeper  layers  of  the  skin  and  mucous  mem- 
branes. 

Other  conditions  may  present  an  abnormal  amount  of  pigmenta- 
tion, either  general  or  local.  Patchy  yellow  spots  may  appear,  usu- 
ally but  not  always,  on  the  forehead  and  face,  in  persons  who  suffer 
from  habitual  constipation  or  chronic  "biliousness";  dilatation  or 
chronic  ulcer  of  the  stomach ;  pregnancy  with  uterine  diseases ;  can- 
cer or  tuberculosis  of  the  abdominal  viscera  or  the  peritoneum  ;  diseases 
of  the  liver,  especially  cirrhosis  and  the  chronic  congestion  due  to 
cardiac  lesions ;  exophthalmic  goitre ;  severe  acne,  tinea  versicolor,  and 
following  syphilitic  eruptions.  General  and  deep  pigmentation,  from 
dirt  and  lice,  may  be  seen  in  tramps ;  also,  but  rarely,  in  scleroderma 
and  melanotic  cancer. 

Gray  Skin. — This  has  been  observed  after  the  long-continued 
therapeutic  ingestion  of  silver  nitrate.  It  is  occasioned  by  the  pres- 
ence of  minute  deposits  of  the  albuminate  of  the  metal  in  the  skin. 

II.  THE    HEAT   OF   THE   SKIN 

This  may  be  estimated  roughly  by  placing  the  hand  upon  the 
skin,  or  accurately  by  the  use  of  a  surface  thermometer.  The 
temperature  of  the  skin,  however,  is  not  an  index  of  the  internal 
temperature,  because  a  high  degree  of  fever  may  coexist  with  marked 
coldness  of  the  surface,  as  in  the  cold  stage  of  intermittent  malarial 
fever.  *■ 

{a)  Gefieral  coldness  of  the  surface  is  usually  associated  with  a 
poor  capillary  circulation,  the  blood  returning  slowly  to  a  spot  which 
has  been  rendered  anaemic  by  pressure.  It  occurs  in  all  chills  and 
rigours,  in  many  forms  of  general  cyanosis,  and  in  all  afebrile  diseases 


82  THE   EVIDENCES  OP  DISEASE 

attended  by  a  weak  or  failing  heart,  (b)  General  abnormal  heat  of 
the  surface  may  and  usually  does  exist  in  all  fevers  and  diseases  at- 
tended with  decided  febrile  temperatures,  but,  as  stated,  this  is  by  no 
means  always  the  case. 

(c)  Local  coldness  of  the  surface  may  be  due  to  vasomotor  spasm,, 
arterial  or  venous  thrombosis,  or  other  obstruction  to  the  circulation 
in  a  localized  area ;  (d)  local  heat,  to  inflammations  or  new  growths 
under  that  portion  of  the  skin  which  exhibits  the  increased  tem- 
perature. 

III.  THE    MOISTURE    OF   THE    SKIN 

The  amount  of  moisture  may  be  greatly  increased — Jii/peridrosis / 
or  entirely  absent — anidrosis. 

(«)  Hyperidrosis. — More  or  less  profuse  sweating  is  not  incom- 
patible with  fever,  as  in  acute  rheumatism  and  other  diseases,  but 
occurs  more  frequently  when  the  temperature  is  normal  or  subnor- 
mal. In  general,  hyperidrosis  is  attendant  upon  debility  (as  in  con- 
valescence), great  weakness  (as  in  collapse),  dyspnoea,  infectious  and 
septic  conditions,  tuberculosis  (night  sweats),  severe  pain,  and  the 
use  of  diaphoretics. 

Partial  or  localized  sweating  is  an  occasional  event  in  connection 
with  certain  ailments.  Sweating  of  the  hands  or  the  feet  attends^ 
some  conditions  of  general  debility,  or  may  be  a  constitutional  pecul- 
iarity. Sweating  of  the  head  is  seen  in  rachitis ;  unilateral  or  one- 
sided sweating  of  the  head  or  face,  in  migraine,  neuralgia,  and  other 
affections  of  the  nervous  system,  suppurative  parotitis,  and  pressure 
on  the  sympathetic  by  a  thoracic  aneurism ;  unilateral  sweating  of 
the  body  (hemidrosis),  exceptionally  in  hemiplegia.  Partial  sweating 
is  usually  caused  by  deranged  innervation  of  the  vasomotor  nerves. 

{b)  Anidrosis. — Diminution  or  absence  of  perspiration  is  observed 
in  many  febrile  diseases,  especially  if  the  temperature  is  high  and 
prolonged.  It  accompanies  diseases  in  which  there  is  a  profuse  dis- 
charge of  fluid  from  the  bowels,  kidneys,  or  stomach.  If  the  skin  is 
stretched  or  altered  in  structure  so  that  the  cutaneous  circulation  is 
hindered,  as  in  general  dropsy  or  anasarca,  or  in  myxoedema,  anidro- 
sis exists  as  a  direct  result. 

(c)  Alterations  in  Character. — In  rare  instances  alterations  in  the 
composition  or  colour  of  the  perspiration  are  noted.  In  uridrosis, 
occurring  with  diseases  in  which  the  action  of  the  kidneys  has  been 
impaired,  the  sweat  has  a  urinous  odour  and  deposits  white  scales  or 
crystals  of  urinary  solids  upon  the  skin.  Yellow  sweat,  from  the 
biliary  pigments,  may  be  present  in  severe  jaundice.  Blue,  brown,, 
yellow,  or  red  sweat  (chromidrosis)  has  been  observed  in  hysteria.^ 


MOISTURE— RASH   OR  ERUPTION  85 

Very  rarely  bloody  sweat  {hcematidrosis),  a  capillary  hemorrhage  into- 
the  sudoriparous  glands  of  nervous  origin,  or  a  species  of  vicarioua 
menstruation  (metiidrosis),  occurs. 

In  the  consideration  of  sweating  as  a  symptom,  its  normal  in- 
crease, especially  in  warm  weather,  after  exercise,  hot  baths,  hot 
drinks,  and  strong  mental  emotion,  should  not  be  forgotten. 

IV.    RASH   OR   ERUPTION 

There  are  certain  morbid  appearances  or  lesions  of  the  skin  which 
are  of  importance,  because  of  the  fact  that  they  accompany,  or  indeed 
may  be  a  symptom  of,  some  disease  or  condition  affecting  the  body  as- 
a  whole. 

The  cutaneous  lesions  possessing  general  diagnostic  significance 
are  as  follows : 

Cutaneous  or  Suhcutaneous  Hemorrhages. — These  vary  in  size 
from  a  mere  point  to  3  or  more  inches  in  diameter,  and  occur 
most  abundantly  upon  the  lower  extremities.  Small  hemorrhagic 
spots  (petechias)  are  frequently  found  in  the  hair  follicles.  Larger 
hemorrhages  (ecchymoses)  are  diffuse.  If  recent,  their  colour  ia 
dark  red,  but  as  absorption  progresses  this  tint  alters  to  a  reddish 
brown  or  dark  yellow.  Petechial,  ecchymotic,  and  pigmented  points 
or  areas  may  be  readily  distinguished  from  hyperaemic  or  inflamma- 
tory redness  by  pressure  made  with  the  finger,  or  better  with  a  glass^ 
slide.  Under  pressure  a  hemorrhagic  spot  becomes  more  obvious 
because  of  the  surrounding  anaemia,  while  the  redness  of  hyperaemia 
or  inflammation  will  vanish. 

The  diagnostic  value  of  hemorrhages  into  or  beneath  the  skin 
depends  entirely  upon  the  symptom  group  in  which  they  are  found. 
They  may  be  infarctions,  dependent  upon  the  lodgment  of  septic 
emboli  in  the  smaller  arteries,  as  in  pyaemia ;  a  consequence  of  alter- 
ations in  the  blood,  as  in  pernicious  anaemia ;  an  accompaniment  of 
infectious  diseases,  as  in  typhus  fever ;  a  result  of  the  ingestion  of  cer- 
tain drugs,  as  in  mercurial  poisoning ;  an  effect  of  traumatism,  as  in 
contusions  ;  or  of  mechanical  obstruction  to  the  return  flow  through 
the  veins,  local  or  general,  as  in  cyanosis ;  and,  finally,  of  neurotic  or 
unknown  origin,  as  in  locomotor  ataxia  and  the  various  forms  of 
arthritic  or  hemorrhagic  purpura.  In  all  cases  there  must  exist 
either  alterations  in  the  composition  of  the  blood  which  will  allow  it 
to  pass  through  the  uninjured  vessel  walls,  or  histological  changes  in 
the  vessel  walls  due  to  traumatic,  neurotic,  or  other  pathological 
causes,  which  render  them  abnormally  permeable. 

The  most  important  diagnostic  associations  are  with  fever,  as  in 
the  infectious  or  septic  diseases;  with  fever  and  joint  pains,  as  ia 


84 


THE  EVIDENCES  OF  DISEASE 


peliosis  rheumatica ;  and  with  hemorrhages  from  the  nose,  stomach, 
intestines,  and  other  mucous  surfaces,  as  in  purpura  haemorrhagica. 

The  diseases  and  conditions  in  which  petechia  and  ecchymoses 
may  occur,  and  the  poisons  which  may  produce  them,  are  as  follows : 


Acute  exudative  erythema. 

Acute  yellow  atrophy  of  liver. 

Anaemias  (especially  pernicious). 

Cancer  (especially  later  stages,  of 
stomach  and  liver). 

Cerebro-spinal  meningitis  (epi- 
demic variety). 

Convalescence  from  fever  (in  the 
legs). 

Cyanosis  (all  forms). 

Diphtheria. 

Epilepsy  (from  venous  stasis). 

Erythema  nodosum. 

Elea-bites  (in  debilitated  persons). 

Haemophilia. 

Henoch's  purpura. 

Hepatic  cirrhosis  (at  a  late  stage). 

Jaundice  (in  severe  forms). 

Measles  (if  severe). 

Myelitis  (acute  and  transverse). 

Old  age  (in  the  extremities). 

Peliosis  rheumatica  (Schonlein's 
disease). 

Pertussis  (from  venous  stasis). 

Purpura  haemorrhagica. 

Purpura  simplex. 

Pyaemia. 

Eenal  cirrhosis  (at  a  late  stage). 


Sarcoma  (of  skin  and  bones). 

Scarlatina. 

Scurvy. 

Septicaemia. 

Snake  venom  (poisoning  by). 

Stigmata  (bleeding  points  in  hys- 
teria). 

Tuberculosis  (with  extreme  debil- 
ity). 

Typhoid  fever. 

Typhus  fever. 

Ulcerative  (malignant)  endocar- 
ditis. 

Variola. 

Yellow  fever. 

Belladonna  (poisoning  or  idiosyn- 
crasy). 

Copaiba  (poisoning  or  idiosyn- 
crasy). 

Ergot  (poisoning  or  idiosyncrasy). 

Mercury  (poisoning  or  idiosyn- 
crasy). 

Phosphorus  (poisoning  or  idio- 
syncrasy). 

Potassium  iodide  (poisoning  or 
idiosyncrasy). 

Quinine  (poisoning  or  idiosyn- 
crasy). 


Herpes  Facialis. — These  are  small  vesicles  ("  cold  sores  ")  contain- 
ing a  clear  fluid,  grouped  upon  a  reddened  and  slightly  elevated  base. 
The  fluid  becomes  puriform,  and  in  a  few  days  the  lesion  dries  and 
scales  off.  They  are  not  attended  by  pain,  thus  differing  from  herpes 
zoster.  They  form  most  frequently  upoil  the  lips  {herpes  lahialis)^ 
also  upon  the  nose,  cheeks,  or  ear,  and  may  appear  in  the  mouth. 
Herpes  facialis  is  associated  with  acute  catarrh  of  the  respiratory 
passages;  ephemeral  fever  ;  pneumonia,  in  which  it  is  of  some  diag- 
nostic value ;  cerebro-spinal  fever,  in  which  it  may  be  quite  extensive ; 
and  with  the  rapidly  rising  temperatures  of  intermittent  fever  and 
pyaemia. 


RASH  OR  ERUPTION  85 

Sudamina. — These  consist  of  small,  clear  vesicles,  appearing  in 
great  numbers  upon  all  parts  of  the  body,  but  especially  upon  the 
trunk.  They  give  a  sensation  of  roughness  to  the  hand  as  it  is 
passed  over  the  skin,  and  with  a  good  light  the  minute  pearly  vesi- 
cles may  be  seen.  They  are  formed  after  a  prolonged  period  of  ani- 
drosis  when  the  sweat  glands  begin  to  act.  The  dry  epidermis 
obstructs  the  flow  from  the  sweat  tubules,  each  vesicle  corresponding 
to  the  opening  of  a  sudoriparous  gland.  Their  diagnostic  value  is 
nil. 

Erythematous  or  Inflammatory  Eruptions. — Erythema  is  an  in- 
flammatory hyperaemia  of  the  skin,  either  simple  or  exudative ;  and, 
if  associated  with  or  replaced  by  more  active  inflammatory  processes, 
its  varieties  constitute  a  class  of  cutaneous  lesions  which  are  of  great 
value  in  medical  diagnosis,  because  they  are  essential  events  or  fre- 
quent accompaniments  of  many  serious  and  important,  usually  febrile 
and  infectious,  diseases.  There  are  certain  fevers  in  which  the  skin 
lesions  are  characteristic  (eruptive  fevers  or  exanthemata).  The 
diseases  accompanied  by  more  or  less  diffused  and  characteristic 
eruptions  are  as  follows  : 
'^   ''  Measles.  Influenza  (rare). 

Eubella.  Miliary  fever  (sweating  sickness). 


Scarlatina.  Pyaemia. 

Varicella.  Relapsing  fever. 


s 

e 

^  [  Variola.  '  Septicaemia. 

Cerebro-spinal  fever.  Syphilis. 

Dengue.  Typhoid  fever. 

Glanders  (acute).  Typhus  fever. 

Erysipelas.  Ulcerative  endocarditis. 

Drug  Eruptions. — The  possible  occurrence  of  erythematous  or 
other  eruptions  as  a  result  of  the  ingestion  of  overdoses  of  certain 
medicinal  substances,  or  of  individual  idiosyncrasy,  must  be  borne 
in  mind,  as  otherwise  a  mistaken  diagnosis  may  readily  be  made. 
The  drugs  which  may  cause  puzzling  rashes  or  eruptions  are  :  Anti- 
pyrine,  arnica,  arsenic,  atropine,  belladonna,  cannabis  indica,  capsi- 
cum, carbolic  acid,  chloral,  copaiba,  copper,  cubebs,  croton  oil,  digi- 
talis, iodoform,  lead,  mercury,  morphine,  opium,  potassium  bromide, 
potassium  iodide,  quinine,  salicylates,  salicylic  acid,  santonin,  silver, 
sulphur,  tar,  and  tartar  emetic. 

Roseola. — Fugitive  roseolous  rashes  not  infrequently  initiate  the 
eruptive  fevers,  antedating  the  true  exanthem,  and  may  thus  cause 
confusion.  The  diseases  which  may  be  preceded  by  evanescent  rosy 
rashes  are  cholera,  diphtheria,  malaria,  measles,  scarlatina,  typhoid 
fever,  typhus  fever,  and  variola.  The  roseola  may  be  mistaken  for 
•8 


86  THE   EVIDENCES  OF  DISEASE 

a  beginning  measles,  rubella,  or  scarlet  fever.  It  may  also  follow 
childbed  and  surgical  operations. 

Urticaria. — Xettle  rash  may  exist  as  an  accompaiiinient  or  result 
of  certain  diseases,  and  the  ingestion  of  certain  poisons  and  articles 
of  food.  It  is  largely  of  neurotic  pathogeny.  It  occurs  in  connec- 
tion with  the  following  diseases,  drugs,  and  foods :  Cerebro-spinal 
fever,  dengue,  gastro-intestinal  disorders  (especially),  liydatid  cysts 
(after  tapping),  malaria  (especially  in  children),  menstruation  (dis- 
orders of),  mental  emotion,  neurotic  oedema,  parasites  (intestinal), 
pulmonary  diseases  (bronchial  mucous  membranes),  purpura,  rheuma- 
tism, typhoid  fever,  variola,  antipyrine,  quinine,  buckwheat  cakes, 
mineral  waters  (in  excess),  mushrooms,  oatmeal,  pastry,  pork,  shell- 
fish, and  strawberries  (especially). 

Furuncles  (boils)  and  carbuncles  are  apt  to  occur  in  connection 
with  diabetes  {q.  v.),  and  repeated  attacks  demand  a  careful  examina- 
tion of  the  urine. 

V.  CICATRICES  OR  SCARS 

Whether  old  or  recent,  scars  may  possess  considerable  diagnostic 
value  as  indicative  of  previous  diseases  or  injuries,  thus  confirming 
or  suggesting  a  diagnosis  of  the  present  condition,  as  follows  : 

{a)  Linear  scars,  striae,  or  lineae  albicantes,  occur  from  over- 
stretching of  the  skin  and  consequent  separation  and  atrophy  of 
its  fibres,  in  obesity,  oedema,  pregnancy,  and  large  abdominal  tumours. 

(Z»)  Small  circular  pits  or  depressions,  especially  upon  the  face, 
are  significant  of  varicella  or  variola. 

(c)  Small  scars  upon  the  face  may  result  from  acne ;  upon  any 
part  of  the  body,  from  furuncles  or  carbuncles,  the  latter  especially 
upon  the  nape  of  the  neck. 

{d)  Scars  of  irregular  shape,  usually  depressed  and  adherent,  are 
due  to  tuberculous  or  scrofulous  disease  of  the  glands,  and  are  seen 
significantly  in  the  location  of  the  cervical,  axillary,  and  inguinal 
glands.  They  may  also  be  a  consequence  of  tuberculous  disease  of 
the  bones.     Lupus  of  tuberculous  origin  leaves  large  fiat  scars. 

{e)  The  scars  of  syphilitic  ulceration  are  large  and  nearly  circular. 
Non-traumatic  scars,  if  single,  upon  the  forehead  or  the  legs,  in  a 
person  below  middle  age,  are  usually  specific. 

(/)  Scars  upon  the  head  or  spine  or  over  important  peripheral 
nerves  may  throw  light  upon  the  cause  of  cerebral  symptoms,  or  dis- 
ease of  the  cord  and  spinal  nerves.  The  scars  which  may  result  from 
injuries  sustained  during  convulsions,  epileptic  or  other,  should  be 
borne  in  mind. 

{g)  Scars  of  little  importance  are  the  contracted  large  or  small 


DROPSY  AND  (EDEMA  8Y 

cicatrices  from  burns,  the  symmetrical  linear  scars  from  wet-cupping, 
and  the  multiple  minute  scars  of  pustulation  from  the  external  appli- 
cation of  croton  oil  and  tartar-emetic  ointment. 

VI.     DROPSY,   CEDEMA,   ANASARCA 

Dropsy  is  the  generic  term  indicating  an  accumulation  of  watery 
fluid  in  one  or  more  of  the  serous  cavities,  or  a  diffusion  of  such  fluid 
through  the  areolar  tissue  of  the  body  or  its  organs,  or  a  combination 
of  these  conditions.  (Edema  is  the  effusion  of  watery  fluid  into  the 
tissue  of  a  part.  Anasarca  is  a  subcutaneous  oedema  diffused  over 
the  body  at  large — general  oedema. 

(1)  Dropsy  of  Cavities. — Dropsies  involving  the  cavities  of  the 
body  have  received  particular  names.  Dropsy  of  the  peritoneal 
cavity  is  designated  as  ascites  or  hydroperitoneum ;  joints,  hydrar- 
throsis ;  brain,  hydrocephalus ;  pleural  cavity,  hydrothorax ;  Fallopian 
tube,  hydrosalpinx ;  pericardium,  hydropericardium ;  pelvis  of  the 
kidney,  hydronephrosis ;  and  adnexa  of  the  testicle,  hydrocele.  Drop- 
sies of  cavities  {q.  v.)  are  considered  elsewhere. 

(2)  Recognition  of  (Edema. — The  existence  of  oedema  is  in  most 
cases  readily  perceived.  There  is  painless  swelling,  the  skin  is  pale, 
smooth,  and  shining,  and  if  pressure  is  made  with  the  point  of  the 
finger,  especially  over  a  bony  surface  (tibia,  malleolus),  pitting  will 
occur,  and  an  appreciable  time  will  elapse  before  the  depressed  skin 
regains  its  former  level.  The  part  is  apt  to  be  unduly  cool,  and  a 
serous  fluid  will  ooze  out  from  a  needle  puncture.  (Edema  is  to  be 
discriminated  from  subcutaneous  emphysema  by  the  fine  crackling 
produced  by  pressure  in  the  latter  condition ;  from  the  thickened 
skin  due  to  infiltration  of  mucin  in  myxoedema  {q.  v.)  by  the  fact 
that  in  the  latter  the  swelling  is  firm,  and  does  not  pit ;  from  phleg- 
monous inflammations,  by  the  lack  of  pain  and  redness ;  from  local- 
ized overgrowths  of  connective  tissue,  which  are  hard,  and  do  not 
pit  on  pressure  ;  and  from  scleroderma. 

(3)  Pathology  of  (Edema. — In  general,  oedema  is  directly  due  to  a 
disturbance  of  the  relation  between  the  amount  of  fluid  which  trans- 
udes from  the  capillaries  and  that  which  is  absorbed  and  carried 
away  by  the  lymphatics.  If  the  lymphatics  are  obstructed,  or  if 
from  any  cause  the  capillaries  become  abnormally  permeable  and 
allow  more  fluid  to  escape  than  can  be  removed,  the  excess  of  fluid 
will  accumulate  in  the  connective-tissue  spaces  and  lymph  radicles. 
The  character  of  the  minute  changes  in  the  vessel  walls  which  allow 
free  transudation  of  serum  is  still  unsettled. 

(4)  Causes  of  (Edema. — The  causes  and  varieties  of  dropsy  may  be 
classed  as  follows :  («)  Venous  obstruction ;  {b)  toxaemic  or  hydrae- 


88  THE  EVIDENCES   OP  DISEASE 

mic  conditions  of  the  blood;  (c)  effect  of  inflammation  upon  the 
neighbouring  circulation ;  {d)  vasomotor  or  other  causes  belonging 
to  the  nervous  system;  (e)  lymphatic  obstruction;  and  (/)  idio- 
pathic or  essential  oedema,  the  nature  of  which  is  as  yet  undis- 
covered. 

Venous  Obstruction. — The  diseases  which  may  be  attended  by 
general  oedema  are  those  which  tend  to  prevent  the  return  flow  of 
blood  to  the  right  side  of  the  heart.  Here  belongs  the  rather  char- 
acteristic oedema  of  cardiac  origin  occurring  when  the  heart  muscle 
fails  from  valvular  defects  or  other  causes.  Cardiac  oedema  is  at 
first  localized  and  makes  its  appearance  primarily  in  the  feet,  whence 
it  may  extend  upward.  It  is  most  marked  in  the  lower  extremities 
after  standing  or  walking  during  the  day,  and  lessens,  or  in  slight 
cases  disappears,  after  a  night's  recumbency.  When  extreme,  it  may 
involve  the  entire  body,  the  scrotum  or  labia  majora  being  enor- 
mously swollen,  and  effusion  taking  place  into  the  closed  cavities  of 
the  chest  and  abdomen.  Under  such  conditions  cyanosis  is  usually 
present,  so  that  the  list  of  diseases  causing  cyanosis  by  venous  ob- 
struction (p.  77)  will  serve  also  for  those  which  produce  oedema  by 
venous  obstruction.  Local  oedema  may  be  caused  by  thrombosis  of 
or  pressure  upon  a  venous  trunk. 

Toxmniic  oedema,  due  directly  or  indirectly  to  poisons  circulating 
in  the  blood,  has  its  principal  exemplification  in  renal  dropsy.  In 
marked  cases  it  is  universal,  affecting  the  entire  body  to  a  greater 
extent  than  in  any  other  disease.  Characteristically  it  begins  first  in 
the  face,  and  is  especially  obvious  around  and  under  the  eyes,  because 
of  the  large  amount  of  loose  areolar  tissue  in  this  locality,  thus  giving  a 
puffy  and  swollen  aspect  to  the  countenance.  It  is  greatest  in  the 
morning,  after  hours  of  recumbency,  and  lessens  during  the  day  if  the 
patient  sits  or  stands.  In  aggravated  cases  the  entire  surface  of  the 
body  will  pit  on  pressure.  It  occurs  particularly  in  the  more  acute 
forms  of  nephritis,  such  as  those  which  constitute  a  sequel  of  scarla- 
tina or  a  complication  of  pregnancy. 

Hydraemic  oedema,  caused  by  impoverished  blood,  is  observed  in 
all  the  anaemias,  usually  a  slight  or  moderate  oedema  of  the  feet  and 
ankles  after  standing  or  walking.  The  oedema  of  the  feet  and  ankles 
which  may  appear  toward  the  end  of  all  wasting  diseases,  and  in 
cachexial  conditions,  as  well  as  in  the  recent  convalescent  on  begin- 
ning to  sit  or  walk,  belongs  to  this  category. 

Collateral  (Edema. — This  appears  to  a  greater  or  less  extent  in 
the  neighbourhood  of  localized,  usually  suppurative,  inflammations, 
and  is  caused  partly  by  obstruction  of  the  lymphatics,  partly  by  over- 
distention  of  the  capillaries  resulting  from  the  afflux  of  blood  to  the 


TOPOGRAPHICAL  OCCURRENCE  OP  (EDEMA  89 

point  of  inflammation.  This  form  of  cedema  may  be  of  considerable 
significance  to  the  internalist,  as  in  the  oedema  of  the  thorax  indica- 
tive of  empyema,  or  of  the  right  hypochondrium  in  abscess  of  the 
liver. 

(d)  (Edema  of  Nervous  Origin. — This  is  seen  in  a  most  striking 
form  as  angioneurotic  oedema  {q.  v.),  a  singular  disease  in  which 
cedematous  swellings  appear  and  disappear  at  brief  intervals  upon  the 
face  or  extremities.  Peripheral  multiple  neuritis  and  beri-beri  are 
other  examples  of  nervous  disease  associated  with  oedema,  but  in 
these  the  oedema  is  general.  The  "  blue  oedema  "  of  Charcot  is  hard, 
bluish,  the  temperature  of  the  part  is  lowered,  and  it  is  associated 
with  sensory  or  motor  disturbances  of  hysterical  origin. 

{e)  Lymplicedema. — This  is  due  to  a  transudation  of  lymph  through 
the  walls  of  the  lymphatic  vessels,  or  to  a  distention  of  the  lymph 
spaces  from  mechanical  obstruction.  It  is  usually  localized  or  con- 
fined to  a  single  limb.  It  has  for  its  cause  laceration  of  a  lymphatic 
trunk,  or  occlusion  of  such  a  vessel  by  external  pressure  or  internal 
obstruction,  e.  g.,  Filaria  sanguinis  hominis,  of  which  macromelia 
and  elephantiasis  are  results.  General  lymphoedema  sometimes 
occurs  in  lymphadenoma  or  Hodgkin's  disease.  This  form  of 
oedema  differs  from  haemic  oedema  in  that  the  oedematous  tissues 
are  much  harder,  inflexible  and  brawny,  and  lymph  oozes  from  the 
cut  surface. 

(/)  (Edema  not  due  to  a  discoverable  morbid  condition  is  not 
infrequent.  The  "probationer's  feet"  of  the  training  school,  the 
swelling  of  the  feet  and  ankles  after  long  marches  or  pedestrian 
trips,  and  the  so-called  essential  oedemas  of  children  belong  under 
this  heading. 

(5)  TopograpMcal  Occurrence  of  (Edema. — The  following 
clinical  classification  of  oedema  is  useful.     Two  or  more  diseases  or 
conditions,  each  of  which  is  attended  by  oedema,  may  coexist — e.  g., 
cardiac  disease,  hepatic  cirrhosis,  and  anaemia : 
A.  General  (Edema  or  Anasarca. 

1.  Beginning  at  the  feet  and  extending  upward — cardiac  weak- 

ness or  disease. 

2.  Beginning  in  the  face  and  extending  downward — ^renal  dis- 

ease. 

3.  Attends  beri-beri  and  may  attend  multiple  peripheral  neu- 

ritis. 

4.  Attends  trichinosis,  first  over  affected  muscles,  then  becoming 

general.     Differs  from  previous  forms  by  the  absence  of 
swelling  in  scrotum  and  labia. 

5.  Lymphoedema  in  Hodgkin's  disease. 


90  THE  EVIDENCES  OF  DISEASE 

B.  (Edema  of  Upper  Half  of  Body. 

1.  In  renal  dropsy,  early  stage. 

2.  Of  arms,  head,  and  neck,  in  thoracic  aneurism,  large  double 

hydrothorax,  and  mediastinal  tumour  pressing  on  superior 
vena  cava  above  the  entrance  of  azygos  veins. 

3.  Of  arms,  head,  neck,  and  thorax,  when  point  of  pressure  is 

below  azygos  veins. 

4.  Sudden  or  acute  oedema,  as  in  3,  is  due  only  to  the  very  rare 

rupture  of  an  aneurism  into  the  superior  vena  cava, 

5.  (Edema  of  one  arm  is  caused  by  the  pressure  of  enlarged 

lymphatic  glands  or  tumours  upon  axillary  or  subclavian 
vein,  or  thrombosis  of  the  vein. 

C.  (Edema  of  Loiuer  Half  of  Body. 

1.  Cardiac  dropsy,  early  stage. 

2.  With  ascites  in  hepatic  cirrhosis. 

3.  Pressure  upon  inferior  vena  cava  by  abdominal  tumours,  en- 

larged liver,  spleen,  pancreas,  or  mesenteric  glands. 

4.  Chronic  malarial  poisoning  with  enlarged  liver  and  spleen. 

5.  CEdema,  usually  moderate  in  amount,  with  anaemias,  cachexiae, 

wasting  diseases,  long-continued  slight  hemorrhages. 

6.  Long  standing  or  walking,  first  rising  in  convalescence,  some- 

times from  no  ascertainable  cause. 

7.  CEdema  of  one  leg,  from  thrombosis  of  femoral  vein,  paral- 

ysis, pressure  on  vein  by  tumour  of  groin  or  abdomen. 

8.  Lymphoedema. 

D.  Circumscribed,  usually  Single,  (Edematous  Swellings  {Collateral 
(Edema  attending  Local  Inflammations). 

1.  Over  praecordial  space  in  purulent  pericarditis. 

2.  Over  affected  side  in  empyema. 

3.  Over  mastoid  process  in  inflammation  of  mastoid  cells. 

4.  Over  parotid  gland  in  mumps  or  parotid  suppuration. 

5.  Over  deep-seated  muscular  abscesses,  especially  in  typhoid 

fever. 

6.  Over  right  hypochondriac  region  in  hepatic  abscess. 

7.  Over  region  of  appendix  in  some  cases  of  appendicitis. 

8.  Over  one  posterior  lumbar  region  in  perinephritic  abscess. 

9.  Associated  with  subcutaneous  infection  in  any  part  of  the 

body. 

E.  Circumscribed  Multiple  (Edematous  Stvellings  {usually  acute,  dis- 
persed, and  more  or  less  transient). 

1.  Angioneurotic  oedema. 

2.  Purpuric  oedema. 

3.  Giant  urticaria. 


VENOUS  DISTENTION  :91 

VII.   CONDITION    OF  THE   VEINS 

Unusual  distention  or  overfilling  of  the  surface  veins,  and  perhaps 
of  the  jugular  veins,  may  be  observed.  Abnormal  venous  distention 
may  be  general  or  local,  and  is  frequently  preceded,  accompanied,  or 
followed  by  oedema  and  cyanosis.  CEdema,  if  marked,  may  hide  the 
overfilling  of  the  veins. 

The  diagnostic  indications  of  these  phenomena  are  as  follows : 

General  Venous  Distention. — Caused  by  all  conditions  which  hin- 
der the  return  flow  of  venous  blood  as  a  whole,  thus  embracing  many 
of  the  cardiac  and  pulmonary  lesions  which  are  responsible  for  the 
production  of  cyanosis  {q.  v.)  and  general  oedema  {q.  v.),  particularly 
when  the  right  ventricle  is  failing,  or  when  mitral  and  tricuspid  valv- 
ular defects  are  present.  Asthma  and  emphysema  lead  to  hyper- 
distention  by  interfering  with  the  pulmonary  circulation,  and  a  rare 
cause  is  pressure  upon  both  venae  cavae  by  mediastinal  growths.  It 
is  seen  acutely  in  the  paroxysms  of  pertussis,  and  in  general  convul- 
sions. 

Localized  Venous  Distention. — Any  condition  which  hinders  the 
return  flow  through  a  venous  trunk  of  appreciable  size  will  cause  a 
localized  overfilling  of  the  smaller  veins  which  drain  through  it,  as 
well  as  of  the  veins  which  communicate  with  it  and  its  branches,  and 
constitute  a  collateral  circulation.  The  significant  localized  disten- 
tions are  : 

1.  Of  jugular  veins  alone,  with  or  without  pulsation  :  pressure  by 

mediastinal  tumour  or  thoracic  aneurism. 

2.  Of  veins  of  one  arm  :  thrombosis  of,  or  pressure  on,  axillary 

vein. 

3.  Of  veins   of   one  leg:  thrombosis  of,  or  pressure  on,  femoral 

vein. 

4.  Of  veins  of  both  legs  :  thrombosis  of,  or  pressure  on,  femoral 

veins  or  inferior  vena  cava  by  abdominal  or  pelvic  tumours, 
by  ascites,  or  other  pressure-producing  disease. 

5.  Of  superficial  veins  of  skull  between  ear  and  vertex  :  thrombo- 

sis of  longitudinal  sinus. 

6.  Of  single  small  veins  over  sternum  :  mediastinal  tumour. 

7.  Of  superficial  abdominal  veins  (collateral  circulation) :  hepatic 

cirrhosis,  ascites,  enlarged  spleen,  or   other  abdominal  tu- 
mours or  thrombosis  causing  obstruction  to  the  portal  cir- 
culation. 
Venous  Pulsation  {q.  v.)  is  considered  elsewhere. 


92  THE  EVIDENCES  OF  DISEASE 

VIII.    EMPHYSEMA  OF  THE  SKIN 

This  consists  in  the  presence  of  air  or  gases  in  the  subcutaneous 
cellular  tissue.  At  first  glance  the  resulting  swelling  has  the  appear- 
ance of  oedema,  but  it  yields  lightly  and  readily  to  pressure,  and  does 
not  pit.  The  decisive  test  is  the  fine  crepitation  or  crackling  which 
is  perceived  by  the  palpating  finger,  resembling  that  produced  by 
pinching  an  inflated  normal  lung.  The  swelling  may  be  very  consid- 
erable, and,  like  oedema,  it  is  most  marked  where  the  subcutaneous 
cellular  tissue  is  most  abundant  and  loosely  attached.  It  is  espe- 
cially noticeable  when  occurring  over  the  neck  and  upper  part  of  the 
thorax,  owing  to  the  obliteration  of  the  normal  depressions.  It  is  an 
infrequent  finding,  and  when  it  occurs  is  usually  confined  to  certain 
localities,  but  very  rarely  may  be  diffused  over  the  greater  part  of 
the  body.  The  source  of  the  air  or  gas  is  either  from  without, 
through  a  wound ;  from  within,  by  rupture,  traumatic  or  otherwise, 
of  an  air  or  gas-containing  organ ;  or  from  cellular  tissue  infected 
by  gas-producing  micro-organisms. 

The  topographical  occurrence  of  subcutaneous  emphysema,  and 
the  particular  lesions  causing  it,  exclusive  of  infections,  are  as  follows : 

Face  and  Neck. — Wounds,  perhaps  of  insignificant  size,  of  the 
neck,  breast,  and  lower  part  of  the  face,  especially  those  involving 
the  mucous  membrane  of  the  mouth.  Perforation  or  rupture  of  the 
oesophagus  caused  by  traumatism,  ulceration,  or  cancer,  the  air  pass- 
ing to  the  external  surface  by  way  of  the  mediastinum. 

NecTc  and  Thorax. — Eupture  of  larynx  or  trachea  by  ulceration  or 
traumatism,  allowing  air  to  enter  the  tissues.  Cavities  in  an  adher- 
ent lung,  rupturing  into  the  substance  of  the  chest  walls,  and  subse- 
quent violent  cough  driving  air  into  the  tissues.  Eupture  of  air  cells 
from  greatly  increased  intrapulmonary  air  pressure  (caused  by  the 
taking  of  a  deep  inspiration  and  the  subsequent  voluntary  or  invol- 
untary closure  of  the  glottis)  which  occurs  in  heavy  lifting,  the 
expulsive  efforts  of  labour,  playing  upon  wind  instruments  (lips  tak- 
ing the  place  of  the  glottis),  crying,  shouting,  and  violent  cough, 
especially  in  pertussis.  If  pulmonary  emphysema  is  present,  it  pre- 
disposes to  this  accident.  From  the  ruptured  air  cells  the  air  passes 
under  the  visceral  pleura  or  through  the  interalveolar  tissue  into 
the  mediastinum  and  thence  to  the  connective  tissue  of  the  neck. 
Wounds  of  the  lung  tissue  or  axilla  and  supraclavicular  spaces. 

Abdomen. — From  stomach  or  intestines,  after  adhesions  to  the 
abdominal  walls  have  been  formed,  and  rupture  has  occurred,  due  to 
ulceration  or  traumatism.  If  also  septic  material  from  the  digestive 
tract  passes   into   the   skin,  there  may  be  diffuse   inflammatory  or 


SIGNIFICANCE  OP  JOINT  SYMPTOMS  95 

necrotic  processes  in  the  subcutaneous  tissues,  associated  with  the 
presence  of  gas-producing  organisms. 

Starting  from  any  point  of  entrance,  emphysema  may  spread  over 
wide  areas.  The  extent  of  its  diffusion  depends  either  upon  the 
aspiration  or  suction  force  of  the  tissues  into  which  the  air  is  solicited,, 
or  upon  the  degree  of  the  air  pressure  in  the  air-containing  viscua 
from  which  it  is  driven  into  the  areolar  spaces. 

IX.    CONDITION   OF  THE  JOINTS 

The  joints,  large  or  small,  may  present  deviations  from  the  nor- 
mal in  comparative  size,  shape,  colour,  position,  or  mobility. 

Examination  of  the  Joints. — One  should  observe  if  the  joint  is 
swollen,  distorted,  or  reddened,  and  note  also  the  position  (extended, 
partly  flexed)  in  which  it  is  preferably  kept  by  the  patient.  Try  pas- 
sive motion  to  determine  its  mobility,  and  the  presence  of  creaking 
or  grating  on  movement.  Palpate  the  joint  to  ascertain  whether  it. 
is  tender  or  hot ;  to  discover  irregularities  or  thickening  of  the  ends, 
of  the  bones  forming  the  joint  or  the  edges  of  their  articular  sur- 
faces ;  to  determine,  by  trying  for  fluctuation,  if  the  joint  contains, 
an  excess  of  fluid  ;  and,  by  finding  bogginess  or  firm  bulging  along 
the  line  of  the  joint,  whether  the  synovial  membrane  is  thickened.. 
Finally,  if  the  motion  of  the  joint  is  limited,  make  an  effort  to  decide 
whether  it  is  due  to  shortened  and  spastic  muscles  (contractures),  to- 
anchylosis  (fibrous  or  bony),  or  to  changes  in  the  bone  (exostoses  and 
outgrowths)  by  which  the  joint  is  locked. 

Significance  of  Joint  Symptoms. — In  a  certain  proportion  of  cases 
the  nature  and  associations  of  the  joint  lesions  can  be  readily  deter- 
mined ;  in  others  the  differential  diagnosis  is  extremely  difficult  and 
requires  a  most  careful  consideration  of  the  associated  signs  and 
symptoms,  as  well  as  of  the  character  of  the  local  articular  altera- 
tions.    The  latter  are  by  no  means  always  characteristic. 

Rheumatic  Fever. — First  one  joint  (usually  the  larger  first),  then 
another  becomes  swollen,  red,  and  tender.  Suddenness  of  onset, 
fever,  acid  sweats,  and  sudamina,  the  rapid  occurrence  of  anaemia, 
and  particularly  a  shifting  of  the  inflammation  from  one  joint  to- 
another  are  characteristic  of  this  disease. 

Chronic  Rheumatism. — The  joints  are  painful  (especially  in  the 
morning),  stiff,  and  perhaps  slightly  swollen,  not  often  deformed. 
Fever  is  rarely  present  and  the  disease  is  essentially  chronic. 

Gout. — The  paroxysm  begins  suddenly.  The  proximal  joint  of 
the  great  toe  is  first  and  most  commonly  attacked,  then  the  ankle,, 
knee,  and  small  joints  of  hand  and  wrist.  The  joint  is  excessively- 
painful  ;  the  skin  hot,  tense,  and  shining. 


^4  THE  EVIDENCES  OP   DISEASE 

Arthritis  Deformans. — In  young  persons  many  joints  are  involved, 
first  small,  then  large;  in  older  patients  one  or  two  large  joints 
only  may  be  affected.  The  joints  may  be  only  slightly  painful. 
Owing  to  the  changes  which  occur  in  the  bones  and  articular  car- 
tilages, the  joints  become  extremely  deformed  and  there  is  grating  or 
creaking  upon  movement.  This  disease,  above  all  others,  locks  the 
joints  in  a  more  or  less  fixed  position. 

Post-febrile  or  Secondary  and  Septic  Arthritis. — During  the  period 
of  convalescence  from  certain  of  the  specific  infections,  one  or  a 
number  of  joints  may  become  swollen,  tender,  and  contain  an  effu- 
sion which  may,  but  does  not  often,  proceed  to  suppuration.  These 
are :  Gonorrhcea^  followed  by  rheumatism  (so  called),  usually  mon- 
articular, affecting  only  one  of  the  larger  joints  and  lasting  for 
months  or  years ;  scarlet  fever,  pain  and  swelling  of  multiple  joints 
resembling  rheumatic  fever ;  cerebrospinal  meningitis,  which  is  fre- 
quently complicated  by  simultaneous  pain,  swelling,  and  effusion 
(serous  or  purulent)  of  many  joints ;  smallpox,  joint  swellings  dur- 
ing the  period  of  desquamation  ;  dengue,  attended  by  red,  swollen,  and 
painful  large  and  small  joints ;  pycemia,  in  which  one  or  more  joints 
may  become  inflamed,  with  rapid  suppuration  and  destruction  of  the 
joint;  typhoid  fever,  dysentery,  and  glanders.  Here  also  may  be 
mentioned  the  acute  arthritis  of  infants,  a  sudden  inflammation  of  a 
single  large  joint,  usually  the  hip  or  knee,  which  becomes  rapidly 
purulent ;  and  acute  osteomyelitis  (a  condition  which  is  liable  to  be 
mistaken  for  a  much  less  fatal  ailment),  in  which  there  are  boring 
pain,  swelling,  and  tenderness,  usually  of  one,  possibly  of  more  than 
one,  of  the  ends  or  epiphyses  of  the  bones  entering  into  the  formation 
of  the  larger  joints,  generally  in  the  lower  end  of  the  femur  or  in  the 
tibia,  and  attended  with  high  fever  and  serious  constitutional  dis- 
turbances. 

Diseases  of  the  Blood. — In  haemophilia  there  may  be  joint  symp- 
toms resembling  those  of  acute  rheumatism,  affecting  mainly  the 
larger  articulations ;  in  the  arthritic  forms  of  purpura  there  are 
multiple  joint  swellings ;  and  in  scurvy  there  may  be  actual  or  ap- 
parent arthritis. 

Diseases  of  the  Nervous  System. — The  association  of  chorea  with 
multiple  arthritis,  probably  indeed  with  rheumatic  fever,  is  well 
known ;  in  hysteria  one  of  the  joints  may  be  tender  and  rendered 
immovable  by  contracture,  giving  rise  in  some  instances  to  a  diffi- 
cult diagnostic  problem ;  and  there  may  be  multiple  arthritis  in 
acute  myelitis. 

In  locomotor  ataxia  and  syringomyelia  occur  the  curious  joint 
lesions  called  arthropathies.     One  or  more  joints,  usually  the  knee, 


THE  TEMPERATURE  OF  THE  BODY  95 

but  also  the  ankle  or  hip,  may  undergo  a  sudden,  perhaps  great 
swelling,  frequently  without  pain.  The  cartilages  and  bones  dis- 
integrate and  the  joint  may  be  thoroughly  disorganized  and  dislo- 
cated, the  resulting  changes  resembling  those  of  arthritis  deformans. 
The  joint  and  bone  changes  in  hypertrophic  pulmonary  osteo-arthrop- 
athy  may  also  be  classed  here. 

Miscellaneous  affections  are  :  simple  acute  synovitis  with  effusion 
(traumatic,  rheumatic),  most  commonly  involving  the  knee  joint; 
tuberculosis  of  the  joints ;  and  the  osseous  changes  in  rachitis. 


SECTION  XI 
THE  TEMPERATUKE  OF  THE  BODY 

1.  Method  of  Taking  the  Temperature. — Required  is  a  sea- 
soned clinical  thermometer,  with  an  error  of  not  more  than  ^  of  a 
degree.  Before  and  after  using,  it  should  be  washed  with  soap  and 
cold  water  and  an  occasional  cleansing  given  with  alcohol,  ether,  or 
chloroform.  In  case  of  contagious  disease  the  thermometer  should 
be  carefully  sterilized  by  soap  and  water,  alcohol,  and  an  hour's  soak- 
ing in  a  1 :  500  sublimate  solution.  It  is  much  better  to  have  a 
supply  on  hand,  so  that  one  may  be  left  with  each  contagious  case,  to 
be  destroyed  or  sterilized  at  the  termination  of  the  disease.  Each 
time  before  using,  the  mercury  column  should  be  shaken  down  to  95°, 
in  order  that  subnormal  temperatures  may  not  escape  detection.  The 
thermometer  may  be  placed  in  the  mouth,  axilla,  rectum,  vagina,  or 
the  fold  of  the  groin.  The  temperature  of  the  urine  is  sometimes 
tested  in  a  male  suspected  of  malingering. 

(a)  If  the  mouth  is  employed,  neither  a  very  hot  nor  a  very  cold 
di'ink  should  have  been  taken  for  half  an  hour  before.  The  ther- 
mometer should  then  be  slipped  under  the  tongue  to  one  side  and 
the  patient  cautioned  to  keep  the  lips  closed.  It  is  allowed  to  remain 
for  3,  and  if  accuracy  is  desired  for  5,  minutes.  The  special  1-minute 
thermometers  are  convenient,  but  very  easily  broken. 

{h)  If  the  patient  is  comatose,  dyspnoic,  can  not  breathe  through 
the  nose,  or  is  too  young  to  hold  the  thermometer  in  the  mouth,  the 
axilla  may  be  employed.  The  armpit  should  be  carefully  dried  and 
the  bulb  of  the  thermometer  placed  in  its  hollow.  The  arm  should 
then  be  brought  forward  over  the  chest,  the  elbow  touching  the 
thorax,  and  held  in  this  position  for  at  least  5,  and  if  accuracy  is 
desired  8,  minutes. 


96  THE  EVIDENCES  OF  DISEASE 

(c)  If  the  rectum  or  vagina  is  used,  the  thermometer  is  to  be 
oiled  and  introduced  to  the  depth  of  2  inches.  The  rectum  must  be 
empty  of  faeces.  The  temperature  may  be  taken  by  the  rectum  or 
vagina  in  unconscious  patients,  in  those  who  are  being  tubbed, 
in  all  cases  where  extreme  accuracy  is  required,  and  also  where 
there  is  doubt  as  to  a  recorded  reading  or  a  suspicion  of  malingering. 

(d)  The  fold  of  the  groin  may  be  utilized  in  infants  or  plump 
persons,  but  this  resort  is  rarely  necessary.  Very  seldom  is  it  requi- 
site to  take  the  temperature  of  the  urine.  If  done,  a  rapidly  acting 
thermometer  is  held  so  that  the  stream  of  urine  impinges  upon  it 
during  the  act  of  micturition. 

(e)  The  surface  temperature  is  taken  by  a  self-registering  ther- 
mometer, the  base  of  which  has  been  flattened  or  coiled  so  as  to 
present  a  relatively  large  surface  for  contact  with  the  skin.  It  may 
be  held  in  place  by  the  hand,  or  by  a  perforated  elastic  strap  encir- 
cling the  part.  It  is  better  to  use  two  instruments  simultaneously, 
one  applied  to  the  part  it  is  desired  to  test,  the  other  to  the  cor- 
responding part  of  the  opposite  side,  allowing  them  to  remain  at 
least  5  minutes. 

2.  Fkequency  of  Takixg  axd  Manner  of  Recording. — (a) 
Frequency. — In  ordinary  cases  the  temperature  should  be  taken  if 
possible  morning  and  night,  preferably  at  the  same  hour  each  day. 
In  hospital  practice  the  hours  usually  chosen  are  8  or  9  a.  m.,  and  5 
p.  M.  to  8  P.  M.,  varying  somewhat  in  different  institutions.  If  in 
private  cases  a  professional  nurse  is  not  on  duty,  it  is  frequently 
possible  to  instruct  an  intelligent  member  of  the  family  in  the  use 
of  the  thermometer,  or  to  leave  one  with  directions  to  place  it  in  the 
mouth  or  axilla,  and  in  due  time  to  lay  it  carefully  aside  to  be  read 
by  the  physician  at  his  next  call.  If  not  really  necessary,  it  is  advis- 
able to  take  the  temperature  seldom  or  not  at  all,  because  of  the 
exaggerated  importance  which  the  laity  attach  to  a  slight  rise  or  fall. 

In  continued  fevers,  as  in  typhoid,  the  temperature  should  be 
taken  every  4  hours.  If  it  is  a  disease  in  which  the  changes  of  tem- 
perature are  rapid  and  great,  as  in  pyaemia,  it  may  be  advisable  to 
take  it  hourly  or  every  2  or  3  hours.  If  a  chill  should  occur  in  any 
disease,  the  temperature  should  be  taken  during  its  continuance,  and 
again  1  hour  after  its  cessation,  as  otherwise  a  high  and  significant 
temperature  may  be  overlooked.  In  obscure  cases  (e.  g.,  hidden 
tuberculosis  or  suppuration)  the  temperature  should  be  taken  suffi- 
ciently often  during  the  24  hours  to  show  any  possible  variation  from 
the  normal. 

(J)  Records  of  the  Temperature. — In  all  febrile  cases  of  conse- 
quence the  temperature,  pulse,  and  respiration  should  be  noted  upon 


RECORDING  THE  TEMPERATURE 


97 


a  clinical  chart,  because  of  the  self-evident  advantages  of  the  graphic 
method  of  record.     Personally  I  find  the  chart  illustrated  in  Chart  I 


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Chart  I.— Abortive  pneumonia.  Dulness  and  broncho-vesicular  respiration  over  right 
lower  lobe  on  April  8th,  Upper  line,  temperature ;  middle  line,  pulse;  broken  line, 
respiratioiL 


98  THE  EVIDENCES  OP  DISEASE 

suitable  for  private  practice.  It  is  a  distinct  advantage  to  have 
spaces  for  the  date,  the  day  of  disease,  the  bowels,  and  the  urine. 
Xotes  of  certain  events  which  have  a  direct  bearing  upon  the  pulse, 
respiration,  and  temperature — e.  g.,  chill,  hemorrhage,  cold  bath,  or 
the  administration  of  digitalis — may  also  be  entered  upon  the  chart 
in  order  to  show  their  correlation  in  a  more  striking  manner. 

Chart  I  is  arranged  for  a.  m.  and  p.  m.  takings,  and  Chart  XX,  by 
erasing  the  headings  and  ruling  vertical  lines,  for  4-hourly  takings. 
Any  chart  thus  may  be  adapted  to  any  number  of  daily  takings 
which  may  be  required.  It  is  also  practicable,  and  will  avoid  the 
multiplication  of  charts,  to  place  readings  taken  between  the  regular 
times  as  nearly  as  possible  in  their  proper  time  spaces,  and  to  con- 
nect all  the  readings  by  lines  in  red  ink,  while  the  regular  a.  m. 
and  p.  M.  readings  alone  are  connected  by  lines  in  black  ink. 

3.  Normal  Temperatuees. — The  temperature  of  the  body  is 
registered  according  to  the  centigrade  scale,  or  by  that  of  Fahren- 
heit.    The  latter  is  used  in  this  book. 

To  convert  degrees  Fahrenheit  into  centigrade,  if  above  zero,, 
subtract  32,  multiply  by  5,  and  divide  by  9. 

To  convert  degrees  centigrade  into  Fahrenheit,  if  above  zero,, 
multiply  by  9,  divide  by  5,  and  add  33. 

It  is  seen  that  1°  C.  =::  1.8°  F.,  and  1°  F.  =  |°  C. 

The  following  table  by  Stuart  is  useful  for  reference : 

COMPARISON  OF  THERMOMETRIC  SCALES 


Centigrade 

Fahrenheit 

43° 

109.4° 

42° 

107.6° 

41° 

105.8° 

40° 

104° 

39° 

102.2° 

SS** 

100.4° 

Normal  temperature^  37° 

98.6°  Nortnal  temperature. 

36° 

96.8° 

35° 

95° 

34° 

93.2° 

The  normal  temperature  of  the  body  varies  within  narrow  limits. 
The  average  is  98.6°.  Any  temperature  from  97.2°  to  99.5°  may  be 
considered  to  be  within  proper  boundaries,  although  these  may  be 
exceeded  for  very  short  periods  under  certain  circumstances.  It  is 
modified  somewhat  by  a^e,  the  temperature  of  the  newborn  infant  rang- 
ing from  99°  to  99.7° ;  while  between  60  and  70  years  of  age  it  may  vary 


NORMAL  AND  ABNORMAL  TEMPERATURES        99 

from  99.7°  down  to  97°.  Violent  exercise,  especially  in  warm  weather, 
will  raise  it  to  a  slight  extent.  Mental  exertion  or  excitement  is  also 
competent  to  raise  the  temperature  to  a  moderate  degree  (100.4°). 
The  temperature  of  the  air  exercises  little  influence  on  the  tempera- 
ture of  the  human  body.     In  very  hot  weather  it  may  be  99.5°. 

The  most  important  normal  variation  is  that  which  occurs  diur- 
nally.  Under  ordinary  circumstances  the  temperature  is  highest 
between  5  p.  m.  and  8  p.  m.,  and  lowest  between  3  a.  m.  and  6  a.  m. 
The  diiference  between  the  highest  and  lowest  points  is  about  1.8°, 
although  exceptionally  it  may  amount  to  3.6°.  The  influence  of  this 
rhythmical  change  of  temperature  is  seen  in  many  fevers.  In  those 
who  work  by  night  and  sleep  by  day  this  type  is  reversed.  The  tem- 
perature may  rise  .4°  after  a  meal,  the  so-called  "fever  of  digestion." 
The  readings  of  the  thermometer  differ  somewhat  according  to  the 
cavities  in  which  it  is  placed.  It  is  to  be  remembered  that  the  mean 
temperature  of  the  blood  in  the  interior  of  the  body,  as  nearly  as  it 
can  be  ascertained,  is  102.2°. 

TABLE  OF  NORMAL  TEMPERATURES 


Mean  or  average. 


Fahr.       Cent. 

Normal  (thirty yeai-s  of  age) ,  98.6'    37" 

Infancy  to  six  years  of  age 99.4°    37.4^ 

Old  age  (sixty  to  eighty  years) 

Exercise  (severe,  in  warm  weather) . 

Mental  activity 

Diurnal  variation 


Minimum. 


98.2°     36.8° 


Fahr.      Cent. 


99° 
97° 


Maximum. 


Fahr.      Cent. 


98.6° 


36.2° 

99.5° 

37.5 

37.2° 

99.7° 

37.6 

36.1° 

99.7° 

37.6 

37° 

100.4° 

38° 

37° 

100.4° 

38° 

36.7° 

99.4° 

37.5 

Of  Cavities  or  Fluids 

Axilla 98.6°  (37°  C).  Mouth 98.6°  (37"  C). 

Urine 98.6°  (37°  C).  Rectum 100.4°  (38°  C). 

Vagina 100.9°  (38.3°  C). 

The  normal  surface  temperature  of  the  head  (Gray)  is,  for  the  left 
side,  an  average  of  93.8°  ;  for  the  right,  92.9°.  The  average  temper- 
ature of  the  thoracic  walls  is  96.8°  ;  of  the  abdominal  walls,  95.9°. 

4.  Abxormal  Temperatures. — Heat  production  {thermogenesis) 
depends  upon  the  destructive  metabolisms,  mainly  processes  of  oxi- 
dation, which  are  constantly  going  on  throughout  the  tissues  of  the 
body.  The  skeletal  muscles  and  the  glands,  especially  the  liver,  con- 
stitute the  chief  seats  of  heat  production. 

Heat  dissipation  {thermolysis)  takes  place  mainly  through  the 
expired  air,  and  by  conduction,  radiation,  and  evaporation  from  the 
skin.     As  from  77  to  85  per  cent,  of  the  total  heat  loss  passes  oft 


100  THE   EVIDENCES  OF   DISEASE 

from  the  cutaneous  surface,  the  skin  must  be  considered  as  the  prin- 
cipal factor  in  heat  dissipation. 

As  the  normal  temperature  of  the  body  varies  within  such  narrow 
limits,  there  must  be  some  means  of  regulating  the  relative  amounts 
of  heat  production  and  heat  dissipation,  in  order  that  they  may 
balance  each  other  with  exactness,  and  under  widely  differing  cir- 
cumstances. It  is  quite  certain  that  a  heat-regulating  {thermotaxic) 
mechanism  exists  as  a  part  of  the  nervous  system,  although  the 
mode  of  operation  and  location  of  the  heat  centres,  and  the  nerve 
paths  through  which  the  work  is  accomplished,  are  as  yet  uncer- 
tain, experimental  work  upon  this  point  not  having  given  decisive 
results. 

The  abnormal  temperatures  are  those  which  are  over-normal,  {A) 
fever ;  and  under-normal,  (B)  subnormal  temperature. 

{A)  FEVER 

A  condition  indicated  by  a  marked  and  more  than  transient  rise 
of  temperature  implies  a  disturbance  of  the  normal  relation  between 
heat  production  and.  heat  dissipation,  from  causes  acting  upon  one 
or  the  other,  or  upon  the  heat-regulating  mechanism.  Heat  produc- 
tion in  fever  is  largely  increased,  because  of  the  more  rapid  destruc- 
tive processes  which  take  place  in  the  body,  as  evidenced  by  the 
larger  amounts  of  urea  and  carbon  dioxide  which  are  excreted,  and 
the  larger  quantity  of  oxygen  which  is  consumed.  But  increased 
formation  of  heat  alone  is  not  sufficient  to  account  for  the  rise  of 
temperature,  as  a  corresponding  increase  in  the  heat  loss  can  readily 
dispose  of  a  large  excess.  It  is  therefore  necessary  to  assume  a  dis- 
turbance of  the  thermotaxic  mechanism,  and  this  perturbation  of 
heat  regulation  is  perhaps  the  most  characteristic  element  in  the 
production  of  fever  heat.  Fever  is  a  complex  process  or  condition 
of  which  the  presence  of  an  elevated  temperature  is  the  most  signifi- 
cant and  practical  indication. 

Clinically  all  cases  of  fever  are  attended  by  certain  symptoms  in 
common,  due  partly  to  increased  tissue  changes,  partly  to  the  in- 
creased heat  of  the  body,  and  partly  to  functional  disturbances  of 
certain  organs.  Besides  the  abnormal  rise  of  temperature,  these 
symptoms  are :  ill  feeling,  or  malaise ;  sleeplessness ;  thirst ;  loss  of 
appetite ;  mental  disturbance,  amounting  possibly  to  delirium ;  in- 
creased frequency  of  pulse  and  respiration ;  lessened  amount  of  urine, 
with  increase  in  urinary  solids,  especially  urea ;  usually  headache 
and  backache ;  and,  if  the  fever  is  long-continued,  general  wasting 
of  the  body.  There  is  also  apt  to  be  constipation,  and  a  chill  may 
initiate  or  accompany  a  sudden  rise  of  temperature. 


FEVER  101 

The  symptoms  accompanying  fever  exhibit  considerable  variations 
in  severity  according  to  the  character  and  cause  of  the  disease,  and 
the  duration  and  height  of  the  pathological  temperature.  There  is 
also  a  diiference  in  the  staying  power  of  individuals,  more  easily 
recognised  than  explained,  which  with  equal  temperatures  and  appar- 
ently similar  causes  will  allow  one  to  continue  about  his  daily  work 
with  slight  subjective  symptoms  and  send  another  to  bed  in  a  con- 
dition of  extreme  weakness  and  discomfort.  The  malaise  may  be 
slight  or  marked.  Thirst  and  dryness  of  the  mouth,  together  with 
anorexia,  epigastric  discomfort  on  taking  food,  and  constipation,  are 
due  to  the  partial  or  almost  entire  suppression  of  the  secretion  of 
the  salivary,  gastric,  pancreatic,  and  intestinal  fluids.  Indeed,  the 
total  fluids  of  the  body  are  diminished  in  quantity,  the  urine  is 
scanty  and  high  coloured,  and  the  solid  tissues  waste  away  because 
of  the  great  activity  of  retrograde  metamorphosis.  The  pulse,  as  a 
rule,  is  abnormally  frequent,  rising  10  beats  for  each  degree  of  fever  ; 
but  there  are  some  exceptions.  Typhoid  fever,  meningitis,  and  pneu- 
monia may  present  a  high  temperature,  and  yet  the  pulse  be  but 
slightly  accelerated ;  while  in  scarlet  fever,  diphtheria,  and  perito- 
nitis, the  pulse  may  be  very  rapid  in  proportion  to  the  fever.  '  The 
respiration  follows  a  similar  rule,  increasing  2  per  minute  to  each 
degree  of  fever,  and  also  has  its  exceptions.  The  variations  in  pulse 
and  respiration  are  doubtless  due  either  to  the  effect  of  overheated 
blood  or  to  the  action  of  toxines  upon  the  centres  in  the  medulla.  A 
third  factor  which  may  cause  an  unduly  rapid  pulse  rate  is  the  de- 
generation of  the  cardiac  muscle  which  in  some  cases  occurs  toward 
the  close  of  a  long-continued  fever.  Backache,  headache,  and  aching 
of  the  limbs  are  nearly  always  present,  but  there  is  considerable  varia- 
tion in  their  severity.  As  a  rule,  they  are  most  marked  at  the  begin- 
ning, and,  as  in  some  of  the  acute  infectious  diseases,  may  possess 
distinct  diagnostic  value  because  of  their  prominence  as  symptoms. 
The  headache  of  typhoid  fever  and  the  backache  of  variola  are  exam- 
ples. The  mental  disturbances  of  fever  may  be  manifested  by  an 
increased  activity  of  the  mind,  passing  into  active  delirium ;  or  by 
mental  torpor,  deepening  into  a  low  muttering  delirium.  The  degree 
or  character  of  the  delirium  or  mental  disturbance  does  not  appear 
to  depend  upon  the  height  of  the  temperature,  but  rather  upon  the 
nature  and  amount  of  the  toxines  circulating  in  the  blood  and  their 
effect  upon  the  nervous  system.  Personal  idiosyncrasy  and  age 
modify  the  liability  to  the  occurrence  of  delirium.  Children,  when 
suffering  from  fever,  are  especially  prone  to  it,  and  some  adults  re- 
semble children  in  this  respect.  Fever  temperatures  are  classified 
according  to  (1)  height  and  (2)  type. 
9 


102 


THE  EVIDENCES  OF  DISEASE 


(1)  Terminology  of  Fever  according  to  Height. — This  is  shown  in 
the  following  table,  somewhat  modified  from  those  of  Wunderlich 
and  Finlayson.  The  figures  of  the  two  scales  in  this  table  do  not 
exactly  correspond,  except  for  those  of  normal  temperature  : 


Noi'mal  temperature 

Subfebrile  temperature 

Slight  fever 

Moderate  fever ]  Eve^inf: .' 

High  fever ]  Kveninf  ' 

Hyperpyrexia,  above 


Centigrade. 


36.2° 
37.5° 
37.5" 

38= 

38^ 

38.5" 

38. 5« 

39.5° 

39.5° 

40.5° 

4V 


Some  astonishingly  high  temperatures  have  been  reported,  so 
high  that  it  taxes  credulity  to  receive  them  as  acknowledged  facts.  A 
temperature  of  122°  is  within  the  bounds  of  belief,  but  temperatures 
of  151°  and  228°,  the  latter  16  degrees  over  the  boiling  point  of 
water,  must,  in  spite  of  the  care  taken  in  the  observations  and  the 
excellent  repute  of  the  observers,  be  classified  with  the  tricks  of  the 
prestidigitateur,  as  impossibilities  apparently  accomplished  by  means 
unknown  to  the  observer. 

In  almost  all  forms  of  fevers  the  temperature  is  apt  to  be  lower 
in  the  morning,  the  remission,  and  higher  in  the  evening,  the  exacer- 
bation. In  exceptional  cases  the  morning  temperature  is  higher 
than  that  of  the  evening.  It  is  spoken  of  as  inversion,  or  the  inverse 
type  of  fever. 

(2)  Terminology  of  Fever  with  Respect  to  its  Type. — This  depends 
upon  its  duration  and  the  amount  of  difference  between  the  highest 
and  lowest  daily  readings  of  the  thermometer,  as  follows : 

1.  Continued  Fever,  in  which  the  temperatures  are  usually  high, 
and  the  daily  differences  do  not  exceed  2°  (see  Chart  II,  A). 

2.  Remittent  Fever,  in  which  the  daily  difference  exceeds  2°,  but 
the  minimum  temperature  is  above  the  normal  limit  (Chart  II,  B). 

3.  Intermittent  Fever,  in  which  at  least  once  in  the  24  hours 
the  maximum  is  very  high,  and  the  lowest  temperature  is  normal  or 
subnormal  (Charts  II,  C  and  III,  A). 

The  terms  intermittent  and  remittent  have  by  custom  acquired 
a  special  meaning,  as  indicating  certain  forms  of  malarial  fever.  In 
this  connection  reference  is  had  to  the  type  and  not  to  the  cause  of 
fever,  which  is  said  to  be  quotidian  when  the  rise  and  subsequent 
fall  to  normal  occurs  once  every  day ;  tertian,  when  it  occurs  every 


FEVER— HEIGHT,   TYPE.   CHARACTER 


103 


other  day,  having  one  day  free  from  fever  in  between ;  and  quartan^ 
when  two  days  of  freedom  from  fever  elapse. 

If  two  paroxysms,  or  rises  and  falls,  occur  in  one  day,  they  are 
spoken  of,  according  to  the  interval  of  apyrexia,  or  freedom  from 


Chart  II.— Types  of  fever.     Continued,  remittent,  and  the  quotidian  and  tertian  types  of 

intermittent. 


fever,  as  double  quotidian,  double  tertian,  or  double  quartan.  A  bet- 
ter knowledge  of  the  life  history  {q.  v.)  of  the  Hmmatozoon  malarim 
(Laveran)  has  modified  somewhat  the  original  meaning  of  these  terms. 


Chart  III. — Types  of  fever.     Intermittent,  quartan  type  ;  also  hectic  and  suppurative  fever. 

4.  Recurring  fever,  a  return  or  recrudescence  of  a  febrile  move- 
ment after  several  days  of  apyrexia. 

5.  Irregular  fever,  in  which  the  temperatures  are  very  irregular — 
sometimes  high,  sometimes  low.  There  is  no  regular  daily  differ- 
ence, and  the  highest  or  lowest  point  may  be  reached  at  any  hour  of 
the  twenty-four.     It  is  essentially  atypical. 


104  THE   EVIDENCES  OF   DISEASE 

It  is  necessary  to  bear  in  mind  that  any  one  of  these  types  may 
resolve  itself  into  any  other  one,  according  to  the  nature,  cause,  or 
complications  of  the  disease  which  it  accompanies.  A  remittent  may 
be  merged  into  the  continued  type,  and  the  continued  type  terminate 
as  an  intermittent.  Nevertheless,  certain  diseases  are  characterized 
by  certain  types  of  fever  with  sufficient  frequency  to  give  the  recog- 
nition of  the  type  a  distinct  and  sometimes  great  diagnostic  value, 
and  the  absence  of  the  type  may  be  an  important  negative  symptom. 

(3)  Manner  of  Invasion,  Course,  and  Termination  of  Fever. — The 
invasion  or  beginning  of  fever  may  be  {n)  sudden  or  (b)  gradual. 

(ff)  Sudden  Invasion. — The  temperature  rises  to  as  high  a  point 
in  the  first  2  or  3  hours  as  it  subsequently  attains  during  the  course 
of  the  disease.  A  rapid  rise  to  a  considerable  height  is  attended  by 
chill,  coldness,  chattering  teeth,  and  a  more  or  less  violent  shaking 
of  the  body.  The  surface  is  pale,  the  skin  cool  and  shrunken,  the 
lips  and  finger  nails  are  blue.  If  the  thermometer  be  placed  in  the 
mouth  or  rectum,  it  may  indicate  a  high  degree  of  fever,  the  coldness 
of  the  surface  being  due  to  the  contraction  of  the  peripheral  arteri- 
oles, which  prevents  the  heated  blood  of  the  interior  from  coming  to 
the  surface.  As  the  contraction  relaxes  the  chill  ends,  and  the  skin 
becomes  abnormally  hot  by  the  restoration  of  the  cutaneous  circu- 
lation. 

{b)  Sloiv  Invasion. — On  the  other  hand,  the  invasion  may  be  slow 
and  gradual,  the  febrile  movement  requiring  several  days  to  reach  its 
ultimate  height.  There  may  be  chilliness,  but  the  decided  rigour  of 
the  rapid  rise  is  absent. 

The  termination  or  defervescence  of  fever  also  may  be  («)  sudden 
or  {b)  gradual. 

(«)  If  the  fever  ends  by  a  sudden  drop  of  the  temperature  to  or 
below  the  normal,  the  termination  is  by  crisis,  and  is  usually  accom- 
panied by  profuse  sweating  and  an  increased  flow  of  urine. 

(Z»)  If  the  decline  of  the  fever  is  slow  and  gradual,  several  days 
elapsing  before  the  temperature  reaches  normal,  the  termination  is 
by  lysis. 

Course. — Certain  fevers,  usually  continued  or  remittent,  possibly 
recurrent  in  type,  pursue  a  sufficiently  definite  general  course  to  per- 
mit a  division  of  the  fever  into  three  periods.  The  first  period,  called 
variously  the  initial  .stage,  initial  period,  stadium  incrementi,  is  that 
during  which  the  temperature  is  rising,  rapidly  or  slowly.  The 
second  or  middle  period,  the  acme,  fastiginm,  stadium  fastigii,  is 
characterized  by  a  high  and  continuous  temperature  with  but  slight 
daily  differences  between  the  maximum  and  minimum.  The  tliird 
and  final  period,  during  which  the  temperature  is  descending  rapidly 


DIAGNOSTIC  SIGNIFICANCE   OF   FEVER  105 

or  slowly  to  the  normal,  is  termed  the  defer veace nee  or  stadium  decre- 
menti.  It  is  obvious  that  of  the  terms  applied  to  the  middle  period 
one  only,  acme,  is  appropriate  to  the  intermittent  type  of  fever, 
because  of  the  usually  brief  duration  of  the  latter. 

Pathological  temperatures  include,  besides  febrile  disturbances, 
subnormal  temperatures.  A  temperature  below  97.2°  is  subnormal, 
and  95°  is  the  temperature  of  collapse.  The  lowest  reported  record 
is  71.8°. 

(4)  Diagnostic  Indications  from  the  Temperature.— Changes  in  the 
temperature  are  much  more  easily  produced  when  it  is  already  abnor- 
mal. Consequently,  if  fever  exists,  agencies  which  in  health  would 
cause  little  or  no  alteration  in  the  temperature  will  give  rise  to 
marked  oscillations  in  the  fever  curve.  Indeed,  without  appreci- 
able cause  it  rarely  remains  stationary,  but  varies  to  a  greater  or 
less  extent  every  hour  and  every  day.  If  hourly  observations  are 
made  for  24  hours  in  almost  any  case  of  pyrexia  many  irregularities 
will  be  revealed  which  can  not  be  explained  by  past  events  or  future 
developments.  Nevertheless,  an  attempt  should  always  be  made  to 
ascertain  the  cause  of  any  decided  or  unexpected  variation,  as  such 
changes  may  possess  an  important  diagnostic  or  prognostic  value. 

Putting  aside  for  the  present  the  variations  due  to  disease,  it  is 
well  to  remember  that  an  increase  in  the  fever  may  be  due  to  mental 
excitement,  pain,  an  excessive  amount  of  clothing,  an  overheated 
room,  and  the  ingestion  of  food.  On  the  other  hand,  an  unusually 
cool  room,  cold  sponging,  and  the  cold  tub  are  fever-reducing  agents. 
If  a  slow  loss  of  blood  occurs,  as  when  menstruation  takes  place  dur- 
ing fever,  the  temperature  is  lowered  to  some  extent,  and  a  large, 
sudden  hemorrhage  may  cause  a  drop  even  below  the  normal. 

Causes  of  Fever. — The  ascertained  presence  of  fever  is  capable  of 
a  wide  range  of  interpretation,  because  of  the  large  number  of  condi- 
tions and  diseases  of  which  it  is  a  symptom  or  concomitant.  Its  exist- 
ence requires  a  careful  search  for  its  cause,  and  one  should  not  rest 
contented  until  he  has  found  a  satisfactory  explanation  of  its  pres- 
ence or  has  exhausted  his  diagnostic  resources.  In  general,  fever  is 
caused  by  or  attends  : 

(a)  All  inflammations.,  acute  or  subacute,  the  great  majority  of 
which  are  recognised  as  being  dependent  upon  the  presence  of 
pyogenic  micro-organisms  in  the  inflamed  area,  whence  toxic  material 
enters  the  general  circulation. 

(Z»)  All  infectious  diseases  due  to  specific  micro-organisms  and 
their  products,  whether  attended  or  not  by  local  inflammatory  lesions. 

(c)  Certain  toxmmias  resulting  from  the  ingestion  of  poisonous 
material,  or  absorption  of  putrefactive  products  from  the  digestive 


106 


THE  EVIDENCES  OF   DISEASE 


tube,  or  the  formation  of  toxic  material  in  the  glands  or  tissues  of 
the  body. 

(fZ)  Some  non-toxic  diseases  or  conditions  of  the  nervous  sy stein 
in  which  the  normal  working  of  the  heat-regulating  mechanism  is 
interfered  with  by  direct  or  reflex  causes. 

Diagnostic  Classification  of  Fever. — It  is  obvious  that  an  attempt 
to  catalogue  the  special  diseases  or  conditions  attended  by  pyrexia  is 
impracticable,  but  clinically  one  may  classify  fever  according  to  the 
diagnostic  indications  of  its  manner  of  invasion  and  termination,  its 
course,  type,  and  variations  as  follows : 

(a)  Sudden  Invasion. — A  rapid  rise  to  a  high  point  (Chart  IV 
characterizes  erysipelas,  gastro-intestinal  disease  in  children,  mid- 
dle-ear or  mastoid  inflammation,  malaria,  osteo-myelitis,  pneumo- 
nia, scarlet  fever,  tonsilitis  (lacunar),  and  all  conditions  in  which 
large  quantities  of  fever-producing  ptomaines  rapidly  enter  the  cir- 


AV 

Pfc 

Ahiph 

AA^Pt 

AN 

Pt 

n 

PH 

AMPM 

SUDDEN    INVASION-NO.   1 

Temperature    continuing    high.      Rise 
frequently    accompanied    by   a   chill    in 
adults,  and  occasionally  by  a  convulsion 
in  children. 

Erysipelas. 

GaSTRO-INTESTINAL  DISEASES  IN  CHILDREN. 

Middle-ear  or  mastoid  inflammation. 

Osteomyelitis. 

Pneumonia  (lobar). 

Scarlet  fever. 

Tonsilitis 

s 

1 

to 
g 

1 

105 
104 
103 

tod 

101 

100 

9d 

98 

> 

/ 

S/ 

r 

i 

r 

\j 

/ 

■" 

V 

3 

5 

1 

1 

1  _ 

1 

Chart  IV. — -Diagrnostic  indications  to  be  derived  from  a  sudden  inva.^ion  of  fever.     No.  1. 


culation.  There  is  apt  to  be  a  chill  in  the  adult,  and  in  children 
perhaps  a  convulsion.  The  initial  outbreak  of  fever  occurring  in  the 
diseases  classified  later  under  the  intermittent  type  might  also  be 
included  here. 

(b)  Gradual  Invasion. — A  gradual  rise  of  temperature  (Chart 
Y)  attends  the  great  majority  of  febrile  diseases,  except  as  men- 
tioned in  the  previous  paragraph.  Typlioid  fever  is  the  typical 
fever  of  slow  invasion,  requiring  a  week  or  more  to  reach  the  height 
it  will  ultimately  attain. 

(c)  Crisis. — The  fevers  which  terminate  by  a  sudden  fall  of  tem- 


DIAGNOSTIC  SIGNIFICANCE   OP  FEVER 


107 


perature  (Cliart  VIII)  to  or  below  the  normal  point  are  erysipelas, 
measles,  lobar  pneumonia,  relapsing  fever,  and  typhus  fever.  The 
crisis  or  rapid  defervescence  is   usually  accompanied  by  sweating. 


Chart  V. — Diagnostic  significance  of  a  gradual  rise  of  temperature. 


increased  flow  of  urine,  and  improvement  in  the  pulse  rate  and 
respiration.  Occasionally  a  "  pseudo-crisis  "  occurs  from  1  to  3  days 
before  the  true  crisis,  the  temperature  falling  rapidly  toward  the 


Chart  VI. — Diagnostic  significance  of  a  gradual  termination  of  fever. 

normal  point,  but  soon  rising  to  or  above  the  previous  average.     It 
is  especially  liable  to  be  seen  in  pneumonia.     The  diagnostic  import 


108 


THE  EVIDENCES  OP  DISEASE 


of  other  sudden  falls  of  temperature  will  be  considered  in  the  subse- 
quent paragraph  on  the  continued  type  of  fever. 

(d)  Lysis. — A  slow  defervescence  or  subsidence  of  the  elevated 
temperature  is  encountered  in  the  majority  of  febrile  diseases  (Chart 
VI).  It  is  not  infrequently  the  case  that  pyrexial  illnesses  which 
customarily  end  by  crisis  may,  by  reason  of  complications  or  other 


SUDDEN    INVASION-NO.   2 

With  chill  or  convulsion.  Temperature 
rapidly  falling.  frequently  with  sweats, 
and  either  remaining  normal  (dotted  line) 
or  recurring  at  regular  or  irregular  in- 
TERVALS. 

Hepatic  disease  (obstructive,  suppurative, 
cirrhotic,  or  carcinomatous), 
hodgkins'  disease. 

Malarial  intermittent  (quotidian,  tertian). 
Morphine  habit  (exceptionally). 
Py/emia  (times  of  rise  irregular). 
Suppuration. 
Syphilis  (exceptionally). 
Tuberculosis. 
Ulcerative  endocarditis. 


Chart  VII. — Uiasnostie  indications  to  be  derived  from  a  sudden  invasion  of  fever.     No.  2. 


disturbing  causes,  terminate  by  lysis.  The  diseases  which  invariably 
and  characteristically  end  by  lysis  are  acute  rheumatism,  broncho- 
pneumonia, pleurisy,  and  typhoid  fever. 

(e)  Bitermittent  Fever. — A  sudden  rise,  brief  duration,  and  sudden 
fall,  the  latter  usually  with  free  sweating,  occurring  one  or  more  times 
in  24  hours,  creates  a  suspicion  of  hepatic  disease,  Hodgkin's  disease, 
malaria,  morphine  habit  (exceptionally),  pyaemia  (time  of  maximum 
temperature  very  irregular),  suppuration,  syphilis,  tuberculosis,  or 
ulcerative  endocarditis  (Chart  VII). 

The  intermittent  fever  of  suppuration  and  tuberculosis  may  have 
regularly  a  normal  morning  temperature  with  an  evening  exacerba- 
tion. If  the  minimum  temperature  in  any  of  these  diseases  remains 
above  the  normal  the  fever  becomes  of  the — 

(/)  Remittent  Type. — The  remittent  type  may  be  present  at  some 
period  during  the  course  of  any  disease  which  is  attended  by  fever. 
Almost  all  fevers  exhibit  morning  remissions.  A  remittent  type  of 
fever  (Chart  II)  is  especially  characteristic  of  tuberculosis  and  sup- 


DIAGNOSTIC  SIGNIFICANCE  OP   FEVER 


10^ 


puration  {hectic  fever,  q.  v.).  The  remittent  may  become  intermit- 
tent, or  the  intermittent  change  into  the  remittent.  If  the  daily 
difference  between  the  highest  and  lowest  temperatures  of  the  latter 
becomes  less  than  2°  it  changes  its  form  to  the — 

{g)  Continued  Type. — Continued  fever  exists  in  erysipelas,  acute 
pneumonia,  acute  tuberculosis,  typhoid,  and  typhus  fevers.  It  is 
especially  characteristic  of  typhoid  fever  and  pneumonia.  Sudden 
changes  of  the  temperature  during  the  course  of  a  continued  fever 
are  usually  indicative  of  complications.  If  the  change  consists  of  a 
sudden  rise,  it  points  toward  a  beginning  inflammation  or  an  exten- 
sion of  the  already  present  local  lesions.  If  there  is  a  sudden  drop 
to  or  below  the  normal  line  (Chart  VIII),  it  may  betoken  collapse, 
impending  death,  perforation  of  the  bowels,  or  an  internal  hemor- 
rhage— the  last  two  in  typhoid  fever.  It  is  necessary  to  discriminate 
the  sudden  drop  which  indicates  the  crisis  in  diseases  which  may 
terminate  in  this  manner  from  the  drop  of  collapse  or  hemorrhage. 
This  may  be  done  by  noting  the  accompanying  pulse  and  respira- 


A^ 

m 

AMP» 

AM  PI 

Atfp» 

At 

p» 

Ah 

f\i 

i\ 

PM 

p  RAPID   FALL,  without   improvement   in 
j     pulse  and  respiration,  and  followed  by 
;     a  steady  rise,  abdominal  pain,  or  bloody 
•    stools,  will,  in  typhoid  fever,  indicate    ' 
Perforation  or  H/emorrhage. 

[♦RAPID   FALL,  without   improvement   in  i 

PULSE    AND    respiration,    AND    WITHOUT   A 

subsequent  rise,  may  indicate 
Collapse, 
impending  death. 

-^crisis,  rapid   fall.  with   sweating,   in- 
creased amount  of  urine,  and  coinci- 
dent improvement  in  pulse  and  respira- 
tion, occurs  in 
erysipelas. 
Measles. 
J           Pneumonia  (lobar). 
Relapsing  fever. 
Typhus  fever. 

- 

"S 

1 

'«> 
2 

1 

105 
104 
103 
102 
101 
100 
99 
98 

/ 

/ 

i 

/ 

S/ 

/ 

f 
1 

1 
1 

\ 

f 

Si 

\ 

1 

\ 

r 

i 

1 

i 

f 

% 
1 

i 

1 

1/ 

Ni 

^ 

.  i 

y 

\ 

97 

Chart  Vlll.— Diagnostic  indications  to  be  derived  from  a  sudden  fall  of  temperature. 

tion  and  the  general  condition  of  the  patient,  all  of  which  in  crisis 
will  show  a  distinct  alteration  for  the  better,  thus  forming  a  strik- 
ing contrast  to  the  change  for  the  worse  which  may  be  seen  in 
collapse. 

If  the  elevated  temperature  in   continued  fever  is   maintained 


110  THE  EVIDENCES  OF  DISEASE 

beyond  the  usual  duration  of  the  disease  which  it  attends,  search 
should  be  made  for  complications  or  for  persistent  local  lesions.  In 
some  cases,  especially  typhoid  fever,  an  undue  continuance  of  fever 
may  be  found  to  be  due  to  inanition,  the  "fever  of  starvation." 

(h)  Inversion  of  the  Continued  Type. — High  morning  and  low 
evening  temperatures  may  occur,  although  seldom,  in  pneumonia, 
tuberculosis,  typhoid  fever,  and  dentition.  This  type  is  not  neces- 
sarily of  bad  prognostic  import. 

(i)  Recurring  Type. — A  return  or  recrudescence  of  a  fever  which 
has  ceased  may  be  caused  by  a  relapse  of  the  previous  disease,  the 
onset  of  a  new  malady,  or  the  beginning  of  a  late  complication  of 
the  original  disease.  Eelapsing  fever  {q.  v.)  is  the  typical  recurring 
fever. 

{k)  Irregular  Fever. — The  principal  diagnostic  importance  of  an 
ii-regular  fever  is  of  a  negative  character,  its  presence  militating 
against  the  existence  of  any  febrile  disease  which  has  a  characteristic 
temperature  curve,  such  as  typhoid  fever  or  lobar  pneumonia. 

(/)  Solitary  Observation. — Single  observations  of  the  temperature 
may  possess  some  diagnostic  value — e.  g.,  the  single  chill  during 
and  after  which  the  temperature  rises  to  about  104°.  When  this 
occurs  one  may  apprehend  in  advance  malaria,  pneumonia,  puer- 
peral fever,  pyaemia,  scarlet  fever,  suppuration,  or  other  febrile 
diseases  characterized  by  a  sudden  invasion.  A  single  high  morn- 
ing temperature  should  create  a  suspicion  of  an  acute  infectious 
disease. 

(m)  Hyperpyrexia. — A  rise  of  temperature  to  an  unusual  height, 
107°  to  110°,  may  happen  in  connection  with  acute  rheumatism, 
injury  to  the  cervical  portion  of  the  spinal  cord,  malarial  intermit- 
tent or  remittent  fever,  scarlet  fever,  sunstroke,  tetanus  shortly 
before  death,  typhoid  fever,  and  yellow  fever.  It  occurs  very  rarely 
in  erysipelas,  hysteria,  pneumonia,  and  relapsing  fever.  It  may  also 
result  from  trickery  by  the  use  of  friction,  pressure,  hot-water  bags, 
or  poultices. 

Temperatures  over  106°  are  usually  of  unfavourable  prognostic 
import,  but  the  degree  of  danger  varies  according  to  the  nature  of 
the  disease  and  the  duration  of  the  hyperpyrexia.  Single  brief  high 
temperatures  may  be  well  borne  if  an  interval  of  apexia  intervenes,  as 
in  malarial  intermittents ;  but  persistent  high  temperatures  in  a  long- 
continued  disease,  such  as  typhoid  fever,  are  of  evil  omen. 

{n)  Localized  Rise  of  Temperature,  except  in  surgical  diseases,  is 
not  of  great  diagnostic  importance.  The  local  heat  of  the  surface  is 
increased  over  a  pneumonic  lung,  and  there  may  be  a  rise  of  tem- 
perature in  areas  affected  by  vasomotor  paralysis.    Cerebral  thermom- 


CHILLS  111 

etry  occasionally  affords  some  assistance  in  obscure  cases  of  brain 
tumour,  but  the  abnormal  elevation  must  amount  to  at  least  3°. 

(o)  Subnormal  Temperatures. — The  diagnostic  import  of  rapidly 
occurring  falls  of  the  temperature  of  the  body  as  a  whole  to  a  point 
below  the  normal  have  been  considered  in  connection  with  fever. 
Persistent  subnormal  temperature  may  be  present  in  connection  with 
convalescence  from  fevers,  in  acute  alcoholism,  melancholia,  myxoe- 
dema,  starvation  (sometimes  elevated),  wasting  diseases,  and  in  poi- 
soning from  carbolic  acid  or  other  intoxicant.  Locally,  abnormal 
coldness  of  an  edematous  or  cyanosed  part  may  be  observed. 

CHILLS 

A  true  chill  is  always  associated  with  a  more  or  less  elevated  tem- 
perature, although  the  surface  of  the  body  is  cold  and  pale.  The 
bulk  of  the  blood  is  retained  in  the  interior  zones,  and  as  a  result  the 
larger  viscera  are  more  or  less  engorged.  The  teeth  chatter,  the  lips 
and  nails  are  cyanotic  from  the  impeded  circulation,  and  the  skeletal 
muscles  rapidly  contract  and  relax.  There  are  all  degrees  of  chill, 
from  the  "  creepiness,"  which  is  so  often  made  the  subject  of  com- 
plaint, through  decided  chilliness,  up  to  a  hard  chill  or  rigour,  which 
may  be  so  severe  as  to  be  associated  with  danger  to  life  in  the  ma- 
lignant forms  of  malarial  septicaemia. 

True  chill  must  be  discriminated  from  the  so-called  "nervous 
chill,"  which  is  seen  upon  occasions  of  excitement  in  individuals 
with  a  susceptible  and  easily  disturbed  nervous  system.  In  the 
latter,  while  the  chattering  of  the  teeth  and  shaking  of  the  body 
may  be  as  marked  as  in  the  true  chill,  the  colour  and  temperature  of 
the  surface  remain  normal,  while  the  thermometer  demonstrates  the 
absence  of  fever.  As  a  result  of  hysteria,  neurasthenia,  or  depressed 
conditions  in  general,  there  may  be  sensations  of  chilliness  or  cold- 
ness, without  shaking  and  without  fever.  The  shivering  which  may 
attend  the  dilatation  of  the  cervix  during  labour  and  the  relaxa- 
tion of  the  sphincter  vesicae  and  sphincter  ani  during  urination  and 
defecation  is  well  known,  as  are  the  chills  attending  the  passage  of 
a  renal  calculus  or  a  gallstone. 

Almost  all  pyrexial  diseases,  whether  of  infectious,  inflammatory 
and  suppurative,  malarial,  septic  or  pyaemic  origin,  are  ushered  in  by 
chilliness  or  a  marked  chill.  Acute  pneumonia,  peritonitis,  pyaemia, 
suppuration,  if  extensive,  septicaemia,  malaria,  and  ulcerative  endo- 
carditis are  the  diseases  in  which  a  rigour  or  severe  chill  is  most 
likely  to  occur.  Chill  and  intermittent  fever  may  follow  the  passage 
of  a  renal  calculus  or  an  attack  of  severe  pain. 


112  THE  EVIDENCES  OF  DISEASE 


SECTION  xn 

EVIDENCE    OF    GEXEEAL    DIAGXOSTIC    VALUE 

DEEIVED   FROM   THE   DIGESTIVE   AXD 

GEXITO-URINARY   SYSTEMS 

There  are  symptoms  pertaining  to  the  digestive  system  and 
urinary  apparatus  which  may  be  quite  independent  of  local  disease, 
or  if  the  latter  is  present  it  may  be  secondary  to  morbid  processes 
elsewhere.  These  symptoms  are  the  condition  of  the  appetite,  the 
presence  of  unusual  thirst,  the  occurrence  of  nausea  and  vomiting, 
the  character  and  frequency  of  defecation,  the  amount  and  frequency 
of  urination,  and  certain  genital  symptoms. 

I.  APPETITE 

The  appetite  for  food  may  be  diminished  or  lost,  anorexia ;  in- 
creased, bulimia  ;  or  depraved,  pica. 

(a)  Anorexia. — Lack  of  appetite  is  most  frequently  caused  by 
fever,  of  which  it  is  often  the  first  notable  symptom,  and  is  apt  to 
persist  during  the  course  of  the  pyrexia.  It  is  also  found  in  debilitat- 
ing and  wasting  diseases,  conjoined  or  not  with  fever,  as  in  cancer  or 
chronic  phthisis.  A  remarkable  loss  of  appetite  is  seen  in  some 
cases  of  hysteria,  in  which  the  desire  for  food  is  absolutely  extin- 
guished {atiorexia  nervosa),  perhaps  for  long  periods.  The  loss  of 
appetite  due  to  worry,  anxiety,  grief,  or  suspense  is  familiar  to  all. 
It  is  a  symptom  common  to  all  the  dyspepsias,  and  such  patients 
often  fancy  that  they  are  hungry,  but  at  the  smell  or  sight  of  food, 
or  after  the  first  morsel  is  taken,  the  sensation  of  hunger  is  replaced 
by  that  of  aversion  or  positive  nausea.  Anorexia  may  arise  from  too 
long  continuance  of  an  insufficient  dietary,  originally  resorted  to 
because  of  gastric  distress  after  eating,  so  that  the  normal  desire  for 
food  lessens  from  disuse.  It  is  seen  not  infrequently  in  dyspeptics 
who  practise  self-prescribed  abstinence,  one  article  after  another 
having  been  stricken  off  the  diet  list.  The  lack  of  appetite  in  the 
chronic  alcoholic  subject  is  familiar,  as  well  as  the  acute  anorexia  of 
an  impending  attack  of  delirium  tremens.  Epidemic  influenza  is  a 
cause  of  prolonged  anorexia.  The  sense  of  hunger  in  chloro-anaemia 
is  usually  deficient.  Musser  emphasizes  the  frequent  loss  of  appetite 
in  diseases  attended  with  suppuration. 

(b)  Bulimia. — The  bulimia  may  be  permanent  {polyphagia)  or 
paroxysmal.  An  inordinate  craving  for  food  is  observed  in  conva- 
lescence from  diseases  which  have  been  attended  with  fever.     The 


THIRST— VOMITING  113 

voracious  appetite  of  a  typhoid-fever  convalescent  is  proverbial.  A 
large  appetite  is  frequently  characteristic  of  diabetes.  A  child  suf- 
fering from  pertussis  with  frequent  paroxysms  of  cough  will  occa- 
sionally be  greedy  for  food  because  the  vomiting  which  accompanies 
the  cough  does  not  allow  time  for  sufficient  absorption  to  satisfy  the 
demands  of  the  tissues.  The  patient  with  chronic  gastritis  is  apt  to 
have  a  more  than  excellent  appetite,  except  for  breakfast.  Bulimia 
may  be  a  symptom  in  some  of  the  insanities,  and  is  a  characteristic 
of  certain  idiots.  Sudden  and  paroxysmal  attacks  of  bulimia  may 
occur  in  hysteria,  epilepsy,  Graves'  disease,  cerebral  tumours,  and 
diabetes  mellitus.  Acoria  is  an  absence  of  the  sense  of  satiety. 
This  feeling  of  "  emptiness "  occurs  usually  in  hysteria  or  neuras- 
thenia. 

(c)  Pica. — A  craving  for  the  ingestion  of  unusual  or  injurious 
substances,  possibly  of  a  repulsive  nature  {coprophagy),  may  be  sig- 
nificant of  insanity  or  idiocy.  Less  marked  perversions  of  normal 
desires  may  be  seen  in  pregnancy,  in  chloro-anaemia,  in  hysteria,  and 
in  childhood,  although  the  perversion  usually  amounts  to  no  more 
than  capriciousness. 

II.  THIRST 

(a)  Absence  of  Thirst. — It  is  important,  mainly  with  reference  to 
treatment,  to  bear  in  mind  that  the  sense  of  thirst  is  blunted  or 
annulled  in  typhoid  fever. 

(b)  Increased  Thirst. — This  is  present  in  many  diseases.  It  is 
common  to  all  febrile  conditions.  It  is  intense  in  diseases  attended 
with  profuse  watery  discharges  from  the  bowels,  like  the  various 
forms  of  cholera,  and  in  sudden  large  hemorrhages.  Profuse  sweat- 
ing (disease,  hot  weather,  exercise)  is  attended  with  a  marked  thirst. 
Acute  gastritis  or  persistent  vomiting,  especially  when  resulting 
from  irritant  poisoning,  gives  rise  to  great  thirst,  and  an  unusual 
desire  for  fluids  is  common  in  chronic  gastritis  and  cancer  of  the 
stomach.  Persistent  thirst  should  always  lead  to  an  examination  of 
the  urine,  especially  if  combined  with  a  large  appetite  and  progressive 
loss  of  weight,  as  such  symptoms  attend  diabetes,  both  mellitus  and 
insipidus.  A  rare  cause  of  thirst  is  xerostomia,  or  "  dry  mouth,"  in 
which  there  is  an  arrest  of  the  salivary  secretion. 

III.  VOMITING   AND  THE  GROSS    CHARACTER  OF  THE  VOMITUS 

A  sensation  of  nausea  usually  precedes  the  act  of  vomiting, 
although  nausea  alone  may  be  present,  and  sudden  vomiting  may 
occur  without  antecedent  sickness.  On  the  other  hand,  one  may 
suffer  from  most  distressing  nausea  with  a  total  inability  to  relieve 


;l]L4  THE  EVIDENCES  OP   DISEASE 

it  by  vomiting,  owing  to  a  lack  of  completeness  in  the  required  mus- 
cular efforts.     With  nausea  there  is  generally  salivation. 

(1)  Muscular  Mechanism. — The  muscular  mechanism  of  the  act  of 
vomiting  involves  a  sudden  deep  inspiration,  a  subsequent  immediate 
closure  of  the  glottis,  and  a  contraction  of  the  diaphragm.  At  the 
same  moment  the  cardiac  orifice  of  the  stomach  is  opened  by  the 
contraction  of  the  longitudinal  fibres.  A  violent  expiratory  con- 
traction of  the  abdominal  muscles  immediately  follows,  by  which 
the  contents  of  the  stomach  are  forced  outward,  the  glottis  remain- 
ing closed  and  the  diaphragm  contracted.  The  chief  factor  in  the 
act  appears  to  be  the  contraction  of  the  abdominal  walls,  the  muscu- 
lar layer  of  the  stomach  walls  playing  a  very  small  part.  Persistent 
vomiting  may  cause  a  reverse  peristalsis  of  the  duodenum  with  a 
consequent  passage  of  bile  into  the  stomach  and  its  ajjpearance  in  the 
vomitus.  If  for  any  reason  the  cardiac  orifice  fails  to  relax  or  the 
abdominal  muscles  to  contract,  nausea  with  inability  to  vomit  results. 

(2)  Nervous  Mechanism. — The  centre  for  the  act  of  vomiting  (Fig. 
17)  lies  in  the  medulla  in  close  proximity  to  the  respiratory  centre. 
It  is  for  this  reason  that  nausea  may  sometimes  be  relieved  by  rapid 
breathing,  and  that,  particularly  in  children,  a  temporarily  increased 
respiration  rate  is  frequently  significant  of  nausea.  Impulses  are 
sent  out  from  this  centre  to  the  diaphragm  by  the  phrenic  nerves, 
to  the  stomach  and  esophagus  by  the  pneumogastric,  and  to  the 
abdominal  muscles  by  the  intercostal  nerves. 

(3)  Vomiting  Centre. — The  vomiting  centre  may  be  stimulated  to 
send  out  its  impulses  either  directly  by  certain  toxic  substances  con- 
tained in  the  blood  which  flows  through  it,  e.  g.,  the  hypodermic  use 
of  apomorphia,  or  indirectly  by  impressions  received  from  the 
periphery  or  from  the  brain  above.  For  the  most  part  the  centre  is 
excited  to  action  by  indirect  or  reflex  irritation.  This  is  true  even 
in  gastric  diseases,  for  the  irritated  nerves  of  the  gastric  mucosa 
must  send  their  stimulus  to  the  centre  to  be  reflected  to  the  muscles 
concerned  in  the  act  of  vomiting.  Children  vomit  more  readily  than 
adults,  partly  because  the  nervous  system  is  more  excitable,  partly 
because  of  the  more  vertical  position  and  less  marked  cardiac  curva- 
ture of  the  stomach. 

(4)  Causes  of  Vomiting.— The  diseases  and  conditions  which  may 
cause  vomiting  are  many.  Consequently,  vomiting,  as  an  isolated 
symptom,  possesses  very  slight  diagnostic  value  and  requires  a  care- 
ful consideration  of  the  accompanying  symptoms  in  order  to  deter- 
mine its  cause.  In  the  majority  of  cases  these  are  sufficiently  dis- 
tinctive, but  there  are  instances  in  which  a  most  painstaking  inves- 
tigation will  leave  the  clinician  in  doubt.     Xo  case  should  be  classed 


VOMITING 


115 


as  of  purely  neurotic  origin  until  the  blood  and  the  urine  have  been 
questioned  by  appropriate  methods. 


Ideational. 


Cerebral  disease 


VOMITING   CENTRE. 


Fig.  17. — Diagram  of  the  vomiting  centre  in  the  medulla,  and  the  manner  in  which  stimuli, 
both  toxsemic  and  reflex,  may  act  upon  it. 


116  THE  EVIDENCES  OP   DISEASE 

In  any  case  of  vomiting  the  following  queries  should  be  an- 
swered : 

(a)  Has  any  article,  medicinal  or  dietetic,  been  ingested  which  is 
capable  of  causing  nausea  ? 

{b)  Has  the  previous  health  been  good  ?  In  other  words,  is  it  an 
event  in  a  chronic  disease  or  a  primary  symptom  in  an  acute  malady  ? 
If  there  is  gastric  pain  or  headache,  is  it  relieved  by  vomiting  ? 

(c)  Is  there  fever,  headache,  abdominal  pain,  or  evidence  of  col- 
lapse ? 

{d)  Is  there  obstinate  constipation  or  jaundice  ? 

(e)  What  abnormalities  are  found  in  the  urine  and  the  blood  ? 

Clinically  we  may  consider  (A)  the  indications  to  be  derived  from 
the  presence  of  vomiting,  (B)  the  indications  to  be  derived  from  the 
macroscopic  character  of  the  vomited  material. 

A.    INDICATIONS    DERIVED    FROM   THE    PRESENCE 
OF  VOMITING 

As  to  its  origin,  vomiting  may  be  centric  or  toxsemic,  due  to 
direct  stimulation  of  the  vomiting  centre  by  any  toxic  or  irritating 
agent  in  the  blood,  or  it  may  be  a  reflex  act  from  disease  or  irritation 
of  many  organs,  but  this  classification  of  vomiting  can  at  best  be 
only  approximately  accurate.  The  following  enumeration  may  serve 
to  give  a  comprehensive  view  of  the  possibilities  in  a  given  case : 

1.  Centric  or  ToxaBmic  Vomiting. — (a)  Acute  alcoholism,  the 
hypodermic  use  of  apomorphia,  and  the  inhalation  of  chloroform, 
ether,  or  sewer  gas  are  the  principal  examples  of  centric  vomiting 
caused  by  foreign  poisons. 

(b)  Toxaemic  vomiting  may  also  be  caused  by  poisons  of  non- 
bacterial origin  circulating  in  the  blood,  as  in  Addison's  disease, 
anaemia  (acute  or  chronic) ;  diabetes,  heralding  the  approach  of  dia- 
betic coma ;  irregular  gout  (biliousness) ;  paroxysmal  haemoglobi- 
nuria,  preceding  the  appearance  in  the  urine  of  the  colouring  matter 
of  the  blood ;  and  nephritis,  perhaps  as  the  earliest  symptom  of  the 
disease,  in  which  case  it  is  apt  to  occur  in  the  morning.  The 
unknown  toxic  agent  of  rlieumatic  fever  will  in  rare  instances 
cause  obstinate  vomiting. 

(c)  Other  varieties  of  centric  vomiting  are  due  to  bacterial  toxines 
in  the  blood.  It  occurs  almost  invariably  at  the  onset  of  scarlet 
fever,  and  with  varying  frequency  in  erysipelas,  measles,  variola, 
acute  pneumonia,  yellow  fever,  malarial  fever,  epidemic  parotitis 
(mumps),  roseola,  and  sometimes  syphilis.  Vomiting  which  takes 
place  later  in  such  diseases  is  more  apt  to  be  due  to  uraemia. 
Vomiting  may  be  a  feature  in  the  course   of   other  infectious  and 


REFLEX   VOMITING  117 

septic  diseases,  as  in  acute  miliary  tuberculosis,  acute  yellow  atrophy 
of  the  liver,  ulcerative  endocarditis,  and  gangrene  of  the  lungs. 

2.  Reflex  Vomiting,  (a)  Cerebral. — When  vomiting  is  due  to 
irritations  sent  from  the  cerebrum  to  the  centre  in  the  medulla,  it  is 
somewhat  characteristically  projectile  and  frequently  unattended 
with  nausea  or  epigastric  pain.  It  may  be  caused  by  cerebral  tumour 
or  abscess;  and  intracranial  hemorrhage,  embolism,  or  thrombosis, 
particularly  hemorrhage.  Musser  has  seen  sudden  and  continuous 
vomiting,  with  a  slow  full  pulse  and  a  flushed  face,  as  a  premonitory 
symptom  of  apoplexy,  and  I  *  can  add  a  personal  case  of  the  same 
kind.  Chronic  and  acute  hydrocephalus  may  be  attended  with  vom- 
iting. 

Vomiting  is  a  common  and  sometimes  the  first  symptom  of  men- 
ingitis, especially  in  children,  and  may  continue  throughout  the  dis- 
ease. Anaemia  of  the  brain  may  be  responsible  for  nausea  and  vomit- 
ing, as  in  vomiting  from  loss  of  blood,  severe  anaemias,  syncope, 
shock,  and  collapse ;  also  concussion,  laceration,  or  compression  of 
the  brain,  especially  during  recovery  in  the  moderately  severe  cases. 
Vomiting  shortly  after  an  epileptic  convulsion  is  common.  It  may 
be  caused  by  a  disgusting  sight,  taste,  or  odour,  or  the  emotion  may 
be  purely  subjective.  Most  obstinate  and  intractable  vomiting  may 
be  of  hysterical  origin,  and  may  be  of  daily  occurrence  in  children  or 
young  people  who  are  overburdened  with  school  work,  the  so-called 
"  juvenile  vomiting."  It  is  usually  attended  with  gastric  pain,  and 
perhaps  with  severe  headache,  pallor,  dilatation  of  the  pupils,  and  a 
slow  pulse.  Paroxysms  of  vomiting  and  inability  to  take  food,  lasting 
from  1  to  10  days,  appearing  in  persons  apparently  healthy  before 
and  after  the  attack,  the  paroxysms  recurring  at  definite  inter- 
vals, constitute  a  very  uncommon  disease,  the  periodic  vomiting  of 
Leyden. 

Neurasthenia,  especially  if  lithaemia  coexists,  is  the  cause  of  occa- 
sional attacks  of  vomiting,  more  particularly  after  fatigue  of  mind  or 
body.  The  vomiting  of  sea-sickness  is  familiar.  A  paroxysm  of 
Meniere's  disease  usually  terminates  with  nausea  and  vomiting,  as 
does  migraine  or  hemicrania,  and  the  so-called  bilious  or  lithaemic 
headache. 

Muscular  asthenopia  and  refractive  errors,  particularly  astigma- 

*  "  That  right  line  '  I '  is  the  very  shortest,  simplest,  straightforwardest  means 
of  communication  between  us,  and  stands  for  what  it  is  worth  and  no  more.  Some- 
times authors  say,  '  The  writer  has  often  remarked  ' ;  or  '  The  undersigned  has  ob- 
served ' ;  but  '  I '  is  better  and  straighter  than  all  these  grimaces  of  modesty ;  and 
I  shall  ask  leave  to  maintain  the  upright  and  simple  perpendicular.'' — Thackeray, 
Roundabout  Papers. 
10 


118  THE  EVIDENCES  OP  DISEASE 

tism,  may  be  an  occasional  cause  of  nausea,  after  injudicious  use  of 
the  eyes,  proceeding  in  some  cases  to  actual  vomiting. 

(b)  Pharynx,  Larynx,  Lungs,  and  Thyroid  Gland. — As  an  irrita- 
tion of  the  fauces  by  titillation  will  cause  reflex  vomiting,  so  the  dis- 
eases which  are  attended  with  a  severe  paroxysmal  cough  may  also 
produce  it,  as  in  whooping  cough,  the  irritative  cough  of  phthisis,  and 
the  cough  due  to  enlarged  bronchial  glands  or  mediastinal  tumour. 
A  sudden  attack  of  vomiting  and  abdominal  pain,  in  some  cases 
accompanied  with  a  profuse  watery  diarrhoea  and  jaundice,  constitutes 
a  not  infrequent  symptom  during  the  course  of  exophthalmic  goitre. 

(c)  Stomach. — Diseases  affecting  the  stomach  are  responsible  for 
the  majority  of  cases  of  vomiting.  Xeurotic  vomiting  occurs  in  hys- 
teria, and  attacks  of  pain  and  vomiting  constitute  the  gastric  crises 
of  locomotor  ataxia.  Severe  vomiting  is  a  prominent  symptom  of 
acute  or  subacute  gastritis  from  putrefying,  indigestible,  or  irritating 
food,  or  from  overloading  of  the  stomach.  The  vomiting  of  chronic 
gastritis  is  usually  in  the  morning,  so  also  is  the  "  dry  retching  "  of 
the  laity,  nausea  and  ineffectual  attempts  to  vomit,  in  the  same  dis- 
ease. Vomiting  (often  blood-streaked  or  coffee  ground)  is  almost  in- 
variably present  in  gastric  cancer  and  cirrhosis  during  the  middle  or 
later  stages  of  the  disease.  Vomiting  due  to  dilatation  of  the  stomach 
may  occur  several  hours  after  a  meal,  or  at  intervals  of  several  days, 
in  which  case  the  amount  of  vomited  material  may  be  very  large  and 
contain  food  which  has  been  eaten  many  hours  previously.  Vomit- 
ing due  to  gastric  ulcer  is  apt  to  occur  2  or  more  hours  after  eating, 
and  is  preceded  by  the  most  constant  symptom  of  this  lesion,  viz., 
pain,  which  usually  begins  immediately  after  eating  and  increases  in 
intensity  until  vomiting  takes  place,  after  which  the  pain  subsides. 
If  the  ulcer  perforates,  vomiting  often  begins  and  is  attended  by  col- 
lapse, great  and  increasing  pain,  fever  and  other  symptoms  of  acute 
peritonitis. 

Vomiting  may  be  due  to  the  administration  of  the  medicinal 
emetics,  and  to  irritant  poisons.  With  the  latter  there  is  usually 
pain,  collapse,  and  subsequently  more  or  less  violent  purging.  Poi- 
soning by  antimony  can  not  be  distinguished  by  the  symptoms  alone 
from  cholera,  epidemic  or  sporadic.  The  history,  environment,  and 
season  may  arouse  suspicion.  The  presence  of  bloody  stools  in  arsen- 
ic poisoning  will  discriminate  it  from  cholera.  Paris  green  may  be 
detected  in  the  vomited  material.  Poisoning  from  copper  colours 
the  vomit  green,  turning  to  blue  upon  the  addition  of  ammonia.  In 
phosphorus  poisoning  vomiting  begins  several  hours  after  taking  the 
poison,  and  the  vomited  material  smells  strongly  of  the  drug  and 
may  be  phosphorescent  in  the  dark. 


REFLEX  VOMITING  119 

(d)  Intestines  and  Peritoneum. — Vomiting  is  a  most  common 
symptom  at  the  onset  of  appendicitis ;  and  in  every  case  of  acute 
vomiting  accompanied  with  abdominal  pain,  the  caecal  region  should 
be  carefully  palpated  to  discover  possible  muscular  rigidity  or  tender- 
ness. It  is  early,  severe,  and  prolonged  in  cholera  infantum,  cholera 
Asiatica,  and  sporadic  cholera.  In  a  perforating  duodenal  ulcer,  or 
a  perforating  ulcer  of  other  parts  of  the  intestine,  vomiting  with 
collapse  occurs  in  connection  with  the  symptoms  of  acute  peritonitis. 
In  the  acute  enteritis  of  adults  and  the  acute  enterocolitis  of  children 
vomiting  is  a  frequent  event. 

In  every  case  of  vomiting  associated  with  abdominal  pain  the 
possible  existence  of  hernia  (femoral,  inguinal,  umbilical,  and  the 
rarer  varieties  of  obturator,  ventral,  diaphragmatic,  and  retroperito- 
neal hernia)  should  not  be  forgotten,  as  a  small  knuckle  of  intestine 
nipped  in  the  neck  of  a  hernial  sac  may  easily  be  overlooked  without 
a  systematic  and  careful  examination.  Often  the  hernial  protrusion 
is  so  slight  as  to  cause  no  palpable  swelling  or  tumour,  the  diagnosis 
resting  upon  the  localized  tenderness  and  the  exclusion  of  other  con- 
ditions. 

The  acute  varieties  of  peritonitis  are  almost  invariably  attended 
with  vomiting,  which  in  acute  general  peritonitis  is  an  early  and  per- 
sistent symptom. 

Vomiting  may  be  caused  by  obstruction  of  the  intestine,  and  is 
one  of  the  cardinal  symptoms  of  this  condition.  The  development 
of  this  symptom  depends  much  upon  the  location  of  the  obstruction. 
A  lesion  in  the  upper  part  of  the  small  intestine  is  characterized  by 
the  rapid  appearance  of  vomiting,  often  of  a  violent  and  expulsive 
nature ;  whereas,  in  obstruction  in  the  large  intestine,  vomiting  comes 
on  tardily,  following  general  tympanites,  or,  indeed,  there  may  be 
only  a  belching  of  gas  without  vomiting. 

(e)  Liver  and  Gall  Bladder. — Vomiting  may  be  a  symptom  of  dis- 
eases of  the  liver,  especially  those  which  cause  jaundice,  such  as 
catarrh  of  the  bile  ducts  with  its  attendant  gastro-duodenal  catarrh  ; 
hepatic  colic  ;  and  of  obstruction  of  tlie  common  duct  by  gallstones 
or  new  growths.  The  vomiting  of  "  biliousness  "  has  been  referred 
to. 

(/)  Kidney. — Uraemic  vomiting  has  been  mentioned.  Attacks 
of  renal  colic,  if  severe,  are  attended  with  nausea  and  vomiting. 
Suppurative  pyelitis  has,  in  my  experience,  been  characterized  by 
persistent  nausea  and  occasional  vomiting.  An  abrupt  onset  of  vom- 
iting, usually  with  localized  pain  and  diminution  of  the  flow  of  urine, 
may  be  indicative  of  a  movable  kidney  which  has  become  twisted 
upon  its  pedicle. 


120  THE  EVIDENCES  OP  DISEASE 

{g)  Pancreas. — Vomiting  preceded  by  sudden  pain  in  the  epigas- 
trium, followed  by  collapse,  may  be  indicative  of  a  possible  acute 
pancreatitis ;  and  when  attended  with  paroxysmal  attacks  of  colicky 
pain  and  persistent  jaundice  may  be  a  symptom  of  cancer  of  the 
pancreas. 

(h)  Uterus,  Ovaries,  Tubes. — The  reflex  nausea  and  vomiting  of 
pregnancy  is  familiar.  Marked  displacement  of  the  uterus,  pregnant 
or  non-pregnant,  may  also  be  a  causal  factor.  Vomiting  may  be  a 
symptom  of  septic  endometritis,  salpingitis,  and  ovaritis.  The  atro- 
cious dysmenorrhoea  which  characterizes  certain  cases  of  anteflexion 
of  the  cervix  in  neurotic  young  women  is  often  attended  with  vomit- 
ing and  partial  syncope. 

(i)  Bladder  and  Prostate  Gland. — Chronic  cystitis  may  occasion- 
ally cause  vomiting,  absorption  of  some  elements  of  the  decomposing 
urine  having  taken  place.  In  acute  cystitis  and  prostatitis  the  reflex 
irritation  from  inflammatory  disease  of  these  sensitive  organs  may  in 
itself  be  sufficient  to  produce  nausea. 

(j )  Other  Associations  of  Vomiting. — Some  persons  who  appear 
to  have  a  peculiar  susceptibility  of  the  nervous  system  will  vomit 
after  severe  exertion,  although  the  general  health  may  be  above  sus- 
picion. Vomiting,  with  abdominal  pain,  occasionally  with  diarrhoea, 
is  observed  in  the  early  stage  of  trichinosis  before  general  infection 
has  occurred. 

In  this  connection  rumination,  regurgitation,  eructations,  hic- 
cough, and  pyrosis  may  be  considered. 

3.  Rumination  or  Merycism. — This  is  the  act  of  returning  swal- 
lowed solid  food  to  the  mouth,  when  it  is  again  chewed  and  swal- 
lowed. It  is  a  neurosis,  involuntary  at  first,  but  becoming  voluntary 
by  custom  in  some  cases. 

4.  Regurgitation. — Frequent  regurgitation  of  the  liquid  portions 
of  food  may  occur,  and  is  due  either  to  relaxation  of  the  cardiac  ori- 
fice of  the  stomach,  or  to  the  existence  of  a  sac  or  diverticulum  of 
the  esophagus,  into  which  fluid  enters  and  from  which  it  is  expelled 
at  irregular  intervals. 

5.  Eructations. — The  frequent,  spasmodic  expression  of  gas  from 
the  stomach  by  way  of  the  mouth  (eructation,  belching)  is  a  common 
symptom.  The  gas  expelled  may  be  offensive  (siilphuretted  hydro- 
gen) or  odourless,  consisting  mainly  of  air.  The  gas  may  come  from 
the  esophagus,  and  in  this  case  consists  of  air  which  has  been  swal- 
lowed. The  belchings  may  take  place  singly  and  at  infrequent  inter- 
vals, or  in  paroxysms,  2  or  3  times  a  minute,  the  attack  lasting  for 
hours. 

In  the  majority  of  cases  eructations  of  gas,  particularly  if  offen- 


PYROSIS— HICCOUGH  121 

give,  are  significant  of  acute  indigestion,  overfeeding,  acute  or  chronic 
gastritis,  and  other  organic  affections  of  the  stomach  and  of  the 
pancreas.  It  may  be  a  pure  neurosis,  occurring  in  neurasthenia  or 
hysteria,  as  well  as  in  patients  who  are  otherwise  healthy  or  who 
have  been  worried  and  excited.  In  these  instances  the  gas  is  odour- 
less. The  terminal  stage  of  an  attack  of  angina  pectoris  may  be 
attended  by  explosive  eructations  of  gas ;  and,  rarely,  the  belching 
may  signify  the  presence  of  an  aneurism  of  the  thoracic  aorta. 

6.  Pyrosis. — A  burning  sensation  in  the  epigastrium,  frequently 
extending  up  behind  the  sternum  to  the  pharynx,  and  sometimes 
accompanied  by  the  regurgitation  of  a  watery  acrid  or  acid  fluid,  is 
termed  pyrosis.  In  common  parlance  the  sensation  is  called  "  heart- 
bum  "  ;  the  regurgitation,  "  water  brash." 

Pyrosis  is  often  accompanied  by  eructations,  and,  like  the  latter, 
may  be  symptomatic  of  gastric  or  pancreatic  disease,  or  may  be  a 
neurosis.  While  it  is  most  frequently  associated  with  a  too  acid  gas- 
tric juice  (hyperacidity),  it  may  exist  with  a  neutral  reaction  of  the 
stomach  contents. 

7.  Hiccougll. — This  symptom  results  from  a  sudden  contraction 
of  the  diaphragm  which  may  be  repeated  at  more  or  less  regular  inter- 
vals. The  attack  may  last  for  a  minute  or  for  several  hours,  and 
may  recur  during  days  and  months. 

The  causes  of  hiccough  are  as  follows : 

It  occurs  in  diseases  of  the  abdominal  viscera — e.g.,  gastritis, 
gastrectasia,  cancer  of  the  stomach ;  enteritis,  internal  and  external 
strangulation  or  other  cause  of  intestinal  obstruction,  appendicitis, 
cholera;  suppurative  pancreatitis;  disease  of  liver;  peritonitis,  espe- 
cially if  it  involves  the  diaphragmatic  peritoneum ;  and  tympanites. 

Diseases  of  the  nervous  system  are  not  infrequent  causes — viz., 
epilepsy,  tumour  of  the  brain,  meningitis,  hydrocephalus,  shock, 
mental  emotions,  and  hysteria.  To  the  latter  many  excessively  ob- 
stinate cases  are  due. 

Certain  constitutional  conditions  appear  to  be  responsible  for 
otherwise  inexplicable  paroxysms  of  hiccough,  such  as  diabetes,  gout, 
and  chronic  nephritis.  Other  causes  are  gangrene  of  the  lung,  dia- 
phragmatic pleurisy,  dysmenorrhoea  and  pregnancy,  alcoholism,  Addi- 
son's disease,  large  hemorrhages,  and,  last  but  not  least,  severe  typhoid 
fever  and  the  typhoid  state. 

The  milder  forms  of  hiccough  are  ordinarily  of  little  consequence, 
but  its  onset  in  conditions  which  are  known  to  be  serious  adds  nota- 
bly to  the  gravity  of  the  prognosis. 


122  THE   EVIDENCES  OF  DISEASE 


B.    INDICATIONS   DERIVED   FROM   THE   MACROSCOPIC 
CHARACTER  AND  AMOUNT  OF  THE  VOMITUS 

The  first  act  of  vomiting  expels  the  food  contents  of  the  stomach, 
if  such  be  present,  the  character  of  which  may  furnish  a  clew  to  the 
cause  of  the  vomiting.  If  the  vomiting  continues,  or  if  the  stomach 
is  empty,  the  vomitus  will  consist  of  a  watery  fluid  (partly  swallowed 
saliva),  mucus,  and  finally  bile.  In  certain  cases  the  vomitus  may 
contain  streaks  of  blood,  or  consist  almost  entirely  of  blood.  Still 
more  rarely  there  may  be  a  faecal  odour  or  visible  fascal  matter  in  the 
vomit. 

(a)  Watery  Fluid  and  Mucus. — If  the  vomit  comes  from  an  empty 
stomach,  is  watery,  and  contains  considerable  mucus,  it  usually  indi- 
cates a  gastric  catarrh,  although,  if  nausea  has  existed  for  some  time 
previous  to  the  vomiting,  the  mucus  may  have  been  swallowed.  It 
may  be  acid  or  alkaline.  If  the  latter,  the  watery  part  usually  con- 
sists of  swallowed  saliva.  If  it  is  clear,  containing  little  or  no  mucus, 
and  has  a  very  sour  smell,  and  on  examination  responds  to  the  tests 
for  hydrochloric  acid,  it  is  gastric  juice,  constituting  hypersecretion. 
If  on  quantitative  examination  the  proportion  of  hydrochloric  acid 
exceeds  the  normal  0.3  per  cent,  there  is  hyperchlorhydria.  Vomit- 
ing of  overacid  gastric  juice  occurs  persistently  or  periodically  in  the 
gastric  neuroses  ;  in  the  terminal  vomiting  of  migraine  ;  in  hysteria ; 
in  the  gastric  crises  of  locomotor  ataxia,  exophthalmic  goitre,  and 
movable  kidney ;  and  in  gastric  ulcer  before  and  after  healing. 

{b)  Bilious  Vomiting. — Vomit  containing  bile,  green  or  greenish- 
yellow,  makes  its  appearance,  as  a  rule,  only  after  frequent  and  vio- 
lent vomiting. 

Vomiting  of  grass-green  bile,  occurring  early  and  perhaps  with 
slight  effort,  in  connection  with  each  act  of  vomiting,  is  a  symptom 
of  some  diagnostic  value  in  peritonitis,  and  commonly  precedes  f  secal 
vomiting  in  intestinal  obstruction, 

(c)  Hsematemesis. — The  vomited  blood  may  be  bright  red  and 
fluid,  in  which  case  it  has  remained  but  a  short  time  in  the  stomach. 
If  it  has  been  in  the  stomach  for  a  sufficient  length  of  time  to  be 
partially  digested  by  the  gastric  juice,  it  has  the  appearance  of  coffee 
grounds.  It  may  be  in  the  form  of  clots,  reddish  or  brown,  indicat- 
ing a  stay  of  medium  duration. 

It  is  necessary  to  discriminate  between  hsematemesis  and  hgemop- 
tysis,  or  hemorrhage  from  the  mucous  membrane  of  the  bronchi. 
In  the  latter  the  blood  is  bright  red,  frothy,  and  alkaline.  It  is 
raised  by  an  act  of  coughing,  not  vomiting,  and  physical  examina- 
tion of  the  lungs  usually  reveals  signs  of  its  pulmonary  origin.     If  it 


H^MATEMESIS  123 

is  from  the  stomach,  tarry  stools  may  be  passed,  and  there  will  usu- 
ally be  evidences  of  disease  of  some  of  the  abdominal  organs. 

It  is  to  be  remembered  that  the  presence  of  certain  substances  in 
the  vomited  material  may  give  the  appearance  of  fresh  blood,  such 
as  red  wine,  grape  juice  from  black  grapes,  red  jellies,  preserves  made 
from  strawberries,  raspberries,  huckleberries,  currants,  cranberries, 
mulberries,  and  red  cherries,  or  the  fruits  themselves. 

Coffee-ground  vomit  may  be  simulated  by  coffee  or  cocoa,  strong 
broths  or  soups,  bile,  bismuth  salts,  and  ferruginous  preparations,  all 
of  which  may  produce  a  brownish  or  blackish  coloration  of  the  stom- 
ach contents. 

If  there  is  doubt  as  to  the  presence  of  blood  in  the  vomit,  a  drop  should  be 
placed  under  the  microscope  to  determine  the  presence  of  red  corpuscles.  If 
these  are  not  found,  the  test  for  haemin  may  be  applied  by  filtering  some  of  the 
vomited  matter  and  evaporating  a  small  amount  of  the  filtrate  to  dryness  in  a 
porcelain  or  glass  dish,  after  which  the  dried  material  is  to  be  scraped  off, 
placed  upon  a  slide,  a  minute  quantity  of  common  salt  added,  and  a  cover  glass 
placed  upon  it,  after  which  a  drop  of  acetic  acid  is  allowed  to  flow  under  the 
cover  glass  by  capillary  attraction.  It  is  then  heated  with  care  over  an  alcohol 
flame  for  a  minute  until  bubbles  are  seen  under  the  cover  glass,  acetic  acid 
being  added  from  the  edge  until  a  slight  reddish-brown  tint  shows  itself.  The 
acid  is  then  permitted  to  dry  out,  the  slide  being  removed  to  a  greater  height 
above  the  flame.  When  thoroughly  dried,  a  drop  of  water  or  glycerin  is  dif- 
fused under  the  cover.  It  is  now  placed  under  the  microscope,  using  a  power 
of  at  least  300  diameters,  when,  if  blood  be  present,  minute  crystals  of  haemin 
are  visible. 

Large  and  suddenly  fatal  hemorrhages  from  the  stomach  may  be 
due  to  the  rujjture  of  an  aneurism  into  the  esophagus  or  stomach, 
to  rupture  of  varicose  esophageal  veins,  to  gastric  ulcer,  to  a  large 
spleen,  and  to  cirrhosis  of  the  liver.  Death  has  taken  place  before 
the  occurrence  of  vomiting,  the  stomach  containing  3  or  4  pounds  of 
blood.  In  the  majority  of  cases  gastric  hemorrhage  is  not  imme- 
diately fatal  and  the  bleedings  recur  for  a  considerable  length  of 
time.  This  is  particularly  the  case  in  ulcer  of  the  stomach,  cirrhosis 
of  the  liver,  and  carcinoma  of  the  stomach — the  diseases  which  are 
responsible  for  the  greater  part  of  the  gastric  hemorrhages  which  are 
met  with  in  practice.  The  large  bleedings  are  accompanied  by  the 
customary  signs  of  internal  hemorrhage  [q.  v.).  The  vomiting  of 
small  amounts  of  blood,  sometimes  only  a  few  bright-red  streaks  in 
mucus,  or  a  moderate  quantity  of  coffee-ground  material,  occurs  in  a 
number  of  diseases  and  conditions.  A  brief  recapitulation  of  the 
causes  of  haematemesis  may  prove  to  be  useful. 

1.  Swallmced  Blood. — Vomiting  of  blood  is  not  synonymous  with 
gastric  hemorrhage.     In  epistaxis  and  haemoptysis  the  blood  may  be 


124  THE  EVIDENCES  OF  DISEASE 

swallowed  unconsciously.  It  is  also  swallowed  for  purposes  of  decep- 
tion by  malingerers  and  hysterical  persons,  the  blood  having  been 
obtained  from  an  extraneous  source  or  from  self-made  wounds  of 
the  buccal  mucous  membrane.  Blood  from  a  bitten  tongue  may  be 
vomited  after  an  epileptic  seizure,  and  an  infant  may  vomit  blood 
coming  from  a  fissured  nipple  while  nursing. 

2.  Injury. — Blows,  kicks,  wounds,  or  other  injuries  in  the  epi- 
gastric region  may  be  followed  by  haematemesis.  Streaks  of  blood 
are  not  infrequently  ssen  as  a  result  of  the  violent  straining  which 
attends  severe  and  persistent  vomiting. 

3.  Stomach. — Hemorrhage  may  result  from  gastric  ulcer,  and  gas- 
tric cancer  (occasional  and  moderate  coffee-ground).  The  vomit  of 
chronic  gastritis  and  gastrectasia  may  present  streaks  of  blood.  Vi- 
carious menstruation  by  way  of  the  stomach  in  cases  of  amenorrhoea 
must  be  considered  a  rare  and  perhaps  non-existent  phenomenon. 

4.  Portal  Obstruction. — Cirrhosis  of  the  liver  frequently,  cancer 
of  the  liver  seldom,  and  an  enlarged  spleen  at  times,  by  causing  ex- 
treme passive  congestion  of  the  gastric  mucous  membrane,  will  pro- 
duce haematemesis ;  so  also  with  congestion  of  the  liver  and  the 
portal  system  secondary  to  cardiac  valvular  disease,  especially  mitral 
stenosis. 

5.  Poisons. — The  corrosive  poisons — arsenic,  strong  acids  and 
alkalies — may  be  responsible  for  streaks  of  blood  in  the  vomitus. 

6.  HcBmic  Conditions. — Bleeding  from  the  stomach,  more  or  less 
profuse,  may  result  from  severe  anaemias,  of  whatever  origin ;  it  is  an 
occasional  symptom  of  cholaemia,  and  may  be  due  to  haemophilia.  It 
is  sometimes  an  early  event  in  leucaemia,  occurs  infrequently  in 
Hodgkin's  disease,  and  may  be  present  in  scurvy,  purpura  haemor- 
rhagica,  and  chronic  nephritis.  The  poisons  of  the  acute  infectious 
diseases  may  so  disorganize  the  walls  of  the  vessels  of  the  gastric 
mucous  membrane  that  blood  escapes  from  them  into  the  stomach. 
It  has  been  observed  in  severe  malarial  fevers,  typhus  fever,  epidemic 
influenza,  relapsing  fever,  yellow  fever  (black  vomit),  malignant 
smallpox,  and  dengue.  It  has  also  occurred  in  phosphorus  poison- 
ing and  acute  yellow  atrophy  of  the  liver.  It  is  a  rare  symptom  in 
pyaemia. 

{d)  Faecal  Vomitiilg. — The  presence  in  the  vomit  of  material  com- 
ing from  the  intestine  is  indicated  by  a  distinctly  fsecal  odour.  Very 
rarely  masses  or  particles  of  a  clearly  feculent  character  and  consist- 
ence may  be  found.  Faecal  vomiting  is  indicative  of  intestinal  ob- 
struction from  any  of  the  recognised  causes,  or  of  an  intense  general 
peritonitis,  or  of  an  abnormal  communication  between  the  stomach 
and  intestine. 


THE   VOMIT  US— DEFECATION  125 

(e)  Pus  in  the  Vomit. — An  amount  of  pus  in  the  vomit  sufficient 
to  be  seen  by  the  naked  eye  is  of  very  infrequent  occurrence.  If 
present,  it  is  usually  indicative  of  the  rupture  of  an  abscess  of  a 
near-by  organ  into  the  stomach,  as  in  hepatic  or  pancreatic  suppura- 
tion, although  it  may  result  from  phlegmonous  or  diphtheritic  inflam- 
mation of  the  gastric  walls. 

(/)  Parasites  in  the  Vomit. — The  parasites  which  have  been 
vomited  are  segments  of  taeniae,  ascarides  or  roundworms,  Oxyuris 
vermicularis  or  threadworms,  trichinae,  fragments  of  echinococcus 
cysts  if  rupturing  into  the  stomach  from  the  liver  or  spleen,  and  the 
anchylostomum  duodenale.  The  appearance  of  any  one  of  these, 
except  taenia  and  ascaris,  is  extremely  rare. 

{g)  Odour  of  the  Vomit. — The  significance  of  a  faecal  odour  has 
been  mentioned.  The  garlicky  odour  of  phosphorus  and  the  char- 
acteristic odour  of  carbolic  acid  may  reveal  the  nature  of  the  toxic 
agent  in  cases  of  poisoning.  An  ammoniacal  odour  is  indicative  of 
uraemia. 

IV.  DEFECATION   AND  THE  GROSS  CHARACTER  OF  THE  STOOLS 

In  every  case  of  illness  it  is  customary  and  desirable  to  inquire  as 
to  the  character,  regularity,  and  frequency  of  the  bowel  movements 
and  the  character  of  the  stools. 

The  bowels  normally  move  once  daily  without  pain.  The  colour 
of  the  stool  varies  from  a  bright  to  a  blackish  brown,  and  is  due  for 
the  most  part  to  the  presence  of  reduced  bilirubin  {liydrohiliruhin). 
The  average  weight  of  the  stool  is  about  5  oz,  (160  grammes).  It 
is  firm  in  consistence,  sausage  shaped,  about  6  inches  long,  and  is 
composed  of  insoluble  or  unabsorbed  portions  of  the  food,  intestinal 
mucus  and  other  secretions  of  the  digestive  tube,  epithelial  cells,  and 
bacteria. 

The  rhythmical,  wormlike  contractions  of  the  intestine,  by  which 
its  contents  are  passed  toward  the  rectum,  are  dependent  upon  the 
presence  of  automatic  motor  centres  in  its  muscular  wall.  These 
centres  are  to  a  certain  extent  under  the  control  of  the  splanchnic, 
which  sends  to  them  both  inhibitory  and  motor  fibres,  and  which 
affords  also  the  vasomotor  and  sensory  nerve  supply  of  the  intestine. 
Normal  peristalsis,  therefore,  depends  upon  the  functional  integrity 
of  the  nervous  mechanism,  the  healthy  condition  of  the  intestinal 
musculature,  and  the  presence  of  adequate  and  not  excessive  stimula- 
tion, the  last  of  which  is  ordinarily  found  in  the  contact  of  the  chyme 
with  the  intestinal  walls  and  in  the  passage  of  blood  containing  the 
normal  proportion  of  oxygen  and  carbon  dioxide  through  the  intes- 
tinal blood  vessels. 


126  THE  EVIDENCES  OP  DISEASE 

The  deviations  of  more  or  less  diagnostic  importance  which  may 
be  encountered  relate  to  constipation,  diarrhoea,  incontinence  of 
faeces,  painful  defecation,  tenesmus,  and  the  colour,  shape,  consist- 
ence, and  abnormal  contents  of  the  stools. 

A.    CONSTIPATION 

There  may  be  considerable  variations  in  the  frequency  of  defeca- 
tion which  are  quite  consistent  with  good  health.  Certain  individ- 
uals habitually  evacuate  the  bowel  twice  or  thrice  daily,  having  other- 
wise a  feeling  of  discomfort,  while  a  movement  every  3,  3,  or  -t  days 
may  be  the  rule  in  persons  who  present  no  evidence  of  ill  health. 

Constipation,  which  may  be  roughly  defined  as  a  lack  of  intestinal 
peristalsis,  is  therefore  a  relative  term,  and  its  existence  is  to  be 
determined  by  inquiry  as  to  the  habits  of  the  individual  in  this 
respect  for  a  series  of  years.  It  is  commonly  easy  in  practice  to  de- 
cide between  normal  and  pathological  infrequency.  Constipation  due 
to  a  mechanical  cause,  as  in  intussusception,  constitutes  intestinal  ob- 
struction. 

If  constipation  becomes  habitual,  it  may  cause,  in  varying  degrees, 
a  feeling  of  lassitude  or  debility,  headache,  mild  vertigo,  mental  tor- 
pidity, and  low  spirits — symptoms  commonly  attributed  to  the  absorp- 
tion of  toxic  material  from  the  intestinal  canal.  These  symptoms 
are  manifested  most  frequently  in  neurasthenic  and  hypochondriacal 
individuals,  less  often  in  those  of  a  non-nervous  temperament. 

As  a  symptom,  constipation  is  common  to  many  diseases  and  con- 
ditions. In  the  following  paragraphs  an  attempt  is  made  to  state 
the  most  important  facts  which  should  be  borne  in  mind  when  seek- 
ing to  determine  the  diagnostic  indications  of  constipation  in  a  given 
case. 

1.  Constipation  may  be  a  constitutional  trait  and  is  not  infre- 
quently hereditary. 

2.  Dietetic  causes  are  not  uncommonly  responsible  for  the  existence 
of  constipation.  If  the  food  is  of  such  a  nature  as  to  be  almost  com- 
pletely absorbed  (milk,  meat,  meat  extracts,  eggs),  there  is  an  insufii- 
cient  amount  of  waste  material  to  give  a  normal  stimulus  to  peristal- 
tic action.  For  obvious  mechanical  reasons,  a  certain  bulk  or  volume 
of  faecal  matter  is  required,  in  order  that  the  intestine,  the  colon  in 
particular,  may  easily  grasp  and  propel  it  to  its  proper  destination. 
For  similar  reasons,  a  too  small  amount  of  food,  even  if  of  proper 
composition,  will  have  the  same  effect. 

Constipation  may  also  arise  from  a  too  scanty  taking  of  fluids, 
whereby  the  faeces  become  dry  and  hard,  thus  lacking  the  smooth- 
ness which  normally  enables  them  to  slide  without  friction  along  the 


CAUSES  OF  CONSTIPATION  127 

mucous  lining  of  the  intestine.  Overloading  the  intestines  with 
food  of  a  coarse  and  bulky  nature  may  give  rise  to  constipation  by 
overdistending  and  weakening  the  intestinal  tube.  Beverages  which 
contain  tannin,  like  tea  or  red  wines,  may  lessen  intestinal  secretion 
and  so  cause  constipation. 

3.  Negligence  in  the  regularity  of  defecation  and  of  eating,  imper- 
fect mastication,  sudden  changes  in  the  quantity  and  quality  of  food, 
sedentary  habits  and  consequent  insufficient  exercise,  are  more  or 
less  potent  factors  in  causing  intestinal  torpidity. 

4.  Alterations  in  the  quantity  or  quality  of  the  digestive  fluids 
may  induce  constipation  ;  so  also  may  a  deficiency  of  bile,  by  depriving 
intestinal  peristalsis  of  a  powerful  stimulus. 

5.  Profuse  and  long-continued  siveating  from  heat,  exercise,  dis- 
ease, or  drugs,  or  polyuria  of  diabetic  or  other  origin,  may  produce 
constipation  by  lessening  the  fluidity  of  the  intestinal  contents. 

6.  Fever,  unless  the  disease  has  diarrhcea  as  a  symptom,  is  usually 
attended  by  constipation,  because  of  the  diminished  secretion  of  the 
digestive  and  other  fluids  which  is  the  common  concomitant  of  the 
febrile  process. 

7.  Constipation  may  be  due  to  a  weakened  cotidition  of  the  abdom- 
inal muscles,  on  account  of  which  the  voluntary  expulsive  effort  of 
defecation  can  not  be  made,  as  in  the  distention  resulting  from 
pregnancy,  abdominal  tumour,  and  obesity. 

8.  There  are  certain  local  conditions  which  may  inhibit  the  empty- 
ing of  the  rectum  by  causing  pain,  with  consequent  reflex  spasm  of 
the  anal  sphincter.  These  are  fissure  of  the  anus,  inflamed  hemor- 
rhoids, ulcer  of  the  rectum  in  the  neighbourhood  of  the  anus,  irri- 
table or  inflamed  prostate  gland,  and  a  tender  and  prolapsed  uterus 
or  ovary. 

9.  A  frequent  cause  of  constipation  is  a  deficietit  excitability  of 
the  motor  apparatus  of  the  intestine.  This  may  be  due  to  deranged 
innervation,  or  to  an  atonic  or  degenerated  condition  of  the  muscular 
layer  of  the  intestine,  or  both.  As  a  manifestation  of  disordered 
nervous  action  it  attends  myelitis,  tetanus,  and  meningitis,  and  occurs 
as  a  symptom  in  hysteria,  neurasthenia,  and  anaemia,  or  conditions  of 
malnutrition.  Acute  inflammations  involving  the  peritoneum,  as  in 
peritonitis  and  some  cases  of  appendicitis,  may  cause  a  very  obstinate 
constipation  by  producing  paresis  of  the  intestinal  musculature  ;  so 
also  with  acute  hemorrhagic  pancreatitis.  Chronic  portal  congestion 
from  hepatic  or  cardiac  disease,  or  chronic  inflammation  of  the  intes- 
tinal mucosa  may  lead  to  degeneration  of  the  muscular  fibres,  and 
consequent  loss  of  propulsive  power. 

10.  The  custom  of  taking  purgatives  is  in  some  cases  responsible 


128  THE  EVIDENCES  OF  DISEASE 

for  confirmed  constipation,  because  of  overstimulation  and  consequent 
loss  of  response  to  normal  excitation. 

11.  A  special  loss  of  power  in  the  colon,  mainly  at  the  sigmoid 
flexure,  is  not  infrequently  encountered,  leading  to  a  large  accumula- 
tion of  hard  rounded  masses  in  this  locality.  This  may  result  from 
long-continued  inflammation  of  the  mucous  lining,  dilatation  of  the 
colon,  or  chronic  dysentery  or  ulceration ;  and  occurs  also  in  con- 
nection with  uterine  disease,  hysteria,  and  neurasthenia.  It  may  be 
found  in  very  old  people,  demonstrable  lesions  being  absent. 

12.  Constipation  may  be  due  to  a  contracted  state  of  the  small 
and  large  intestine  (spasmodic  constipation),  the  inhibitory  fibres  of 
the  splanchnic  being  irritated,  as  in  hysteria,  ovarian  or  uterine  dis 
ease,  and  chronic  plumbism ;  and  requiring  sedatives  and  antispas- 
modics rather  than  laxatives. 

13.  It  may  happen  that  constipation  is  an  obtrusive  symptom  in 
cases  of  esophageal  and  pyloric  stenosis,  resulting  from  the  limited 
amount  of  food  which  enters  the  intestine ;  but  ordinarily  the  vomit- 
ing which  occurs  is  sufficient  to  direct  attention  to  the  stomach. 

14.  Acute  intractable  constipation  should  always  suggest  an 
examination  of  the  various  sites  of  hernia  before  concluding  that  an 
intra-abdominal  obstructive  cause,  instead  of  hernial  strangulation, 
is  responsible  for  the  failure  of  laxatives. 

15.  The  most  important  and  serious  condition  which  may  be  indi- 
cated by  constipation  is  some  form  of  intestinal  obstruction.  Obstinate 
constipation  not  yielding  to  appropriate  remedies  should  always 
arouse  suspicion,  especially  if  associated  with  vomiting,  distention, 
and  abdominal  pain.  Such  symptoms  coming  on  abruptly  are  very 
suggestive  of  acute  obstruction.  In  the  chronic  varieties  the  consti- 
pation is  gradual  in  its  coming,  in  some  cases  extremely  variable,  and 
may  be  interspersed  with  acute  exacerbations.  It  should  be  remem- 
bered that  the  faecal  accumulation,  especially  in  obstruction  from 
impaction,  may  become  tunnelled,  and  a  deceptive  regularity  of  the 
bowels,  or  even  a  diarrhoea,  be  present,  requiring  careful  palpation  of 
the  abdomen  and  a  digital  examination  of  the  rectum. 

B.    DIARRHCEA 

Diarrhoea  may  be  acute  or  chronic.  The  stools,  more  or  less  fluid 
in  consistence,  vary  in  number  from  3  or  4  in  24  hours  to  the  almost 
continuous  purging  of  cholera.  According  to  its  cause  it  may  or 
may  not  be  attended  by  fever,  abdominal  pain,  rumbling,  and  dis- 
tention. 

Excessive  peristalsis  with  abnormal  fluidity  of  the  stools  may 
result  from  one  or  all  of  three  things :  {a)  Increased  irritability  of" 


CAUSES  OP  DIARRHOEA  129 

the  nervous  mechanism,  so  that  it  responds  with  unusual  vigour  to 
stimulation,  (b)  The  presence  of  abnormal  or  irritating  substances 
in  the  intestine  or  the  action  of  other  unaccustomed  stimuli  upon 
the  nerves,  (c)  A  hyperaemic  condition  of  the  intestinal  mucosa  with 
hypersecretion  or  transudation. 

Without  attempting  to  recapitulate  in  detail  all  of  the  etiological 
possibilities  of  the  symptom,  diarrhoea,  the  following  paragraphs 
present  those  which  are  of  diagnostic  importance  : 

1.  An  acute  diarrhoea  with  2  to  8  watery  stools,  without  pain  or 
nausea,  may  be  caused  by  psychic  influences^  as  in  the  examination 
diarrhoea  of  students.  It  is  commonly  spoken  of  as  nervous  diar- 
rhoea. 

2.  An  acute,  watery  diarrhoea  of  brief  duration,  with  or  without 
pain,  may  be  an  "  intestinal  crisis"  of  locomotor  ataxia,  exophthalmic 
goitre,  or  movable  kidney. 

3.  A  persistent  diarrhoea  occurring  in  the  early  morning,  2  or  3 
stools  being  passed  at  short  intervals,  with  freedom  for  the  rest  of 
the  day,  and  attended  with  neurasthenic  symptoms,  is  the  "  morning 
diarrhoea  "  of  Delafield  and  others. 

4.  Paroxysmal  diarrhoea,  preceded  and  accompanied  by  much  pain, 
usually  in  the  left  iliac  fossa,  terminating  with  the  discharge  of 
strings  or  membranes  composed  of  mucus,  and  occurring  in  an  indi- 
vidual, usually  a  woman,  who  presents  neurasthenic  or  hysterical 
symptoms,  constitutes  the  disease  known  as  mucous  colic  or  mem- 
branous enteritis. 

5.  Sudden  diarrhoeal  attacks  occurring  at  intervals  of  days  or 
weeks,  as  well  as  a  chronic  diarrhoea,  may  be  due  to  hysteria^  but 
caution  should  be  exercised  in  making  this  diagnosis  before  excluding 
other  possible  causes. 

6.  It  is  a  good  rule  to  examine  the  urine  in  all  cases  of  chronic, 
or  repeated  acute,  diarrhoeas,  as  they  may  be  vicarious  efforts  to 
lessen  the  uraemia  of  nephritis,  or  be  due  to  the  secondary  intestinal 
catarrh  of  the  same  disease. 

7.  By  far  the  most  common  cause  of  diarrhoea  is  some  form  of 
enteritis^  catarrhal,  croupous,  or  ulcerative. 

The  etiological  factors  of  catarrhal  enteritis  {q.  v.)  are  various — 
e.  g.,  sudden  changes  in  the  temperature,  hot  summer  weather,  too 
much  food  or  indigestible  food,  the  presence  of  ptomaines  or  toxines 
(resulting  from  the  activity  of  micro-organisms),  or  inorganic  toxic 
substances  (arsenic,  antimony),  the  profound  exhaustion  resulting 
from  Addison's  disease,  pernicious  anaemia,  syphilis,  and  cancer,  or 
chronic  portal  congestion. 

8.  An  acute  diarrhoea  with  frequent  large  serous  stools,  usually 


130  THE  EVIDENCES  OF   DISEASE 

with  severe  vomiting,  is  indicative  of  cholera  infantum,  cholera  mor- 
bus, cholera  Asiatica,  ingestion  of  poisonous  mushrooms,  or  acute 
antimonial  or  arsenical  poisoning.  In  poisoning  by  arsenic  the  stools 
are  generally  bloody.  More  rarely  there  may  be  serous,  scalding 
stools  in  cancer  of  the  rectum,  and  very  watery,  almost  serous,  evacu- 
tions  may  be  indicative  of  an  unusually  severe  catarrhal  enteritis  or 
the  gastro-intestinal  form  of  epidemic  influenza. 

9.  An  acute  diarrhoea,  the  stools  at  first  fluid-ftecal,  becoming 
small,  bloody,  and  containing  large  amounts  of  mucus,  or  composed 
entirely  of  gelatinous  mucus,  and  voided  with  great  tenesmus,  is 
characteristic  of  acute  dysentery.  Tenesmus,  with  frequent  passing 
of  a  small  amount  of  mucus,  may  be  due  to  acute  inflammation  of 
the  rectum  (proctitis),  syphilitic  ulceration  of  the  rectum,  and  can- 
cer of  the  rectum  or  sigmoid  flexure.  Tenesmus  and  bloody  stools 
in  children  should  invariably  cause  a  suspicion  of  intussusception. 

10.  Fissure  of  the  anus  and  stricture  of  the  rectum  may  produce 
a  diarrhoea  from  irritation,  either  direct  or  reflex,  due  to  accumulated 
faeces. 

11.  It  should  be  remembered  that  while  constipation  is  usually 
present  in  appendicitis,  yet  sometimes  in  adults,  and  not  infrequently 
in  children,  a  diarrhoea  may  be  one  of  the  initial  symptoms. 

12.  In  considering  diarrhcea  as  a  symptom,  the  possibility  of  its 
occurrence  as  an  indication  of  constipation  should  always  be  borne 
in  mind.  An  accumulated  mass  of  faeces  may  become  channelled,  or 
the  presence  of  separate  hard  rounded  masses  in  the  colon  or  its  sig- 
moid flexure  may  cause  colitis  with  frequent  evacuations  of  scybala 
coated  with  mucus  and  sometimes  bloody.  The  diagnosis  is  to  be 
made  by  palpation  of  the  abdomen  and  digital  examination  of  the 
rectum.  This  condition  may  be  present  in  the  latter  stages  of 
typhoid  fever,  and  the  febrile  temperature  thus  be  unduly  prolonged. 

13.  It  is  evident  that  diarrhoea  is  a  symptom  of  wide  affiliations. 
As  a  rule,  the  associated  symptoms  are  such  as  to  explain  its  occur- 
rence. The  cases  in  which  the  clinician  is  particularly  liable  to  fall 
into  the  error  of  supposing  an  acute  or  chronic  catarrhal  enteritis 
to  be  the  only  existing  condition  are  the  diarrhoea  of  constipation, 
cancer  of  the  rectum,  and  intussusception  or  appendicitis  in  children. 

C.    INCONTINENCE    OF    F>ECES 

The  discharge  of  faeces  is  regulated  by  a  centre  in  the  lumbar 
enlargement  of  the  cord  with  afferent  fibres  from  the  rectum  and 
efferent  fibres  to  the  sphincter  ani.  The  lumbar  centre  may  be 
inhibited  or  helped  to  a  considerable  extent  by  voluntary  impulses 
from  the  brain.     So  long  as  the  rectum  is  empty  the  sphincter  is 


F^CAL  INCONTINENCE— PAINFUL  DEFECATION  131 

closed,  largely  by  its  own  elasticity  and  tonus.  When  faeces  enter 
the  rectum,  sensory  impulses  pass  to  the  lumbar  centre  and  the  brain, 
and,  according  to  circumstances,  the  reflex  act  of  defecation  is  either 
resisted  or  facilitated  by  the  will. 

Incontinence  of  faeces,  perhaps  only  for  fluid  or  semifluid  stools, 
may  be  present  as  a  result  of  impaired  intelligence  in  the  insane,  in 
idiots,  and  delirious  persons,  and  in  all  diseases  attended  with  coma 
or  profound  prostration.  It  is  sometimes  a  symptom  of  paralysis  of 
the  sphincter  ani,  or  an  injury  of  the  pelvic  floor,  or  of  disease  of  the 
lower  portion  of  the  rectum  which  interferes  with  sphincteric  con- 
traction. Spasmodic  contractions  of  the  rectum  and  the  abdominal 
muscles  may  forcibly  expel  the  faeces  without  volition  on  the  part  of 
the  patient. 

Incontinence  of  faeces,  therefore,  may  occur  in  the  following  con- 
ditions :  Apoplexy,  uraemia,  epileptic  coma,  meningitis,  insolation, 
hydrocyanic-acid  poisoning,  shock,  typhoid  fever,  the  typhoid  state, 
cholera  morbus,  cholera  infantum,  cholera  Asiatica,  dysentery,  mye- 
litis and  some  other  diseases  of  the  spinal  cord,  the  grave  form  of 
chorea  ;  tetanus  and  strychnine  poisoning,  or  other  diseases  of  which 
convulsions  are  a  manifestation ;  laceration  of  the  perinaeum  involv- 
ing the  sphincter  ani,  or  surgical  overstretching  of  the  latter,  and 
cancerous  or  syphilitic  infiltration  of  the  rectum.  In  medical  prac- 
tice incontinence  of  faeces  is  most  frequently  encountered  in  the 
typhoid  state. 

D.    PAINFUL    DEFECATION 

Pain  during  defecation  may  or  may  not  be  conjoined  with  rectal 
tenesmus.  Very  severe  pain  after  going  to  stool,  which  may  last  for 
several  hours  and  then  gradually  subside,  only  to  be  renewed  at  the 
next  evacuation  of  the  rectum,  the  stools  being  at  times  streaked 
with  blood,  is  very  significant  of  an  anal  fissure.  Pain  may  be  due  to 
the  passage  of  a  large,  hard  mass  of  faecal  matter  or  to  the  presence 
of  hemorrhoids,  prolapsus  ani,  or  an  inflamed  and  swollen  prostate 
gland.  Great  rectal  discomfort  is  not  infrequently  explained  by  the 
presence  of  salpingitis  and  pelvic  peritonitis,  and  may  result  from 
cancer  of  the  cervix,  a  retroflexed  tender  uterus,  coccygodynia,  or 
cancer  of  the  rectum. 

Obviously,  the  principal  diagnostic  requirement  of  pain  occurring 
with  defecation  is  a  digital  and,  if  a  sufficient  cause  does  not  appear 
without  it,  an  instrumental  examination  of  the  pelvic  contents. 


132  THE   EVIDENCES  OF  DISEASE 

E.    RECTAL   TENESMUS 

A  persistent  inclination  to  defecate,  accompanied  by  painful  and 
largely  ineffectual  efforts  so  to  do,  constitutes  rectal  tenesmus,  a 
symptom  of  much  diagnostic  importance.  In  conjunction  with 
colicky  pain  and  stools  of  bloody  mucus,  it  is  characteristic  of  the 
various  forms  of  dysentery,  and  is  found  to  a  much  milder  degree  in 
severe  catarrhal  enteritis.  It  may  be  present  in  the  diarrhoea  caused 
by  irritant  poisons,  especially  cantharides.  Associated  with  vesical  te- 
nesmus it  is  indicative  of  a  calculus  in  the  urinary  bladder  or  a  symp- 
tom of  mucous  colic  (membranous  enteritis).  Eectal  tenesmus  may 
also  be  caused  by  impacted  faeces,  worms,  or  a  foreign  body  in  the 
rectum,  hemorrhoids,  and  proctitis.  It  is  very  commonly  present  in 
cases  of  rectal  polypus,  adenoma,  and  cancer  of  the  rectum.  In 
infants  or  children  tenesmic  stools,  consisting  of  bloody  mucus  with- 
out faecal  matter,  are  significant  of  intussusception.  Earely  rectal 
tenesmus  may  indicate  an  enlarged  and  retroflexed  uterus. 

F.  THE  CHARACTER  AND  ABNORMAL  CONTENTS 
OF  THE  STOOLS 

Valuable  information  may  be  obtained  by  a  naked-eye  inspection 
of  the  stools,  this  inspection  relating  to  their  odour,  reaction,  shape, 
consistence,  colour,  and  contents.  The  microscopical  examination 
of  the  faeces  {q.  v.)  is  considered  elsewhere. 

1.  The  Shape  of  the  Stools. — {a)  A  stool  of  normal  consistence, 
cylindrical  in  shape  but  of  unusually  small  calibre,  is  significant  of 
prolapsus  ani  or  an  annular  stricture  of  the  rectum.  More  rarely  a  stool 
of  this  shape  is  indicative  of  the  early  stage  of  an  intussusception. 

(J)  Ribbon-shaped  or  flattened  stools  of  normal  consistence  arouse 
a  suspicion  of  the  existence  of  stricture  or  cancer  of  the  rectum. 
More  rarely  this  finding  may  indicate  ischio-rectal  or  prostatic  ab- 
scess or  great  enlargement  of  the  prostate,  large  hemorrhoids,  pro- 
lapse of  the  uterus,  or  perhaps  spasm  of  the  anus  and  lower  bowel. 

(c)  Scybala — roundish  masses  of  hardened  faeces — are  found  in 
many  cases  of  habitual  constipation,  especially  when  atony  and  sac- 
culation of  the  colon  coexist.  They  are  of  common  occurrence  in 
gastric  ulcer,  gastric  dilatation,  and  cancer  of  the  rectum.  Tliey  are 
apt  to  be  present  in  the  constipation  resulting  from  the  use  of  opium, 
and  small  round  balls  may  be  shot  out  of  the  anus  during  the  strain- 
ing efforts  attendant  upon  dysentery. 

2.  The  Odour  and  Reaction  of  the  Stools. — A  sour  odour,  as  com- 
pared to  the  faecal  odour  of  the  healthy  adult  stool,  is  normal  for  the 
nursing  infant.     An  unusually  offensive  but  not  putrid  odour  is  found 


CHARACTER  OF  THE  STOOLS  133 

as  a  symptom  of  jaundice  or  other  conditions  in  which  there  is  a  defi- 
ciency of  bile  in  the  intestine ;  in  acute  indigestion,  acute  enteritis, 
typhoid  fever,  erysipelas,  rachitis,  and  occasionally  in  ordinary  con- 
stipation. A  musty,  mousy  odour  is  associated  with  cholera  infantum. 
Ill-smelling  stools  are  caused  by  the  taking  of  sulphur  or  the  eating 
of  eggs,  with  the  consequent  formation  of  sulphuretted  hydrogen. 
Stools  with  a  foul  and  putrid  odour  are  suggestive  of  syphilitic  or 
carcinomatous  ulceration  of  the  rectum  or  gangi'enous  dysentery. 

There  is  at  present  little  of  clinical  value  to  be  learned  from  the 
reaction  of  the  stools.  It  is  normally  faintly  acid  in  the  infant,  and 
an  alkaline  reaction  in  this  case  is  of  some  significance  with  refer- 
ence to  the  nature  of  the  fermentative  processes  which  are  under  way 
in  the  intestine.  It  may  be  either  acid  or  alkaline,  according  to  the 
variety  of  micro-organisms  which  are  present,  in  the  diarrhoeas  of 
infants  and  children. 

3.  The  Consistence  of  the  Stools. — {a)  Semifluid  or  fluid  faecal 
stools  are  found  in  the  great  majority  of  cases  in  which  diarrhoea  is  a 
symptom,  embracing  the  ordinary  diarrhoeas  and  the  various  forms  of 
catarrhal  enteritis.  At  the  onset  of  the  attack  the  solid  or  semisolid 
contents  of  the  rectum  are  discharged ;  but  very  shortly,  owing  to  the 
increased  amount  of  fluid  poured  out  by  the  intestinal  mucous  mem- 
brane, the  stools  become  fluid  or  semifluid  in  consistence,  still,  how- 
ever, retaining  a  faecal  character. 

{h)  Serous  stools,  composed  of  fluid  without  faecal  matter,  are  of 
considerable  diagnostic  importance.  Such  stools  are  significant  of 
cholera  Asiatica,  cholera  morbus,  cholera  infantum,  and  poisoning  by 
antimony.  Arsenical  poisoning  also  may  be  attended  by  a  serous  diar- 
rhoea, and  an  unusually  severe  acute  catarrhal  enteritis  may  present 
this  variety  of  stool.  In  cancer  of  the  rectum  the  evacuations  may 
be  small,  serous,  and  frequent.  Poisoning  by  the  non-edible  mush- 
rooms is  another  possible  but  infrequent  cause  of  serous  stools. 

4.  The  Colour  of  the  Stools. — The  colour  of  the  stool  may  be 
altered  by  the  kind  of  food  which  has  been  eaten.  In  an  exclusive 
milk  diet  the  stools  are  light  yellow,  as  indeed  they  may  be  if  starchy 
foods  form  a  large  proportion  of  the  ingesta.  Fruits  with  deep-red 
juice  and  red  wines  darken  the  stools. 

(«)  Clay-coloured  stools  are  usually  significant  of  a  deficient 
amount  of  biliary  colouring  matter  in  the  intestine,  due  either  to  an 
obstruction  to  the  flow  of  bile  from  the  common  duct  or  to  an  im- 
paired bile  formation.  Obstruction  of  the  common  duct  by  a  cal- 
culus, or  of  the  large  and  small  ducts  by  inflammation  and  conse- 
quent swelling  of  their  lining  membrane,  are  the  most  frequent 
causes  of  clay-coloured  stools.  More  rarely  a  tumour  or  a  movable 
11 


134  THE  EVIDENCES  OF  DISEASE 

kidney,  by  pressing  upon  or  causing  kinking  of  the  common  duct, 
may  be  responsible  for  the  lack  of  colouring  matter.  Light-coloured 
stools  may  be  significant  of  impaired  bile  formation  resulting  from 
anaemia,  rachitis,  or  chronic  lead  poisoning,  as  well  as  cancer,  cirrho- 
sis, or  amyloid  disease  of  the  liver.  Such  stools  occur  also  in  connec- 
tion with  acute  yellow  atrophy  of  the  liver  and  phosphorus  poisoning. 

{b)  Green  stools,  when  occurring  in  infancy,  are  commonly  caused 
by  the  growth  of  a  chromogenic  or  colour-forming  bacterium  in  the 
intestine.  The  greenish  or  greenish-yellow  defecations  resulting 
from  the  administration  of  calomel  are  suiSiciently  familiar,  and,  like 
the  similar  "  bilious  "  stool,  are  caused  by  an  increased  peristalsis 
sweeping  the  bile  out  before  it  undergoes  its  customary  alteration. 
An  unusual  amount  of  bile  may  be  present  in  any  case  of  chronic 
diarrhoea  or  acute  enteritis. 

(c)  Black  stools  may  be  due  to  the  administration  of  iron,  man- 
ganese, or  bismuth.  "  Tarry  "  and  red  stools  are  considered  in  con- 
nection with  the  abnormal  constituents  of  the  faeces. 

5.  Abnormal  Contents  of  the  Stools. — The  stools  may  contain  un- 
digested food,  blood,  mucus,  pus,  membranes,  fat ;  calculi  from  the 
gall  bladder,  intestines,  stomach,  salivary  glands,  or  tonsils ;  foreign 
bodies,  intestinal  parasites,  exfoliated  polypi,  and  segments  of  exfoli- 
ated intussusceptions  and  necrotic  sloughs. 

(a)  Undigested  portions  of  food  (lienteric  diarrhoea)  may  be  in- 
dicative of  an  acute  dyspeptic  diarrhoea,  or  of  imperfect  mastication 
or  digestion.  In  fevers  the  appearance  of  milk  curds  is  an  important 
sign  of  overfeeding,  and  a  similar  discovery  in  the  stools  of  an  infant 
is  a  reliable  sign  of  an  improper  quantity  or  quality  of  food,  and  not 
infrequently  heralds  an  acute  attack  of  gastro-intestinal  disturbance. 

(b)  Blood  in  the  stools  may  show  itself  in  its  characteristic  red 
colour,  or  as  "  tarry  "  stools  (melcena),  according  to  the  source  of 
the  bleeding  and  the  length  of  time  it  has  remained  in  the  intestine. 
If  it  has  its  origin  in  the  upper  portion  of  the  digestive  tract  (stom- 
ach or  small  intestine),  it  is  altered  by  the  action  of  the  digestive 
fluids  so  as  to  assume  a  black  or  brownish-black  appearance,  or  may 
resemble  coffee  grounds.  If  there  is  active  peristalsis,  or  if  the  blood 
is  in  large  amount,  it  may,  even  if  coming  from  the  upper  part  of 
the  small  intestine,  pass  so  rapidly  along  that  it  issues  almost  un- 
changed with  the  stool.  As  a  general  rule,  however,  bright  blood  in 
the  defecation  comes  from  the  lower  part  of  the  bowel,  particularly 
from  the  rectum.  The  more  thoroughly  the  blood  is  mixed  with  the 
faeces,  and  the  more  marked  the  tarry  appearance,  the  greater  is  the 
probability  of  its  origin  from  the  upper  portion  of  the  alimentary 
canal. 


ABNORMAL  CONTENTS  OP  STOOLS  135 

If  there  is  any  question  as  to  the  presence  of  blood  in  the  stools,  it  may  be 
identified  either  by  the  microscope  or  by  chemical  methods,  or  both.  Under 
the  microscope  the  red  cells  may  be  distinguished,  or  if  these  cells  are  disinte- 
grated, brownish-red  masses  may  be  seen  Vhich  are  composed  of  amorphous 
ha^matoidin.  In  a  certain  proportion  of  cases  the  hasmatoidin  may  be  found  in 
crystals  of  the  characteristic  rhombic  shape.  In  the  absence  of  well-preserved 
corpuscles  or  crystals,  the  haemin  test  (page  123)  must  be  applied.  As  a  pos- 
sible source  of  error,  the  red  colour  imparted  to  the  stools  by  the  administra- 
tion of  haematoxylon  or  the  ingestion  of  a  large  quantity  of  red  fruits  or  fruit 
juices  may  be  borne  in  mind. 

1.  Tarry  stools  may  be  indicative  of  a  gastric  hemorrhage  due  to 
ulcer,  cancer,  or  ruptured  varicose  esophageal  veins.  The  blood  may 
have  been  originally  derived  from  the  lungs  or  the  nose,  a  certain 
amount  having  been  swallowed,  so  that  any  case  of  epistaxis,  haemop- 
tysis, or  (especially)  haematemesis  may  be  followed  by  black  and  tarry 
stools.  Duodenal  ulcer  and  multiple  ulcers  of  the  small  intestine 
(syphilitic,  dysenteric,  or  typhoid)  may  also  be  responsible.  Portal 
obstruction  from  any  cause,  particularly  hepatic  cirrhosis  or  cancer, 
may  be  attended  by  melaena  ;  so  also  may  acute  yellow  atrophy  of  the 
liver,  purpura  haemorrhagica,  hemophilia,  and  leucaemia. 

2.  Bloody  stools  in  which  the  red  colour  of  the  blood  has  not  been 
destroyed  by  the  action  of  the  digestive  fluids  may  occur  in  any  of 
the  conditions  enumerated  above  as  causing  tarry  stools,  provided 
the  blood  is  in  sufficient  amount ;  and,  similarly,  some  of  the  diseases 
and  conditions  about  to  be  mentioned  as  possible  causes  of  bloody 
stools  may  give  rise  to  coffee-ground  or  tarry  defecations. 

A  frequent  source  of  blood  in  the  stools  is  a  bleeding  hemorrhoid. 
Cancer  of  the  rectum,  fissures,  and  ulcers  (especially  syphilitic)  may 
give  rise  to  blood-covered  stools,  particularly  if  the  faeces  are  dry, 
hard,  and  lumpy.  Indeed,  the  latter  condition  alone,  in  the  absence 
of  rectal  disease,  may  abrade  the  mucous  membrane  of  the  rectum  so 
as  to  cause  bloody  faeces.  In  children  and  feeble-minded  persons  the 
possible  presence  of  foreign  bodies  should  be  borne  in  mind.  An 
acute  proctitis  is  an  additional  rectal  source  of  blood-stained  stools. 
A  polypus  of  the  rectum,  if  it  becomes  eroded,  may  bleed  profusely. 

Strangulated  hernia  and,  in  a  child,  intussusception  should  be 
suspected,  the  latter  especially,  in  the  presence  of  blood-stained  stools 
composed  principally  of  mucus  and  attended  with  tenesmus.  An 
acute  and  unusually  severe  colitis  in  children  may  manifest  itself  by 
blood-streaked  passages.  The  various  forms  of  dysentery  may  pre- 
sent stools  which  have  the  appearance  of  rusty-red  fleshy  lumps. 
Cancer  or  ulceration  of  the  large  or  small  intestine,  from  whatever 
cause,  as  well  as  the  perforation  resulting  from  such  ulceration,  may 


136  THE  EVIDENCES  OF  DISEASE 

explain  the  appearance  of  blood  in  the  fasces.  According  to  Grainger 
Stewart,  amyloid  disease  of  the  intestine  may  cause  hemorrhage. 
Corrosive  poisons,  especially  arsenic,  may  determine  the  presence  of 
streaks  of  blood  in  the  passages. 

The  rupture  of  an  aneurism  of  the  abdominal  aorta  into  the  ali- 
mentary canal  serves  to  explain  some  cases  of  large  hemorrhage  from 
the  bowel.  Aneurism  or  thrombosis  of  the  superior  mesenteric  artery, 
to  which  attention  has  been  particularly  directed  by  Watson  and 
Elliot,  is  a  condition  which  produces  tarry  or  bloody  stools. 

Engorgement  of  the  portal  circulation  from  cancer  or  cirrhosis  of 
the  liver,  or  as  the  result  of  valvular  disease  of  the  heart,  pulmonary 
emphysema,  or  portal  thrombosis,  demands  consideration  as  a  cause  of 
intestinal  hemorrhage.  In  jaundice,  whatever  its  origin,  blood  may 
be  contained  in  the  stools,  as  well  as  in  phosphorus  poisoning.  In 
various  infectious  diseases,  among  them  yellow  fever,  pernicious  ma- 
larial fever,  dengue,  acute  yellow  atrophy  of  the  liver,  septicaemia, 
pyaemia,  and  typhoid  fever  (usually  from  an  intestinal  ulcer),  blood 
in  varying  quantity  and  colour  may  be  a  constituent  of  the  stools. 

Intestinal  hemorrhage  may  be  a  symptom  of  leucaemia,  haemo- 
philia, purpura  haemorrhagica,  and  scurvy.  In  the  occasional  sudden 
diarrhoeal  attacks  of  exophthalmic  goitre,  bloody  mucus  is  sometimes 
present.  Intestinal  hemorrhage  not  due  to  tuberculous  ulceration 
may  appear  as  an  intercurrent  event  in  pulmonary  phthisis.  Finally, 
injuries  of  the  abdomen  and  intestinal  parasites  may  give  rise  to  bleed- 
ing from  the  bowel. 

3.  Most  Frequent  Causes  of  Blood  in  the  Stools. — It  is  evident 
that  a  decision  as  to  the  origin  of  the  blood  in  a  given  case  can  be 
reached  only  by  a  careful  consideration  of  the  history  and  symptoms, 
as  well  as  a  painstaking  physical  examination.  It  may  be  of  service 
to  bear  in  mind  that  the  most  frequent  causes  of  hemorrhage  from 
the  bowel  are  hemorrhoids,  typhoid  fever,  colitis,  and  cancer  of  the 
colon  ;  that  the  most  frequent  causes  of  la7'ge  intestinal  hemorrhages 
are  typhoid  fever,  portal  engorgement  from  disease  of  the  heart  or 
liver,  haemophilia,  purpura  haemorrhagica,  and  rupture  of  an  aneur- 
ism ;  that  the  most  frequent  causes  of  small  hemorrhages  from  the 
bowel  are  hemorrhoids,  injury  to  the  rectum  or  a  rectal  fissure  by 
the  passage  of  faeces,  ulceration  (syphilitic  or  cancerous)  of  the  rec- 
tum, and  intussusception  in  infants  and  children. 

The  extent  of  an  intestinal  hemorrhage,  and  on  occasion  its  oc- 
currence before  appearing  in  the  stools,  may  be  judged  by  the  con- 
stitutional symptoms,  which  are  those  of  internal  hemorrhage  (q.  v.). 

(c)  Mucus  in  small  and  almost  unnoticeable  quantities  is  present 
in  health  in  the  form  of  small  particles  adherent  to  the  faeces.     An 


ABNORMAL  CONTENTS  OF  STOOLS  137 

increased  amount  is  ordinarily  significant  of  a  catarrhal  process  in 
some  portion  of  the  intestine.  If  in  considerable  quantity,  forming 
a  thick  coating  upon  the  faeces,  or  if  the  entire  defecation  is  com- 
posed of  mucus,  it  indicates  inflammation  of  the  mucous  membrane 
of  the  rectum  or  large  intestine.  If  in  smaller  quantity,  and  con- 
tained in  thin  stools,  or  mixed  and  thoroughly  diffused  through 
faecal  matter,  it  indicates  a  catarrhal  process  in  the  small  intestine. 
Mucus-containing  stools  constitute  a  symptom  of  the  various  forms 
of  dysentery,  entero-colitis,  proctitis,  and  impaction  of  faeces.  The 
characteristic  stool  of  intussusception  is  composed  of  bloody  mucus. 
Membranes,  fragments,  or  tubular  casts  composed  of  altered  mucus 
are  voided  in  the  disease  known  as  membranous  enteritis  {mucous 
colic).  Allied  to  this  disease  are  the  attacks  of  mucous  diarrhoea 
which  may  occur  during  the  course  of  exophthalmic  goitre,  and  in 
connection  with  movable  kidney  and  enteroptosis. 

{d)  Pus  in  the  faeces,  if  in  large  quantity,  is  indicative  of  the 
rupture  of  an  abscess  (pelvic,  periproctitic,  or  perinephritic)  into  the 
alimentary  canal.  In  smaller  quantities  it  is  significant  of  dysen- 
tery, enteritis,  proctitis,  and  syphilitic  or  cancerous  ulceration  of  the 
rectum  or  colon.  It  may  be  derived  from  the  urethra  or  vagina  as  a 
result  of  a  severe  inflammation  of  their  lining  membrane. 

{e)  Membranous  shreds^  not  composed  of  mucus,  are  found  in 
rare  cases  as  the  result  of  a  superficial  necrosis  and  sloughing  of 
the  intestinal  mucous  membrane  which  may  occur  in  the  course 
of  acute  proctitis,  cancer  of  the  colon,  dysentery,  and  relapsing 
fever. 

(/)  Fatty  stools^  which  may  be  recognised  by  their  oily,  greasy 
appearance,  are  found  in  association  with  obstructive  jaundice  be- 
cause of  the  deficient  absorption  of  hydrocarbons  resulting  from  the 
absence  of  bile.  Indigestion  or  overfeeding  in  infants  may  give 
rise  to  fat-containing  stools.  In  the  absence  of  jaundice  or  (in 
infants)  impaired  digestive  capaicity,  the  occurrence  of  a  fatty  diar- 
rhoea should  suggest  cancer  of  the  pancreas,  or  pancreatic  calculi 
impacted  in  the  pancreatic  duct. 

{g)  Gallsto7ies,  if  suspected,  must  be  searched  for  by  breaking  up 
the  faeces  in  a  sieve  while  pouring  water  over  the  mass.  Multiple 
stones  formed  in  the  gall  bladder  are  faceted,  especially  if  ejected 
soon  after  their  emergence  from  the  common  duct  and  before  any 
solvent  action  is  exerted  upon  them  by  the  intestinal  fluids.  Very 
rarely  a  gallstone  is  found  which,  being  very  small,  non-faceted,  and 
crumbling  easily,  may  be  conjectured  to  have  been  formed  in  the 
intra-hepatic  ducts.  Gallstones  are  most  commonly  composed  of 
cholesterin,  in  which  case  they  float  in  water ;  less  frequently  of  in- 


138  THE  EVIDENCES  OF  DISEASE 

spissated  bile  or  calcareous  salts,  and  are  heavier  than  water.     The 
other  calculi  found  in  the  stools  are  very  rare. 

(A)  Foreign  bodies^  when  found,  usually  indicate  childhood,  men- 
tal infirmity,  a  depraved  taste,  or  a  professional  freak.  Conversely^ 
suspect  foreign  bodies  with  such  patients. 

{%)  Intestinal  Parasites  (see  also  Index). — Ascaris  liimhricoides, 
— If  a  cylindrical  worm,  pointed  at  both  ends,  of  a  yellowish  or 
slightly  reddish  colour,  and  varying  from  10  to  30  centimetres  (4  to 
12  inches)  in  length,  is  found  in  the  stools,  it  is  the  Ascaris  lumhri- 
coides,  or  roundworm.  The  patient  is  usually  a  child  and  the  worm 
is  the  most  common  human  parasite.  On  closer  inspection  the 
worm  is  seen  to  be  transversely  striated  and  to  possess  four  longitu- 
dinal bands.  It  exhibits  considerable  motility,  and  this  power  of 
migration  gives  rise,  fortunately  in  rare  instances,  to  serious  conse- 
quences. Thus  this  parasite  has  crawled  from  the  upper  part  of  the 
small  intestine,  which  is  its  ordinary  habitat,  into  the  common  bile 
duct  and  the  intra-hepatic  ducts ;  perforated  the  wall  of  the  intestine 
and  caused  peritonitis  ;  crawled  into  the  stomach,  esophagus,  pharynx, 
and  thence  into  the  Eustachian  tube,  emerging  from  the  external 
ear.  Passing  into  the  larynx,  the  worm  has  caused  death  by  as- 
phyxia ;  into  the  trachea,  pulmonary  gangrene.  As  a  general  rule, 
only  one  or  two  are  present,  but  a  considerable  number  may  exist  in 
the  same  patient.  Great  masses  of  these  worms  have  caused  intes- 
tinal obstruction.     They  may  or  may  not  give  rise  to  symptoms. 

Oxyuris  vermicular  is. — White,  threadlike  worms,  4  to  10  milli- 
metres (I  to  f  inches)  in  length,  found  in  the  faeces,  or  at  the  anus, 
or  in  the  vagina,  are  examples  of  the  Oxyuris  vermicularis,  the  thread 
or  seat  worm.  They  occur  in  patients  of  any  age,  most  commonly 
in  children.     Their  ordinary  habitat  is  the  rectum  and  colon. 

Tapeworms.— 1.  Twfiia  saginata.— White  or  yellowish-white,  flat- 
tened, oblong  bodies,  10  millimetres  (|  inch)  wide,  18  millimetres 
(f  inch)  in  length,  are  the  segments  or  proglottides  of  a  ribbon- 
shaped,  jointed  parasite  of  the  class  of  intestinal  cestodes,  tape- 
worms. In  this  country  there  is  a  very  great  probability  that  it  is 
the  beef  tapeworm,  Tcefiia  saginata  or  mediocanellata. 

The  T.  saginata  varies  from  12  to  20  feet  in  length.  The  head 
is  about  2  millimetres  (Jj  inch)  in  diameter,  square  in  shape,  and 
possesses  four  large  pigmented  sucking  disks,  ivithout  Jiooklets.  The 
neck  is  long  and  threadlike,  gradually  enlarging  and  becoming  seg- 
mented, the  segments  reaching  their  fullest  development  at  or  about 
the  450th,  and  then  containing  ripe  ova.  Each  segment  contains 
both  male  and  female  sexual  organs.  If  the  mature  segment  is 
pressed  between  glass  slides,  the  uterus  is  seen  as  a  median  line 


INTESTINAL  PARASITES— URINATION  139 

with  15  to  35  lateral  branches.  The  period  from  the  time  at  which 
the  worm  is  swallowed  and  attaches  itself  to  the  mucous  membrane 
of  the  intestine  to  the  time  at  which  ripe  segments  begin  to  pass 
from  the  rectum  is  from  3  to  3|^  months.  The  segments  of  this 
worm  possess  motility,  and  are  not  infrequently  found  in  the  cloth- 
ing, having  extruded  themselves  from  the  rectum  between  the  acts 
of  defecation.  The  mature  proglottides  are,  under  favourable  cir- 
cumstances, ingested  by  beef  cattle,  the  ova  are  set  free,  and  the 
embryos,  passing  from  the  stomach  into  the  muscles,  liver,  brain,  or 
eye,  become  encysted  larvae  or  cysticerci. 

2.  Tmnia  solium. — If  the  segments  are  somewhat  shorter  and  nar- 
rower, 8  millimetres  (^  inch)  wide  and  1  centimetre  (f  inch)  in 
length,  and  the  head  of  the  worm  is  but  the  size  of  the  head  of  a 
pin,  and  on  examination  with  a  power  of  40  diameters  is  found  to  be 
provided  with  Jiooklets  as  well  as  suckers,  it  is  the  pork  tapeworm, 
the  TcBfiia  solium.  This  worm  varies  from  6  to  12  feet  in  length, 
and,  with  the  exceptions  noted,  is  similar  in  appearance  to  T.  saginata. 
The  uterus  possesses  fewer  (8  to  14)  lateral  branches  than  the  previous 
variety.  It  is  eaten  by  and  becomes  encysted  in  the  hog,  which  is 
then  referred  to  as  "measled."  It  is  the  common  tapeworm  of 
Europe. 

If  raw  or  imperfectly  cooked  beef  or  pork  is  eaten  by  men,  the 
still  living  larvae  are  liberated,  and,  attaching  themselves  in  the  intes- 
tine, begin  the  adult  stage  of  existence. 

T.  saginata  and  T.  solium  are  the  only  tapeworms  of  clinical  and 
pathological  interest  which  are  ordinarily  found  in  this  country. 

{ /)  Polyjn  which  have  become  detached  from  the  rectum  or  intes- 
tine may  be  passed  in  the  faeces. 

(k)  The  invaginated  segment  of  hoivel  in  intussusception  some- 
times sloughs  away  and  is  passed  per  rectum. 

(?)  Necrotic  sloughs  from  tumours  or  inflammatory  processes  in- 
volving the  intestinal  wall  sometimes  appear  and  must  be  differen- 
tiated from  masses  of  undigested  meat. 

V.  URINATION 

The  diagnostic  information  to  be  derived  from  the  chemical  and 
microscopical  examination  of  the  urine  {q.  v.)  is  discussed  elsewhere. 
"We  consider  here  the  significance  of  abnormalities  of  urination — t.  e., 
dysuria  (painful  urination),  difiicult,  slow,  or  frequent  urination, 
incontinence,  retention,  and  suppression  of  urine. 

Dysuria. — Under  painful  micturition  or  dysuria,  one  includes 
vesical  tenesmus,  a  persistent  inclination  to  urinate,  accompanied  by 
painful  straining ;  and  strangury,  the  performance  of  urination  by  a 


140  THE  EVIDENCES  OP  DISEASE 

spasmodic  and  painful  effort — the  former  term  laying  a  greater  stress 
upon  the  presence  of  a  continuous  desire  to  empty  the  bladder. 

The  diagnostic  indications  of  dysuria  relate,  with  some  excep- 
tions, to  local  disease,  as  follows  : 

Pain  and  burning  during  the  act  of  urination  may  be  caused  by  a 
too  acid  and  concentrated  urine,  as  in  some  lithaemic  cases,  or  for  a 
similar  reason  may  be  symptomatic  of  acute  nephritis.  The  urine 
may  have  become  irritant  in  consequence  of  the  ingestion,  or  absorp- 
tion through  the  skin,  of  cantharides  or  turpentine,  or  such  condi- 
ments as  mustard,  pepper,  and  horseradish. 

Cystitis  is  the  most  frequent  of  all  the  morbid  vesical  conditions 
producing  severe  dysuria.  Discomfort  in  voiding  urine,  as  one  of 
numerous  associated  symptoms,  is  not  an  uncommon  subjective 
complaint  in  neurotic  women  (neuralgia  of  the  bladder,  irritable 
bladder),  and  is  sometimes  accompanied  by  vesical  pain  and  spasm. 
Cancer,  polypoid  or  fungoid  growths,  tuberculous  disease  or  ulcera- 
tion of  the  bladder,  may  also  be  suspected,  but  with  much  less 
probability  because  of  their  comparatively  infrequent  occurrence. 
A  stone  in  the  bladder  or  a  sandlike  deposit  of  calculous  material 
should  not  be  forgotten  as  a  source  of  vesical  irritation,  the  former 
especially  if  there  is  a  history  of  sudden  stoppages  of  the  stream  of 
urine,  with,  in  a  male,  considerable  pain  in  the  head  of  the  penis. 

Certain  urethral  conditions  also  are  suggested  by  dysuria,  such 
as  urethritis,  simple  or  gonorrhoeal;  chancre  or  old  stricture  of 
the  urethra ;  and,  in  association  with  variola  or  varicella,  the  pres- 
ence of  vesicles  in  the  urethra.  The  prostate  gland,  if  inflamed, 
hypertrophied,  or  cancerous,  may  be  the  cause  of  painful  micturi- 
tion. 

In  women,  dysuria  may  be  indicative  of  a  prolapsed  uterus,  cancer 
of  the  cervix,  acute  metritis,  pelvic  peritonitis  and  abscess,  particu- 
larly if  there  are  adhesions  preventing  the  complete  collapse  of  the 
bladder,  in  which  case  the  greatest  pain  is  felt  toward  the  end  of 
micturition.  It  is  sometimes  associated  with  the  various  forms  of 
dysmenorrhoea ;  and  vesical  tenesmus  with  a  discharge  of  mucus  may 
occur  in  connection  with  paroxysms  of  mucous  colic  (membranous 
enteritis).  In  a  recent  case  of  the  latter  disease  in  my  wards  at  the 
Methodist  Episcopal  Hospital  there  was  so  much  vesical  tenesmus 
with  a  discharge  of  bloody  mucus  that  suspicions  of  malignant  dis- 
ease were  entertained,  but  a  cystoscopic  examination  by  Pilcher,  of 
the  surgical  staff,  showed  nothing  but  a  coating  of  mucus  on  the 
inner  lining  of  the  organ.  A  sudden  attack  of  painful  and  spas- 
modic urination  may  be  a  vesical  crisis  of  locomotor  ataxia. 

Inflamed  hemorrhoids,  perineal  abscess,  acute  proctitis,  and  acute 


ABNORMAL  MICTURITION  141 

dysentery  are  not  infrequently  accompanied  by  reflex  dysuria  and 
vesical  tenesmus. 

DiflBcult  or  Slow  Urination. — Any  condition  or  lesion  which  nar- 
rows the  lumen  of  the  urethra  or  impairs  the  muscular  power  of  the 
bladder  walls  will  give  rise  to  slow  or  difficult  urination,  and  perhaps 
to  a  diminution  in  the  size  of  the  stream.  Such  a  symptom,  conse- 
quently, leads  to  a  suspicion  of  a  tight  prepuce,  a  urethral  stricture, 
an  enlarged  or  inflamed  prostate  gland,  or  a  loss  of  tone  of  the  blad- 
der, the  latter  from  overdistention  or  disease  of  the  nervous  mechan- 
ism concerned  in  the  act  of  micturition. 

Frequent  Urination. — Many  of  the  conditions  which  are  respon- 
sible for  dysuria  {q.  v.)  are  also  attended  by  an  abnormal  frequency 
of  urination,  particularly  diseases  of  the  bladder. 

The  cause  of  a  too  frequent  desire  to  empty  the  bladder  is  occa- 
sionally found  in  some  abnormality  of  the  urine — e.  g.,  a  too  concen- 
trated urine,  azoturia  (an  excess  of  urea),  lithuria  (an  excess  of  uric 
acid  and  urates),  and  the  presence  of  irritant  substances.  So  also 
with  the  opposite  condition  of  an  abnormal  increase  in  the  amount 
of  urine  {q.  v.). 

A  frequent  desire  to  urinate  is  a  reflex  symptom  of  the  passage  of 
a  renal  calculus  through  the  ureter,  and  if  the  stone  becomes  im- 
pacted in  the  ureter  this  annoying  symptom  continues.  It  is  also 
associated  with  some  cases  of  pyelitis.  Finally,  frequent  urination 
may  precede  an  ague  fit,  accompany  an  attack  of  angina  pectoris, 
and  constitute  a  symptom  of  sunstroke. 

The  more  or  less  constant  dribbling  of  urine  in  some  cases  of 
retention  should  not  be  mistaken  for  simple  frequency  of  urination. 
Palpation,  percussion,  and,  if  necessary,  the  catheter  should  be  em- 
ployed in  order  to  determine  that  the  bladder  is  empty. 

Incontinence  of  Urine. — An  inability  to  control  the  escape  of  urine 
from  the  bladder,  or  the  passing  of  it  unconsciously,  is  due  either  to 
contraction  of  the  detrusor  (longitudinal)  muscular  layer  of  the 
bladder,  or  to  relaxation  or  paralysis  of  the  sphincters.  If  both  are 
paralyzed,  it  leads  to  retention  plus  incontinence,  manifested  by  dis- 
tention of  the  bladder  with  constant  dribbling.  If  the  compressor 
muscle  is  paralyzed,  and  the  sphincter  is  contracted  or  the  urethra 
obstructed,  retention  alone  ensues. 

Involuntary  or  unconscious  passing  of  urine  may  be  the  direct 
result  of  all  conditions  which  annul  or  interrupt  the  ordinary  and 
normal  voluntary  control  exercised  by  the  brain  over  the  act  of  mic- 
turition. These  conditions  may  pertain  (1)  to  the  brain  itself,  or  (2) 
to  that  portion  of  the  cord  which  puts  the  brain  in  relation  with  the 
vesical  centres. 


142  THE  EVIDENCES  OF  DISEASE 

(1)  The  conditions  or  lesions  which  annul  conscious  cerebral 
activity  are :  all  forms  of  coma  (apoplectic,  alcoholic,  epileptic,  espe- 
cially the  nocturnal  form  of  the  latter) ;  idiocy  and  some  varieties  of 
insanity ;  sunstroke ;  shock ;  and  the  poisons  of  certain  infectious 
diseases,  such  as  severe  diphtheria,  typhus  and  typhoid  fevers,  and 
the  typhoid  state  from  whatever  cause. 

(2)  The  lesions  which  interfere  with  conduction  to  and  from  the 
vesical  centres  in  the  sacral  segments  are  :  injuries  and  tumours  of  the 
cord,  intraspinal  hemorrhage,  transverse  myelitis,  spinal  meningitis, 
and  locomotor  ataxia,  provided  that  the  lesion  does  not  destroy  the 
vesical  centres.  If  the  reflex  arc  is  abolished  by  the  same  lesions 
affecting  the  centres,  total  paralysis  of  the  bladder,  with  retention 
and  dribbling,  will  result.  If  the  paralysis  be  partial  there  is  partial 
retention,  with  occasional  voiding  or  accidental  escape  of  the  urine 
with  any  sudden  muscular  effort.  From  a  diagnostic  standpoint,  the 
presence  of  vesical  disturbance  militates  against  amyotrophic  lateral 
sclerosis,  poliomyelitis,  and  multiple  neuritis,  as  distinguished  from 
myelitis  and  locomotor  ataxia,  in  which  bladder  symptoms  are  more 
or  less  prominent. 

Incontinence  of  urine  may  be  due  to  an  increased  reflex  excita- 
bility of  the  nervous  mechanism,  of  which  nocturnal  enuresis  is  an 
example.  Under  such  circumstances,  and  especially  if  an  unusual 
irritation  is  present,  the  urine  is  passed  involuntarily,  usually  during 
sleep,  when  the  normal  cerebral  control  is  in  abeyance ;  sometimes 
during  waking  hours  when  the  mind  is  profoundly  engrossed.  The 
sources  of  local  irritation  which  should  be  sought  for  are  ascarides 
(seat  worms),  cystitis,  vesical  calculus,  phimosis,  contracted  meatus, 
balanitis,  and  concentrated  or  diabetic  urine.  It  may  also  be  caused 
by  general  weakness  of  the  nervous  system,  or  the  reflex  irritation 
due  to  dentition.  In  women  a  relaxation  of  the  pelvic  floor,  asso- 
ciated with  cystocele,  is  a  common  cause  of  incontinence. 

Increase  of  the  intrapelvic  pressure,  combined  with  lack  of  tone 
of  the  vesical  sphincters,  may  produce  incontinence,  as  in  the  leakage 
of  urine  during  a  paroxysm  of  pertussis  or  other  cough,  sneezing, 
laughing,  or  muscular  effort.  Hydrocyanic-acid  poisoning  is  attended 
with  the  involuntary  discharge  of  urine. 

As  with  frequent  urination,  so  with  incontinence,  the  possible 
presence  of  an  overdistended  bladder  should  not  be  overlooked. 

Retention  of  Urine. — As  previously  stated,  retention  may  alter- 
nate or  coexist  with  incontinence  of  urine  or  frequent  urination. 
The  same  injuries  and  diseases  of  the  cord  which  cause  the  latter 
two  will  also  produce  retention.  It  is  met  with  in  all  forms  of  coma, 
in  typhoid  fever,  and  other  febrile  or  non- febrile  diseases  in  which 


RETENTION  AND  SUPPRESSION   OF   URINE  I43 

the  typhoid  state  occurs,  in  peritonitis  (pelvic  or  general),  and  very 
seldom  it  arises  from  diphtheritic  paralysis.  In  women,  aside  from 
parturition,  which  is  not  inconsistent  with  the  regular  voiding  of  a 
portion  of  the  retained  urine,  the  most  common  cause  of  retention  is 
hysteria. 

Atony  of  the  bladder  consequent  upon  an  unduly  long  postpone- 
ment of  micturition  leads  to  brief  retention  upon  attempting  to 
urinate,  usually  overcome  without  catheterization,  unless  the  prostate 
gland  is  enlarged.  In  the  infant,  irritating  urine  may  cause  so  much 
pain  during  urination  that  after  one  or  two  trials  the  child  will 
refrain  from  so  doing  as  long  as  possible.  In  elderly  men  prostatic 
enlargement  is  the  most  frequent  cause  of  retention.  Stricture  of 
the  urethra,  urethritis,  impaction  of  a  calculus  in  the  urethra, 
usually  near  the  meatus,  cystitis,  or  tumours  of  the  bladder  produce 
it,  and  the  lodgment  of  a  calculus  in  the  ureter  may  by  reflected 
irritation  cause  a  spasm  of  the  vesical  sphincters. 

(/)  Suppression  of  Urine. — When  for  any  reason  urine  is  not 
secreted  by  tlie  kidney,  or,  if  secreted,  does  not  reach  the  bladder,  it 
constitutes  anuria,  or  suppression  of  urine.  Anuria  must  be  sepa- 
rated from  retention  by  using  the  catheter  and  finding  the  bladder 
empty. 

Anuria  not  infrequently  shows  a  striking  absence  of  symptoms. 
In  other  cases  uraemia  {q.  v.)  supervenes.  In  persistent  total  anuria 
death  usually  occurs  within  12  days.  Total  suppression  of  urine  is 
rather  rare.  Ordinarily  a  small  quantity  is  secreted,  but  so  small 
that  it  practically  constitutes  anuria. 

The  various  conditions  and  diseases  which  may  be  attended  by 
suppression  of  urine  are  as  follows  : 

In  acute  congestion,  acute  nephritis,  the  terminal  stage  of  chronic 
nephritis,  renal  abscess,  hydronephrosis  and  pyonephrosis  anuria  may 
exist  because  of  interference  with  the  secreting  tissue  of  the  kidney. 
Poisoning  by  lead,  turpentine,  cantharides  or  phosphorus  and,  very 
rarely,  the  inhalation  of  ether,  may  cause  it.  It  may  be  due  to  the 
prolonged  watery  drain  from  the  blood  in  Asiatic  cholera  and  cholera 
infantum,  and  is  a  possibility  in  cholera  morbus ;  so  also  with  col- 
lapse or  shock  from  injuries,  operations  (especially  those  involving 
the  urinary  tract  in  the  aged),  or  gastro-intestinal  perforations. 

Yellow  fever,  typhoid  fever  and  the  typhoid  state,  the  terminal 
stage  of  acute  yellow  atrophy  of  the  liver,  pernicious  malarial  fevers, 
the  terminal  stage  of  sunstroke,  and,  infrequently,  peritonitis,  may 
conduce  to  a  cessation  of  the  urinary  function,  presumably  by  caus- 
ing hyperaemia  or  disturbed  innervation  of  the  kidneys. 

A  curious  condition,  due  to  disturbed  innervation,  is  the  anuria 


144  THE  EVIDENCES  OF  DISEASE 

of  hysteria,  which  may  be  so  prolonged  as  to  evoke  ursemic  symp- 
toms. More  frequently  the  condition  is  that  of  retention  rather  than 
suppression.  This  diagnosis  should  be  made  with  great  caution,  and 
is  to  be  based  on  well-marked  associated  symptoms  of  hysteria.  While 
not  intending  to  classify  hysteria  with  malingering,  it  is  here  conven- 
ient to  speak  of  those  cases  of  feigned  anuria  which  every  hospital 
physician  sees.  A  successful  device  for  detecting  this  trick  is  to 
catheterize  at  a  certain  hour,  and  2  or  3  hours  after,  when  the  patient 
least  expects  it  and  has  made  no  preparation  for  it,  to  use  the  cathe- 
ter again. 

Kare  causes  of  anuria  are  thrombosis  of  the  inferior  vena  cava 
and  of  the  renal  vein.  This  condition  is  remotely  conjecturable  if 
there  has  been  an  injury  of  the  kidneys,  with  blood,  albumin,  and 
casts  in  the  urine,  followed  by  diminution  and  suppression. 

Obstructive  suppression  embraces  all  conditions  in  which  one  or 
both  ureters  are  occluded  by  outside  pressure  or  obstacles  within 
their  lumen.  Pressure  from  the  outside  may  result  from  an  intra- 
abdominal tumour,  or  a  large  aneurism  of  the  abdominal  aorta,  or 
cancer  of  the  bladder  involving  the  ureters  at  their  entrance.  Obstruc- 
tions within  the  ureter  when  present  are  usually  impacted  calculi. 
Both  ureters  may  be  obstructed  at  the  same  time.  If  only  one  ureter 
is  occluded,  anuria  may  still  follow  because  the  opposite  kidney  is  dis- 
eased or  absent.  Such  cases  are  not  extremely  rare,  two  instances 
having  come  to  my  knowledge  within  the  past  year. 

In  distinguishing  between  obstructive  and  non-obstructive  sup- 
pression, if  any  urine  at  all  is  passed  some  aid  may  be  derived  from 
the  urinary  examination ;  a  high  specific  gravity,  blood,  albumin, 
and  casts,  favouring  the  non-obstructive  form,  while  a  normal  specific 
gravity  and  the  absence  of  abnormal  constituents  argues  for  ureteral 
obstruction.  The  recent  advances  in  cystoscopy  and  ureteral  cathe- 
terization are  of  much  service  in  the  diagnosis  and  treatment  of  some 
forms  of  renal  disease,  provided  the  requisite  skill  can  be  secured. 

VI.    SYMPTOMS   BELONGING   TO  THE   GENITALIA 

1.  Males. — The  genital  symptoms  of  somewhat  general  diagnostic 
value  which  occur  in  the  male  are  urethral  discharges,  priapism, 
pendulous  testicles,  varicocele,  spermatorrhoea,  impotence,  and  mas- 
turbation. 

{a)  Urethral  Discharges. — Discharges  from  the  urethra  may  be 
due  to  a  concealed  initial  lesion  of  syphilis,  simple  or  gonorrhoeal 
urethritis,  or  gleet,  and  inflammation  of  the  prostate  gland.  A  thin 
mucous  discharge  may  be  caused  by  excessive  or  ungratified  sexual 
desire.    From  the  medical  standpoint,  urethral  discharges  may  have  a 


GENITAL  SYMPTOMS— MALES  145 

bearing  upon  the  diagnosis  of  the  manifold  lesions  of  syphilis ;  gonor- 
rhoeal  rheumatism  or  conjunctivitis ;  syphilis,  or  gonorrhoea!  pelvic 
inflammations  in  the  wife  of  the  infected  male ;  and  sexual  neuras- 
thenia or  hypochondriasis. 

(b)  Priapism. — Prolonged  or  abnormally  frequent  erection  of 
the  penis,  with  or  without  sexual  desire,  constitutes  priapism. 

Priapism  may  be  indicative  of  vesical  calculus,  a  distended  blad- 
der, hypertrophy  of  the  prostate  gland,  gonorrhoeal  urethritis,  or 
adherent  prepuce.  It  may  be  a  symptom  of  poisoning  by  cantharides. 
A  loaded  rectum,  inflamed  hemorrhoids,  a  blow  upon  the  perinaeum, 
or  the  irritation  from  seat  worms  (ascarides)  may  be  responsible  for 
it.  It  is  an  occasional  symptom  of  injuries  (cervical  and  lumbar) 
and  diseases  of  the  spinal  cord,  as  in  myelitis  and  spinal  meningitis, 
and  has  been  observed  in  lesions  of  the  pons  and  in  hemorrhage  into 
the  cerebellum.  It  is  at  times  a  premonitory  or  immediate  symptom 
of  an  epileptic  seizure.  Priapism  is  a  not  infrequent  event  in  leucae- 
mia, of  6  weeks'  duration  in  one  case.  It  may  also  be  present  in 
hydrophobia,  tetanus,  rarely  in  diabetes  mellitus,  and  is  sometimes 
caused  by  alcoholic  or  sexual  excesses. 

(c)  Pendnloiis  Testicles. — A  loss  of  tone  in  the  muscular  and  other 
components  of  the  spermatic  cord  and  scrotum,  thus  allowing  the 
testicles  to  droop  unduly,  may  be  a  symptom  of  old  age,  self-abuse 
(especially  if  attended  with  spermatorrhoea),  excessive  sexual  indul- 
gence, and  conditions  of  debility  in  general.  It  is  also  present  in 
connection  with  the  impotence  resulting  from  locomotor  ataxia  and 
diabetes  mellitus. 

{d)  Varicocele. — This  is  a  condition  in  which  the  spermatic  veins 
are  enlarged  and  varicose.  It  may  occur  under  similar  circumstances 
to  (c)  and  is  sometimes  associated  with  neurasthenia  and  hypochon- 
driasis. 

{e)  Spermatorrhcea. — In  a  continent  individual  involuntary  emis- 
sions during  sleep,  if  occurring  at  irregular  intervals  of  2  to  6  weeks, 
are  quite  normal.  If  these  discharges  are  habitually  more  frequent, 
2  or  3  times  a  week  or  perhaps  every  night,  a  pathological  condition 
exists.  If  the  emissions  occur  without  erection,  unconsciously  to  the 
patient,  in  the  daytime  or  while  straining  at  stool,  their  pathological 
character  is  very  marked. 

Before  accepting  the  statement  of  a  patient  that  he  has  spermat- 
orrhoea, especially  if  he  has  been  terrorized  by  the  perusal  of  quack 
literature,  the  history  should  be  gone  over  carefully.  He  not  infre- 
quently believes  that  a  heavy  phosphatic  sediment  in  the  urine  or  a 
thin  mucous  discharge  due  to  prostatic  or  other  irritation  is  escaping 
semen.     Occasionally  there  is  a  fixed  delusion  that  clear  and  normal 


146  THE  EVIDENCES  OF   DISEASE 

urine  is  the  constant  carrier  of  the  testicular  fluid.  A  chemical 
examination  of  the  urine  will  prove  the  nature  of  the  phosphatic 
deposit,  and  a  microscopical  examination  the  presence  or  absence  of 
spermatozoa. 

Spermatorrhoea  is  variously  indicative  of  self-abuse,  excessive 
coitus,  sexual  neurasthenia  as  cause  or  consequence,  and  the  early 
stage  of  locomotor  ataxia.  Sedentary  habits,  an  habitually  loaded 
rectum,  ascarides,  and  the  too  free  use  of  condiments  and  alcoholic 
liquors  may  be  responsible  for  the  slighter  degrees  of  this  symptom. 

Very  often  in  these  cases  there  is  mental  depression,  debility,  lack 
of  energy,  and  a  persistent  brooding  over  a  condition  which  is  sup- 
posed to  be,  and  sometimes  from  this  very  fact  becomes,  incurable. 
The  urine  is  apt  to  be  of  high  specific  gravity,  acid  and  containing 
oxalates,  or  alkaline  with  a  deposit  of  phosphates. 

(/)  Impotence. — An  inability  to  perform  the  act  of  coitus  is  a 
common  and  sometimes  an  early  sign  of  diabetes,  and  is  usually  pres- 
ent in  the  later  stages  of  locomotor  ataxia  or  other  diseases  of  the 
spinal  cord  in  which  there  is  involvement  of  the  bladder  and  rectum 
or  anaesthesia  of  the  glans  penis. 

There  is  an  impotence  which  is  purely  psychical,  emotions  of  fear, 
shame,  or  lack  of  confidence  interfering  with  the  normal  action  of 
the  nervous  mechanism,  erection  failing  to  occur,  or  ejaculation 
taking  place  prematurely.  Impotence  may  come  on  at  an  unusually 
early  age,  although  there  is  no  strict  dividing  line  of  years,  in  those 
who  have  practised  excessive  venery  or  self-abuse. 

{g)  Masturbation. — Modern  writers  attribute  much  less  pathogenic 
power  to  this  habit  than  do  those  of  20  or  30  years  ago.  Its  effects 
are  practically  those  of  excessive  coitus.  It  may  be  a  symptom  and 
not  a  cause  of  insanity  and  sexual  perversion.  On  the  other  hand, 
excessive  masturbation,  like  excessive  venery,  may  cause  sexual  neu- 
rasthenia, and  hypochondria,  spermatorrhcea,  pendulous  testicles, 
"nervousness,"  debility,  and  palpitation  of  the  heart.  Little  impor- 
tance is  attached  to  onanism  and  excessive  coitus  as  causes  of  loco- 
motor ataxia  and  other  organic  diseases  of  the  spinal  cord. 

As  the  majority  of  boys  practise  this  habit  until  enlightened  con- 
cerning its  evils,  it  should  be  suspected  in  cases  exhibiting  anomalous 
nervous  symptoms  without  other  appreciable  cause.  There  is  no 
characteristic  expression  of  the  face  which  will  betray  the  onanist. 
If  he  is  aware  that  he  is  doing  wrong,  the  facial  expression  will 
simply  correspond  to  that  of  a  conscious  wrongdoer. 

2.  Females. — The  symptoms  pertaining  to  the  female  genitalia 
which  possess  a  general  medical  interest  are  vaginal  discharges, 
amenorrhcea,  dysmenorrhoea,  menorrhagia,  and  metrorrhagia. 


GENITAL  SYMPTOMS— FEMALES  147 

(«)  Vaginal  Discharges. — Aside  from  its  constant  presence  as  a 
symptom  of  various  pelvic  disorders,  leucorrhoea,  the  most  common 
of  vaginal  discharges,  may  be  a  symptom  of  anaemia  and  debility 
from  sundry  causes,  as  fatigue,  deficient  food  supply,  phthisis  pul- 
monalis,  and  overlong  lactation.  An  offensive  serous  or  purulent 
discharge,  tinged  or  not  with  blood,  is  a  frequent  symptom  of  carci- 
noma uteri,  and  in  the  absence  of  pelvic  pain  may  give  the  clew  to  an 
obscure  anaemia  and  debility.  In  children,  a  discharge  from  the  geni- 
tals may  be  due  to  a  vulvitis  or  vaginitis,  usually  the  former,  caused 
by  the  migration  of  ascarides  from  the  rectum  and  the  irritation 
consequent  upon  their  presence. 

(b)  Amenorrhoea. — Omitting  the  menopause,  pregnancy,  imper- 
forate hymen,  and  congenital  absence  or  imperfect  development  of 
essential  organs,  cessation  of  the  menses  is  almost  invariably  depend- 
ent upon  some  abnormal  condition  of  the  blood  or  nervous  system, 
or  both. 

It  may  occur  as  a  symptom  of  grave  hysteria  and  melancholia  or 
other  insanities,  or  be  due  to  strong  emotions  (fear,  grief,  worry) 
which  interrupt  the  normal  nervous  balance,  or  to  a  change  of  sur- 
roundings and  occupation,  of  which  the  amenorrhoea  sequent  to  a 
sea  voyage  is  an  example.  Mental  overwork  in  schoolgirls  is  some- 
times responsible  for  the  absence  of  the  menstrual  flow,  so  much 
nerve  force  being  expended  in  one  direction  that  other  functions 
must  suffer. 

Anaemia,  associated  with  a  weakened  nervous  system,  is  the  con- 
dition most  commonly  productive  of  amenorrhoea.  Chloro-anaemia 
and  phthisis  pulmonalis  are  the  underlying  causes  most  frequently 
encountered,  the  anaemia  and  malnutrition  attending  these  maladies 
being  of  such  a  grade  that  the  additional  loss  due  to  menstruation 
can  not  be  afforded.  Indeed,  the  amenorrhoea  of  these  and  other 
diseases  is  a  conservative  consequence,  and  not,  in  opposition  to  a 
natural  false  logic  on  the  part  of  patients,  a  causal  factor.  For  a 
similar  reason,  amenorrhoea  may  be  indicative  of  chronic  nephritis, 
diabetes,  tuberculosis  of  the  kidney,  the  cancerous,  malarial,  or  satur- 
nine cachexiae,  chronic  mercurial  poisoning,  morphine  addiction, 
and  leucaemia.  It  is  not  infrequently  due  to  the  anaemia  which  at- 
tends gastric  ulcer  and  convalescence  from  typhoid  fever  and  the 
exanthemata.  Scanty  menstruation  with  recurring  amenorrhoea  is 
rather  common  in  obese,  anaemic  patients — the  "  fat  anaemics." 

[c)  Dysmenorrhcea. — Of  the  recognised  varieties  of  dysmenorrhoea, 
the  neuralgic  form  only  is  of  direct  medical  interest,  as  it  is  not  asso- 
ciated with  pelvic  lesions  but  is  part  and  parcel  of  a  general  neurotic 
condition  or  a  manifestation  of  some  constitutional  or  blood  disorder. 


148  THE  EVIDENCES  OP  DISEASE 

The  pain  of  neuralgic  dysmenorrhoea  is  somewhat  characteristic. 
It  is  paroxysmal  and  radiating  like  the  neuralgias,  with  its  greatest 
intensity  in  the  hypogastrium,  passing  to  one  or  the  other  iliac  region, 
whence  it  shoots  down  the  corresponding  thigh.  It  begins  before 
the  flow,  and  may  stop  or  continue  after  the  flow  is  established.  It 
bears  no  relation  to  the  amount  or  character  of  the  menstrual  loss, 
and  there  are  none  of  the  usual  symptoms  or  physical  signs  of  pelvic 
lesions.  In  cases  of  sufiicient  severity  to  call  for  treatment,  a  more 
or  less  neuropathic  diathesis  is  almost  invariably  found.  There  is 
apt  to  be  a  hyperaesthetic  condition  of  the  skin  of  the  lower  abdomen, 
with  painful  points  at  the  emergence  of  nerve  branches.  The  char- 
acter and  severity  of  the  pain  may  be  such  as  to  cause  delirium  or 
partial  coma,  and  in  some  intractable  cases,  fortunately  few  in  num- 
ber, the  steadily  recurring  seizures  may  give  rise  to  grave  hysteria, 
and  perhaps  to  epilepsy  or  mania.  The  face  in  marked  cases  is  pale, 
and  the  patient  may  present  the  symptoms  of  collapse  {q.  v.)  with 
lowered  temperature.  In  conjunction  with  neurotic  tendencies,  cer- 
tain general  disorders  may  initiate  or  intensify  the  pain.  In  all  cases 
of  neuralgic  dysmenorrhoea  search  should  be  made  for  malaria,  syph- 
ilis, gout  or  lithaemia,  rheumatism,  and  anaemia. 

A  peculiar  form  of  dysmenorrhoea  is  that  which  is  termed  "  mem- 
branous," in  which  there  is  expelled  with  miniature  labour  pains  a 
hollow,  membranous  cast  of  the  uterine  cavity.  The  membrane, 
when  examined  microscopically,  appears  to  be  the  abnormally  thick- 
ened menstrual  decidua.  While  this  condition  is  attributed  to  an 
endometrial  inflammation,  yet  there  appears  to  be  a  relation  between 
the  nervous  system  and  the  painful  passing  of  membrane.  Certainly 
several  cases  seen  have  exhibited  nervous  idiosyncrasies. 

A  word  may  be  said  here  regarding  intermenstrtial  pain,  which 
has  been  described  by  Palmer  and  others.  It  is  apt  to  begin  about 
two  weeks  after  menstruation  has  ceased.  The  pain,  beginning  grad- 
ually, increases  day  by  day  until  it  reaches  an  unbearable  intensity 
and  finally  passes  away  with  the  advent  of  the  next  menstruation. 
It  is  rather  a  rare  condition,  depending  upon  disease  of  the  ovaries 
and  requiring  their  removal  for  its  relief. 

(d)  Menorrhagia  and  Metrorrhagia.  —  An  excessive  menstrual 
flow  (menorrhagia)  and  an  intermenstrual  flow  (metrorrhagia)  may 
be  caused  by  the  vast  majority  of  diseases  of  the  uterus  and  its  ap- 
pendages. But  either  or  both  may  be,  and  not  infrequently  are,  due 
to  general  diseases  and  conditions. 

The  various  infectious  diseases — influenza,  dengue,  malarial  fever, 
scarlet  fever,  typhoid  fever,  variola,  and  cholera — may  be  attended 
by  excessive  menstruation  or  a  bloody  uterine  flow.     Menorrhagia  is 


SIGNIFICANT  SYMPTOM  GROUPS  149 

not  uncommon  in  the  early  stage  of  phthisis  pulmonalis,  although 
the  reverse  is  usually  the  case. 

Certain  blood  conditions  may  manifest  one  or  the  other  abnor- 
mality. Among  these  are  the  grave  anaemias  (rarely),  more  often 
hsemophilia,  purpura,  scurvy,  leucaemia,  the  uraemia  of  nephritis,  and 
severe  cholaemia  or  jaundice.  Plethora  has  been  assigned  as  a  doubt- 
ful cause.  Certain  intoxications  may  originate  or  increase  uterine 
bleeding,  as  acute  or  chronic  alcoholism,  emmenagogues,  chronic 
lead  poisoning,  and  phosphorus  poisoning.  Among  miscellaneous 
factors,  valvular  or  other  organic  disease  of  the  heart,  cirrhosis  of  the 
liver,  and  acute  articular  rheumatism  should  not  be  overlooked,  nor, 
if  the  age  of  the  patient  be  suggestive,  the  possible  beginning  of  the 
menopause. 

In  searching  for  the  explanation  of  a  menorrhagia  or  metror- 
rhagia, first  eliminate  local  pelvic  causes,  and  then  examine  particu- 
larly for  chronic  cardiac,  renal,  or  hepatic  disease,  syphilis,  and 
malaria. 


SECTION  XIII 

CERTAIN   SYMPTOM   GROUPS  OF  CLINICAL 
SIGNIFICANCE 

There  are  symptom  groups  or  sets  of  correlated  symptoms  which 
it  is  of  service  to  present  here  as  distinct  clinical  pictures.  These 
groups  comprise  coma,  dyspnoea,  fever,  hyperpyrexia,  internal  hemor- 
rhage, shock  or  collapse,  syncope,  weakness  or  debility,  irritant  poi- 
soning, jaundice,  obstruction  to  the  portal  circulation,  hectic  fever, 
pyaemia,  tympanites,  and  the  typhoid  state. 

I.  Coma. — There  is  loss  of  consciousness,  with  stertorous  respirar 
tion  and  expiratory  puffing  of  the  cheeks  and  lips.  The  mouth  is 
partly  open  and  the  tongue  is  dry.  The  cornea  is  insensitive,  and 
one  or  both  pupils  are  either  dilated,  contracted,  or  with  defective 
response  to  light.  There  may  be  an  unusually  slow  pulse.  Involun- 
tary dejection  and  urination  {q.  v.)  may  occur. 

II.  DyspnoBa. — There  is  either  rapid  or  laboured  respiration.  If 
the  dyspnoea  is  severe,  the  face  is  cyanosed  and  wears  an  anxious  ex- 
pression. The  skin  is  covered  with  cold  perspiration,  the  patient 
speaks  in  broken  sentences,  and  may  be  unable  to  lie  down  (or- 
thopncea,  q.  v.). 

III.  Fever. — There  are  slight  chilly  sensations,  the  pulse  is  accel- 
erated, there  are  thirst,  loss  of  appetite,  headache,  backache,  slight  or 

13 


150  THE  EVIDENCES  OF  DISEASE 

severe  aching  of  the  body  and  limbs,  and  a  feeling  of  weakness.  The 
tongue  is  coated,  and  the  urine  is  usually  high-coloured  and  decreased 
in  amount,  with  an  abundant  deposit.  Finally,  the  temperature  is 
found  to  be  elevated. 

IV.  Hyperpyrexia. — If  the  temperature  is  found  to  be  106°  or 
over,  there  may  be  added  to  the  symptoms  just  enumerated  in  III 
dicrotism  of  the  pulse,  delirium,  and  marked  restlessness. 

V.  Internal  Hemorrhage. — The  symptoms  of  internal  or  concealed 
hemorrhage  are  not  sufficiently  distinctive  to  enable  a  positive  diag- 
nosis to  be  made,  without  taking  into  account  the  presence  of  dis- 
eases or  conditions  in  which  such  an  event  is  liable  to  take  place. 
These  symptoms  are  practically  identical  with  those  of  shock  or  col- 
lapse, except  that  air  hunger  and  restlessness  are  especially  promi- 
nent features  in  the  clinical  portrait  of  hemorrhage.  In  the  majority 
of  cases  of  internal  hemorrhage  the  blood  makes  its  appearance  ex- 
ternally, as  in  haematemesis,  haemoptysis,  epistaxis,  metrorrhagia, 
haematuria,  and  bloody  stools,  thus  making  evident  the  nature  of  the 
symptoms.  But  with  a  knowledge  of  the  diseases  and  conditions  in 
which  concealed  hemorrhage  may  occur,  and  by  instituting  a  careful 
search  for  the  existence  of  such  lesions,  the  diagnostician  is  at  times 
enabled  to  predict  the  later  appearance  of  blood  at  some  of  the  natu- 
ral orifices  of  the  body  or  its  finding  at  operation,  as  in  bleeding 
from  a  typhoid  ulcer  or  the  rupture  of  an  ectopic  gestation.  In 
order  to  produce  recognisable  symptoms  the  hemorrhage  must  be 
large.  Slight  hemorrhages  do  not,  of  course,  give  rise  to  appreciable 
symptoms,  nor  do  the  perturbations  caused  by  visible  and  external 
bleeding  differ  from  those  due  to  unseen  bleeding. 

The  symptoms  indicative  of  concealed  hemorrhage  are  as  follows : 
Pain  may  or  may  not  be  present,  depending  on  the  nature  of  the 
lesion  which  causes  the  hemorrhage.  The  face  becomes  pallid, 
pinched,  and  anxious,  and  the  extremities  are  cold.  The  surface  of 
the  body  is  covered  with  perspiration.  The  respirations  are  shallow 
and  sighing,  the  patient  gapes  repeatedly,  and  urgently  desires  more 
air.  There  is  great  restlessness  with  turning  of  the  body  from  side 
to  side.  The  radial  pulse  is  rapid,  weak,  and  thready,  and  may  be- 
come imperceptible.  If  the  hemorrhage  is  large  and  rapid,  syncope 
and  unconsciousness  may  ensue.  The  mind  may  be  clear,  but  more 
commonly  there  is  delirium.  Nausea  is  usually  present,  and  vomit- 
ing may  take  place.  Jactitations  and  convulsions  may  be  added  to  the 
scene.  At  the  onset  of  the  attack  the  heart  beats  violently,  due 
partly  to  excitement  and  partly  to  the  fact  that  the  ventricular  blood 
content  is  rapidly  growing  smaller,  but  very  soon  the  apex  beat  dis- 
appears as  the  systole  becomes  weaker  and  weaker.     If  the  heart  and 


SIGNIFICANT  SYMPTOM  GROUPS  151 

the  large  blood-vessels  are  auscultated,  loud  haemic  murmurs  are 
heard.  When  hemorrhage  takes  place  during  the  presence  of  fever 
the  temperature  falls  rapidly  to  or  below  the  normal  point. 

The  diseases  and  pathological  conditions  in  which  concealed  hem- 
orrhage, suflBcient  to  cause  symptoms,  may  supervene  are : 

(1)  In  the  Thorax. — Bleeding  into  a  large  pulmonary  cavity  or 
the  rupture  of  a  thoracic  aneurism  into  the  mediastinum  or  pleural 
cavities. 

(2)  In  the  Abdomen. — Gastric  ulcer,  duodenal  ulcer,  typhoid 
or  other  ulcers  of  the  intestine,  or  the  rupture  of  an  aneurism 
of  the  abdominal  aorta  into  the  stomach,  intestine,  or  peritoneal 
cavity. 

(3)  In  the  Pelvis. — Concealed  uterine  hemorrhage  before  or  after 
labour  or  rupture  of  an  extra-uterine  fcetation.  Although  in  the 
majority  of  cases  pelvic  haematoma  (effusion  of  blood  between  the 
folds  of  the  broad  ligament)  and  pelvic  hematocele  (effusion  of  blood 
into  the  peritoneal  cavity)  are  due  to  ectopic  gestation,  yet,  as 
these  conditions  do  occur  from  other  causes,  they  are  mentioned  here 
separately. 

(4)  Hwmophilia  and  purpura  haemorrhagica  may  be  responsible 
for  a  variety  of  internal  hemorrhages,  sometimes  of  considerable 
extent. 

(5)  Trauma. — Crushing  injuries,  leading  to  rupture  of  organs  and 
penetrating  wounds,  are  especially  liable  to  concealed  or  internal 
hemorrhage. 

VI.  Shock  or  Collapse. — Although  these  terms  are  ordinarily  con- 
sidered to  be  synonymous,  the  useful  clinical  distinction  drawn  by 
Shrady  should  prevail,  whereby  "  collapse  "  shall  imply  sudden  pros- 
tration occurring  in  cases  not  strictly  surgical,  as  in  irritant  poison- 
ing or  intestinal  perforation  ;  while  "  shock  "  is  limited  to  a  similar 
condition  resulting  from  accidental  or  surgical  traumatism. 

The  symptoms  of  collapse  are  pallor,  anxious  expression,  lowered 
temperature,  cold  perspiring  skin,  thready  or  imperceptible  pulse, 
intense  weakness,  and  intact  or  impaired  intellection.  This  condi- 
tion may  develop  rapidly  or  slowly,  usually  the  former.  Depending 
on  the  resisting  power  of  the  individual  as  well  as  of  the  tissues 
involved,  it  varies  in  severity.  Cases  occur  in  which  collapse  symp- 
toms are  almost  entirely  absent  and  yet  the  autopsy  reveals  lesions 
which  ordinarily  give  rise  to  profound  prostration  at  the  time  of  their 
occurrence,  as  in  some  instances  of  intestinal  perforation.  On  the 
other  hand,  certain  ailments,  commonly  unattended  with  danger, 
may  exhibit  an  apparently  alarming  degree  of  weakness,  as  in  a  form 
of  dysmenorrhoea  frequently  associated  with  an  anteflexed  cervix, 


152  THE  EVIDENCES  OP  DISEASE 

which  presents  a  typical  collapse  invariably  followed  by  a  favourable 
termination. 

The  diseases  and  conditions  causing  collapse  are : 

(a)  Those  already  mentioned  as  attended  with  internal  hemor- 
rhage (q.  v.). 

(b)  The  various  ififectiovs  diseases,  sometimes  at  their  onset,  more 
commonly  at  their  terminal  stages,  as  variola,  pernicious  malarial 
fevers,  typhus  fever,  typhoid  fever,  glanders,  acute  tuberculosis,  ery- 
sipelas, dysentery,  cholera  (stage  of  collapse),  diphtheria,  and  acute 
yellow  atrophy  of  the  liver. 

(c)  Lesions  of  the  Heart  and  Lungs. — A  severe  attack  of  pneumo- 
thorax shows  a  marked  collapse.  So  also  is  it  with  embolism  of  the 
pulmonary  artery,  pulmonary  abscess,  and  pulmonary  gangrene.  Pneu- 
mo-pericardium,  chronic  valvular  disease  of  the  heart,  and  ulcerative 
endocarditis  develop  collapse,  the  latter  two  usually  toward  the  ter- 
mination of  the  illness. 

(d)  Disease  ^vithin  the  Abdomen. — Severe  acute  enteritis  or 
diarrhoea,  intestinal  obstruction,  gastric,  duodenal,  or  intestinal 
perforation,  acute  septic  peritonitis,  intense  hepatic  colic,  perfora- 
tion of  the  diaphragm  by  hepatic  abscess  or  subphrenic  abscess, 
and  acute  pancreatitis  exhibit  collapse  or  prostration  in  varying 
degrees. 

{e)  Narcotic  and  irritant  poisons,  as  in  acute  alcoholism,  acute 
poisoning  from  arsenic,  antimony,  tartar  emetic,  and  chronic  poison- 
ing from  ergot.  In  irritant  poisoning  the  collapse  symptoms  usually 
appear  during  the  later  stages. 

(/)  Traumatism,  particularly  if  there  is  a  rupture  of  one  of  the 
viscera  or  concussion  of  the  brain  or  cord. 

{g)  Other  Causes. — Collapse  also  occurs  with  inversion  of  the 
uterus,  trichinosis,  and  occasionally  hyperpyrexia,  cancrum  oris,  and 
suppurative  tonsilitis. 

VII.  Syncope. — Fainting  or  syncope  is  a  sudden  and  usually  tem- 
porary pallor  and  loss  of  consciousness  from  a  weakening  of  the 
heart's  action.  The  face  is  calm,  the  respirations  are  quiet,  the  pulse 
is  weak  or  imperceptible,  the  pupils  are  dilated  but  responsive  to 
light.  An  attack  of  syncope  may  sometimes  be  anticipated  by  the 
occurrence  of  yawning,  nausea,  and  sighing  respiration.  Fainting 
much  resembles  collapse,  except  that  in  the  former  loss  of  conscious- 
ness takes  place,  the  failure  of  power  is  confined  to  the  heart,  and 
the  attack  is  ordinarily  evanescent. 

VIII.  Weakness  or  Debility. — The  patient  has  a  feeling  of  lan- 
guor and  weakness  and  tires  easily.  There  is  usually  some  shortness 
of  breath  on  exertion  and  the  movements  are  slow  and  made  with 


SIGNIFICANT  SYMPTOM  GROUPS  153 

evident  effort.     The  heart  sounds  are  weak,  especially  the  first,  and 
the  pulse  quickens  unduly  after  gentle  exercise. 

IX.  Poisoniiig  by  Irritants. — In  general,  the  symptoms  of  irritant 
poisoning  (suggestive  but  not  pathognomonic)  are  nausea  and  violent 
vomiting,  with  much  tenderness  and  severe  pain  in  the  epigastrium, 
followed  by  diarrhoea  and  the  evidence  of  marked  collapse.  The 
faeces  may  show  traces  of  blood. 

X.  Jaundice. — A  yellow  or  saffron-coloured  skin  and  conjunctiva, 
general  itching  of  the  body,  depression  of  spirits,  slow  pulse,  dark- 
brown  urine,  and  pale  or  clay-coloured  stools,  constitute  the  symptom 
group  of  obstructive  jaundice  (p.  79). 

XL  Obstructed  Portal  Circulation. — Hydroperitoneum  or  ascites, 
with  enlarged  veins  around  the  umbilicus,  slight  jaundice  or  sallow 
skin,  hemorrhoids,  gastric  disturbances,  and,  when  of  some  standing, 
great  edema  {q.  v.)  of  the  genitals  and  lower  extremities. 

XII.  Suppurative  or  Hectic  Fever. — A  patient  with  bright  eyes 
and  a  clear  mind,  who  is  running  a  temperature  which  rises  in  the 
evening  to  various  heights  and  subsides  in  the  early  morning,  usually 
with  sweating,  with  a  continuously  rapid  pulse,  a  pale  face  with  a 
circumscribed  flush  on  the  cheek,  and  persistent  anorexia,  is  prob- 
ably the  subject  of  suppurative  or  tubercular  disease  of  considerable 
duration.     It  should  not  be  mistaken  for  typhoid  fever. 

XIII.  PysBmla. — If  alone,  or  in  addition  to  the  symptoms  of  sup- 
purative fever,  there  are  irregular,  recurring  chills,  with  nausea  and 
vomiting,  the  temperature  running  suddenly  to  a  high  point  and 
falling  rapidly  with  profuse  sweating,  the  cause  may  be  found  in  the 
formation  of  metastatic  or  embolic  abscesses,  derived  from  a  primary 
suppurative  focus  and  constituting  the  condition  called  pyasmia.  It 
is  not  a  very  uncommon  occurrence  for  pyaemic  chills  and  fever  to  be 
considered  as  of  malarial  origin. 

XIV.  Tympanites, — Meteorism  or  tympanites  consists  of  a  marked 
distention  of  the  stomach  and  intestines  with  gas.  As  a  consequence 
of  the  upward  pressure  against  the  diaphragm,  there  is  dyspnoea,  a 
rapid,  feeble,  or  irregular  pulse,  and  an  upward  displacement  of  the 
apex  beat  (see  also  Abdomen,  General  Distention  of). 

XV.  Typhoid  Status. — The  symptoms  of  this  condition  are  mut- 
tering delirium  or  coma  vigil,  dry  brown  tongue,  teeth  covered  with 
sordes,  twitching  of  the  tendons  {suhsuUus  tenditium),  and  possibly 
picking  at  the  bedclothes  or  grasping  at  imaginary  things  in  the  air 
(cnrphologia).  The  bases  of  the  lungs  may  be  passively  congested 
(hypostatic  pneumonia),  and  ordinarily  the  temperature  is  consider- 
ably elevated,  although  the  typhoid  state  may  exist  with  the  mercury 
at  the  normal  point. 


154  THE  EVIDENCES  OF   DISEASE 

The  typhoid  state  is  common  to  a  number  of  different  diseases 
and  lesions,  as  follows  : 

(a)  Infectious  Diseases. — The  typhoid  state  occurs  with  the  great- 
est frequency  in  infectious  diseases,  especially  lobar  pneumonia, 
erysipelas,  pyaBmia,  and  the  terminal  stage  of  acute  dysentery.  It  is 
also  found,  as  indicated  by  the  name,  in  typhoid  fever  (less  common 
in  cases  treated  by  cold  tubbing),  typhus  fever,  pernicious  malarial 
fevers,  malignant  variola,  malignant  scarlet  fever,  epidemic  influenza, 
acute  yellow  atrophy  of  the  liver,  acute  miliary  tuberculosis,  ulcera- 
tive endocarditis,  puerperal  septicaemia,  anthrax,  and  glanders. 

(b)  Certain  Abdominal  Diseases. — Of  these  the  typhoid  state  may 
develop,  toward  the  close  of  the  disease,  in  jaundice  of  the  obstruct- 
ive form  in  which  the  obstruction  is  insuperable.  It  may  supervene 
also  in  the  course  of  hepatic  abscess,  appendicitis  (especially  if  unrec- 
ognised), acute  enteritis  and  peritonitis  (infrequently),  chronic 
nephritis,  and  pyelitis. 

(c)  Intracranial  Causes. — It  is  sometimes  found  in  meningitis, 
toward  the  end  of  cerebral  embolism  and  thrombosis  with  much  sof- 
tening, and  general  paresis. 

(d)  Other  Causes. — The  typhoid  state  may  be  due  to  purpura 
haemorrhagica  and  acute  phosphorus  poisoning.  It  may  also  be 
produced  by  any  suppurative  inflammation,  particularly  if  pyaemia 
arises  therefrom.  One  of  the  most  typical  examples  of  the  typhoid 
status  that  I  have  seen  was  the  result  of  a  previously  unrecognised 
deep-seated  perineal  abscess,  the  incision  and  drainage  of  which  led 
to  recovery. 


SECTION  XIV 
HEAD  AXD  FACE 

L  Size  and  Contour. — There  are  certain  changes  in  the  size  and 
contour  of  the  head  and  face  which  are  of  diagnostic  importance  in 
the  following  diseases : 

[a)  Hydrocephalus. — The  hydrocephalic  head  is  abnormally  large 
and  usually  globular,  sometimes  pyramidal,  in  shape  (Fig.  18) ;  the 
anterior  fontanel  is  large  and  bulging,  the  sutures  vary  in  width 
from  ^  to  3  inches  or  more,  and  the  veins  of  the  scalp  are  visibly 
distended.  The  face  is  relatively  small  and  the  eyelids  are  raised 
with  difficulty.  The  occipito-frontal  circumference  of  the  head  is 
normally,  at  birth,  a  little  more  than  14  inches,  and  at  1  year  old 
about  18  inches.     An  abnormal  increase  in  this  measurement  is  the 


SIZE  AND  CONTOUR  OP  HEAD 


155 


principal  symptom  by  which  chronic  hydrocephalus  (due  to  ven- 
tricular distention)  may  be  recognised.  It  has  been  known  to  reach 
32  inches  at  8  months  of  age.  Aside  from  the  enlargement  the  most 
characteristic  feature  is  the  prominence  of  the  forehead  at  the  root 
of  the  nose.  The  most  common  error  is  to  mistake  the  rachitic  head 
for  hydrocephalus. 

(b)  Rachitis. — If  the  cranium,  especially  when  viewed  from  above, 
is  elongated,  large,  and  square,  the   vertex   flattened,   the   frontal 
eminences  protuberant,  the  face  small  and  delicate,  the  anterior  fon- 
tanel open  when  it  should 
be  closed,  and  alterations  in      ^'^ 
the  other  skeletal  bones  be 
present,  these  changes  are 
due  to  rachitis  (Fig.  19). 

{c)  Sporadic  Cretinism. 
— If  the  head  is  large  and 


Fig.  18. — Congenital  hydrocephalus. 
Redrawn  from  a  photograph, 
Brother's  case. 


Flu.  1.:.  i;...;.ii.^  ;.^ad;  Italian  c;...u  iv.  ^  _.  ^_;i 
old ;  square,  prominent  forehead  and  flat  ver- 
tex (Holt). 


flat-topped,  the  anterior  fontanel  open  (even  as  late  as  the  tenth 
year),  the  face  broad  and  flat,  with  wide,  negroid  nose,  the  forehead 
low,  the  eyes  wide  apart,  the  mouth  partly  open  and  the  tongue 
slightly  protruding  (Fig.  20),  it  is  a  case  of  sporadic  cretinism. 

{d)  Idiocy. — In  some  cases  the  shape  and  size  of  the  head  may 
suggest  the  presence  of  imbecility  or  idiocy,  but,  as  there  are  no  phys- 
ical changes  which  can  be  considered  characteristic  of  the  various 
forms  of  mental  or  moral  weakness  comprised  under  these  terms,  the 
diagnosis  must  be  made  principally  by  the  psychical  symptoms. 
Hydrocephalus  may  be  the  cause  of  "  hydrocephalic  "  idiocy. 


156 


THE  EVIDENCES  OP  DISEASE 


(e)  Acromegaly. — If  the  head  is  somewhat  enlarged,  with  a  much 
greater  increase  in  the  size  of  the  face,  which  becomes  broadened  and 
elongated,  assuming  an  ovoid  shape  with  the  large  end  downward  in 
consequence  of  the  great  increase  in  size  of  the  maxillae  (especially 
the  lower),  and,  furthermore,  if  the  teeth  are  widely  separated,  the 
tongue,  nostrils,  eyelids,  and  ears  thickened  and  hypertrophied  (Fig. 
21),  it  is  a  case  of  acromegaly  {q.  v.). 


A  B 

Fig.  20. — Sporadic  cretinism.     A  from  Koplik,  B  from  Noyes. 

(/)  Myxmdema. — If  the  patient  has  a  coarse-featured,  round, 
"  full-moon  "  face,  broad,  thick  nostrils,  a  thick-lipped,  large  mouth 
(Fig.  22),  and  a  rough,  dry  skin,  the  existence  of  myxoedema  {q.  v.)  is 
almost  certain,  but  further  confirmatory  evidence  should  be  obtained. 

{g)  Osteitis  Deformans. — If  the  face  is  triangular  in  shape  with 
the  base  upward,  and  the  head  is  lowered  and  carried  forward  so  that 
the  chin  is  below  the  episternal  notch,  a  search  for  other  bone  altera- 
tions is  required,  as  it  may  be  an  example  of  "  Paget's  disease  "  or 
osteitis  deformans. 

{h)  Facial  Hemiatrophy. — If  the  face  presents  an  appearance  as 
if  it  was  composed  of  two  lateral  halves  from  different  individuals, 
with  the  vertical  line  of  junction  sharply  defined,  and  the  hair  of  the 
smaller  side  is  thin  or  absent,  the  eye  sunken,  and  the  skin  altered 


Fig.  '21. — Face  of  acromegaly  (Worcester;. 


ij'iQ.  'ti. — Face  of  myxcedeina  (Gordinier). 


157 


158 


THE  EVIDENCES  OF  DISEASE 


in  appearance  (Fig.  23),  it  is  an  instance  of  facial  hemiatrophy. 
Facial  asymmetry  may  exist  also  with  congenital  torticollis  or  wry- 
neck {q.  v.). 

(i)  Leontiasis  Ossea. — If  the  cranium  is  enlarged  and  globular,  the 
malar  prominences  are  marked,  and  the  orbital  rims  massive  (Figs. 


Fig.  23. — Facial  hemiaiiv 


loiu  Strlimpell. 


24,  25),  the  presence  of  hyperostosis  cranii  or  leontiasis  ossea,  may  be 
suspected. 

(Jc)  Leprosy. — The  tuberous  growths  of  leprosy  {q.  v.)  occurring 
upon  the  face,  together  with  the  resulting  ulceration  and  cicatriza- 
tion, may  slowly  change  the  shape  and  contour  of  the  countenance, 
which  assumes  a  leonine  aspect,  i\iQ  fades  leontina. 

II.  Fontanels  and  Sutures. — {a)  Prominent  or  bulging  fontanels 
(in  infants  or  children)  are  significant  of  chronic  hydrocephalus, 
acute  and  tuberculous  meningitis,  and  meningeal  hemorrhage.  The 
anterior  fontanel  is  frequently  prominent  and  pulsates  strongly  in 
the  acute  febrile  affections  of  infants,  probably  in  consequence  of 
cerebral  hyperaemia. 


FiG.  24.— Leontiasis  ossea  (Edes). 


Fio.  25. — Same  patient  as  in  Fig.  "i-t,  previoui*  to  the  development  of  the  disease  (Edes). 

159 


160  THE  EVIDENCES  OF  DISEASE 

(b)  A  sunken  fo7itanel  is  found  in  wasting  diseases  and  severe 
diarrhceal  or  choleriform  affections,  such  as  marasmus  and  cholera 
Infantum.  In  the  latter  disease  a  depressed  fontanel  is  always  present 
as  one  of  the  symptoms  of  the  hydrencephaloid  state  (spurious 
hydrocephalus).  If  the  depression  is  marked,  the  sutures  may 
overlap. 

(c)  A  vert/  large  fontanel  is  particularly  symptomatic  of  hydro- 
cephalus, and  if  smaller,  but  still  unusually  large,  of  rachitis,  cretin- 
ism, and  hereditary  syphilis.  When  the  infant  is  1  year  old  the  ante- 
rior fontanel  should  not  exceed  1  inch  in  diameter. 

(d)  Delayed  closure  of  the  fontanels,  the  posterior  normally  dis- 
appearing at  the  end  of  the  2d  month,  the  anterior  from  the  14th 
to  the  22d  month,  is  due  ordinarily  either  to  rachitis  or  to  hydro- 
cephalus, particularly  the  former. 

(e)  Abnormally  loide  cranial  sutures,  which  physiologically  are 
fused  by  the  end  of  the  6th,  certainly  by  the  9th,  month,  may  indicate 
rachitis,  hydrocephalus,  or  cretinism. 

III.  Cranial  Bones. — {a)  Craniotabes. — If  in  infants  under  6 
months  of  age  several  spots,  i  to  1  inch  in  diameter,  are  found  on 
the  occipital  bone  or  the  posterior  portion  of  the  parietal  bones,  which 
upon  pressure  by  the  finger  give  a  soft  crackling  sensation,  the  con- 
dition is  termed  craniotabes  and  is  significant  of  rachitis  or  syphilis, 
or  both  conjoined. 

{b)  Meningocele,  Encephalocele,  and  Hydrencephalocele. — A  con- 
genital pulsating  tumour,  varying  in  size  from  a  walnut  to  a  foetal 
head,  bulging  out  between  the  cranial  bones  either  in  the  occipital 
or  the  frontal  regions,  and  if  large,  probably  translucent,  is  a  menin- 
gocele, encephalocele,  or  hydrencephalocele.  The  tumour  is  ordi- 
narily of  the  size  of  an  orange,  pedunculated,  and  pear-shaped  or 
rounded. 

(c)  Nodes. — Soft,  painful,  and  doughy  swellings  of  the  skull,  the 
pain  being  worse  at  night,  and  the  swellings  becoming  harder  as  time 
passes,  are  syphilitic  nodes  (gummatous  periostitis).  If  cerebral 
symptoms  coexist,  it  is  probable  that  similar  nodes  are  forming  on 
the  inner  surface  of  the  cranial  bones. 

IV.  The  Face  as  Indicative  of  Certain  Diseases. — In  addition  to 
the  value  of  the  facial  expression  in  affording  a  clew  to  the  psychical 
condition  of  the  patient  {q.  v.),  the  face  may  present  a  more  or  less 
suggestive  physiognomy  in  certain  diseases  or  conditions.  An  appre- 
ciation of  the  facial  traits  of  disease,  like  the  power  of  making  a 
rapid  diagnosis,  is  based  upon  the  capability  of  comparison  derived 
from  many  observations  and,  when  analyzed,  doubtless  involves 
more  than  the  recognition  merely  of  a  characteristic  countenance. 


THE  FACIES  OF   DISEASE  161 

Nevertheless,  as  a  help  to  an  oftentimes  diflficult  problem,  the  facies 
of  disease  is  not  infrequently  of  great  service. 

The  diseases  and  conditions  which  exhibit,  with  more  or  less  fre- 
quency and  distinctness,  a  characteristic  facies  are :  acute  diffuse 
peritonitis,  dyspnoea,  exophthalmic  goitre,  paralysis  agitans,  phthisis, 
pneumonia,  renal  disease,  typhoid  fever,  impending  death,  and,  in 
children,  mouth-breathing  and  hereditary  syphilis. 

(a)  Acute  Diffuse  Peritonitis. — In  this  disease  the  expression  of 
extreme  anxiety  may  be  very  striking.  The  teeth  are  uncovered  by 
the  raising  of  the  upper  lip,  and  the  whole  expression  is  significant 
of  pain  and  mental  disquiet.  The  respiration  is  somewhat  quick- 
ened because  of  the  fixation  of  the  abdominal  muscles.  In  a  sharp 
and  well-developed  attack,  particularly  if  the  vomiting  has  been 
severe  and  continuous,  the  Hippocratic  countenance  (the  facies  of 
impending  death)  is  seen  more  frequently,  perhaps,  than  in  any  other 
disease  except  cholera.  Localized,  slight  peritonitis  has  no  charac- 
teristic physiognomy,  although  the  faintly  anxious  expression  is 
present  and  significant. 

{h)  Dyspnoea. — In  conditions  which  are  causative  of  diflBcult, 
laborious,  or  painful  breathing,  the  mouth  is  open,  the  lips  and 
tongue  may  be  dry,  the  nostrils  dilate  with  each  inspiration,  and  the 
face  presents  a  bluish  pallor  (cyanosis). 

(c)  Exoplithalmic  Goitre. — The  most  obvious  facial  trait  of  this 
disease  is  the  more  or  less  excessive  protrusion  of  the  eyeballs 
(exophthalmos,  proptosis),  which  may  be  so  great  as  to  prevent  the 
complete  closure  of  the  eyes.  In  a  well-marked  case  the  singular 
staring  expression  is  unmistakable. 

{d)  Hysteria. — The  physician  of  experience  will  sometimes  make 
a  tentative  and  frequently  confirmed  diagnosis  of  hysteria  from  the 
silly  and  vacuous  but  very  amiable  smile  which  greets  his  introduc- 
tion to  the  patient,  or  Avhich  accompanies  the  answer  to  every  ques- 
tion which  is  put.  On  the  other  hand,  a  peculiarly  intense  frowning 
expression  may  appear  in  response  to  every  remark  directly  involv- 
ing the  patient's  symptoms,  the  face  clearing  and  smoothing  when 
the  subject  is  changed  to  one  of  outside  interest.  The  immovable 
face  of  hysterical  coma,  with  its  natural  colour  and  the  quivering 
resistance  of  the  upper  eyelid  when  the  examiner  attempts  to  raise 
it.  is  also  of  value  in  diagnosis. 

(«)  Paralysis  Agitans. — In  this  disease  the  face  presents  a  sphinx- 
like immobility  and  lack  of  expression,  conjoined  usually  with  a 
colour  which  is  apparently  too  healthy  to  correspond  with  the  gen- 
eral condition.  This  stony  visage  (Parkinson's  mask)  is  of  consid- 
erable value  in  the  diagnosis  of  a  doubtful  case. 


162  THE  EVIDENCES  OF  DISEASE 

(/)  Phthisis  Pulmonalis. — In  advanced  phthisis  the  countenance 
is  very  expressive.  The  wide-open,  appealing  eye,  with  its  usually 
white  sclerotic,  the  emaciated  face,  the  pallor  of  which  is  in  strong 
contrast  to  the  spots  of  red  over  the  malar  bones,  the  dilating  alae 
and  panting  respiration,  as  of  a  fugitive,  constitute  a  significant  and 
graphic  portrait. 

{g)  Pneumonia. — In  an  ordinary  frank  pneumonia  the  face  as  a 
whole  is  flushed,  with  a  deeper  tint  of  red  upon  one  cheek,  and  the 
alae  work  strongly  in  consonance  with  the  rapid  respiration.  As  the 
disease  approaches  the  septicasmic  type,  a  general  pallor  brings  the 
malar  flush  into  stronger  relief,  and  in  the  markedly  typhoid  variety 
the  flush  may  entirely  disappear. 

(h)  Renal  Disease. — A  pale,  puffy  face,  with  baglike  swellings  be- 
neath the  eyes,  is  seen  in  those  diseases  of  the  kidney  which  are 
attended  Avith  edema,  more  particularly  the  acute  and  chronic  dif- 
fuse nephritides,  but  it  is  not  infrequently  the  case  that  a  suspicion 
is  aroused  by  a  glance  at  the  patient  which  subsequently  fails  of  con- 
firmation by  the  urinalysis. 

{i)  Typhoid  Fever  and  the  Typhoid  Status. — At  the  height  of  a 
well-marked  case  of  typhoid  fever  the  facies  is  very  characteristic. 
The  expression  is  dull  and  apathetic.  The  mentality  is  impaired 
and  the  patient  is  quite  indifferent  to  his  surroundings.  He  may  be 
in  a  quiet  muttering  delirium.  The  tongue  is  apt  to  be  dry  and  the 
teeth  covered  with  brownish  sordes.  This  facies  is  witnessed  not 
only  in  typhoid  fever  but  in  all  diseases  which  exhibit  the  typhoid 
status  {q.  v.). 

(j)  Impending  Death. — "  A  sharp  nose,  hollow  eyes,  collapsed 
temples ;  the  ears  cold,  contracted,  and  their  lobes  turned  out ;  the 
skin  about  the  forehead  being  rough,  distended,  and  parched ;  the 
colour  of  the  whole  face  being  brown,  black,  livid,  or  lead-coloured." 
Even  in  a  translation  old  Master  Hippocrates'  description  of  the 
face  of  imminent  death  is  intensely  graphic.  As  a  rule,  such  a  coun- 
tenance is  a  sure  precursor  of  a  swift  ending,  except  in  acute  diffuse 
peritonitis,  cholera,  or  starvation. 

In  children : 

{k)  Mouth-breathing. — A  familiarity  with  the  appearance  of  a 
mouth-breather  is  of  great  importance  because  of  the  serious  results 
(ansemia,  gastric  disorders,  phthisis,  et  al.)  which  may  follow  in  neg- 
lected cases  if  the  causative  factors  are  allowed  to  exist  during  the 
developmental  period.  If  the  condition  has  lasted  for  a  considerable 
time — years,  perhaps — the  nostrils  are  small  and  the  nose  itself  rela- 
tively insignificant  in  size,  the  mouth  is  large  and  constantly  open, 
the  lips  are  thick  and  dry,  the  eyelids  droop,  and  the  expression  is 


THE  FACIES— COLOUR  OP  FACE  163 

stupid  and  vacuous.  Further  examination  will  reveal  an  insuflB- 
eiently  developed  thorax. 

(/)  Hereditary  Syphilis. — A  child  suffering  from  a  well-developed 
hereditary  syphilis  has  a  weazened  and  pitifully  old-looking  face, 
very  much  like  that  of  some  species  of  the  quadrumana.  The  skin 
is  yellow  and  wrinkled,  and  it  is  likely  that  labial  fissures,  mucous 
patches,  alterations  in  the  shape  of  the  nose,  and  other  evidences  of 
syphilis  {q.  v.)  will  be  found. 

V.  Colour  of  the  Face. — The  skin  of  the  face,  as  a  part  of  the  gen- 
eral cutaneous  surface,  shares  in  diffused  pallor  or  cyanosis.  But 
there  are  certain  special  alterations  in  the  colour  of  the  face  of  some 
diagnostic  value — viz.,  sallowness,  brownish  discoloration,  and  flush- 
ing of  the  face. 

{a)  Salloicness. — This  is  a  combination  of  pallor  with  a  yellow  or 
brownish-yellow  tint.  It  is  normally  present  in  brunettes  or  natives 
of  hot  climates.  But  the  presence  of  sallowness  should  always  sug- 
gest its  possible  pathological  character. 

A  sallow  face  may  be  indicative  of  one  of  the  cachexias  due  to 
cancer,  lead,  syphilis,  or  malaria.  It  is  also  seen  in  the  anasmias  of 
brunettes.  Addison's  disease  need  only  be  mentioned  as  a  possible 
cause.  Arthritis  deformans  usually  gives  rise  to  a  notable  sallow- 
ness. Very  many,  indeed,  the  great  majority,  of  the  sallow  faces 
seen  in  the  consulting  room  are  due  to  some  disturbance  or  disease 
of  the  digestive  system  and  resulting  anaemia.  Under  this  head 
come  those  who  are  subject  to  habitual  constipation,  chronic  gas- 
tric disorders,  or  chronic  enteritis.  Hepatic  congestion,  cirrhosis 
and  abscess  of  the  liver  are  usually  accompanied  by  a  sallow  com- 
plexion. The  yellowness  of  the  sallow  face  is  to  be  discriminated 
from  the  yellow  tint  of  slight  jaundice  by  the  absence  of  colour  in 
the  sclerotic  and  of  bile  pigments  in  the  urine. 

{h)  Brown  or  hroivnish-yelloio  spots  upon  the  face,  the  so-called 
"  liver  spots  "  of  the  laity,  are  in  the  greater  number  of  instances 
examples  of  the  chloasma  (localized  deposit  of  pigment)  found  in 
connection  with  pregnancy,  chronic  affections  of  the  uterus  or  liver, 
and  exophthalmic  goitre.  The  possibility  of  the  presence  of  Addi- 
son's disease  should  be  considered.  Localized  deposits  of  pigment 
may  be  caused  by  continued  scratching  or  by  the  use  of  counter- 
irritants  or  vesicants.  There  appears  to  be  in  some  individuals  an 
unusual  predisposition  to  the  deposit  of  colouring  matter  in  the  skin 
after  the  local  use  of  mustard,  turpentine,  or  cantharides,  a  fact  not 
to  be  forgotten  for  cosmetic  reasons  in  connection  with  women 
patients.  The  internal  use  of  arsenic  or  the  external  application 
of  the  oil  of  cade  may  cause  permanent  discoloration  of  the  skin. 


164  THE  EVIDENCES  OF  DISEASE 

(c)  Flushing  of  the  face  may  be  of  considerable  duration,  lasting 
for  hours  or  days,  or  it  may  be  sudden  and  evanescent,  passing  as 
quickly  as  it  arrives.  A  permanently  flushed  and  ruddy  face  may 
on  closer  inspection  be  seen  to  be  caused  by  dilated  arterial  twigs  or 
venous  radicles,  in  which  case  it  should  arouse  suspicion  of  athero- 
matous arteries  or  chronic  nephritis.  A  flushed  face  is  character- 
istic of  the  early  stage  or  onset  of  the  majority  of  febrile  tempera- 
tures. It  is  particularly  noticeable  in  malarial  fevers  and  acute 
articular  rheumatism,  and  may  persist  for  days  in  typhoid  fever. 
The  unilateral  flush  of  pneumonia  is  frequently  seen,  and  the  malar 
flush  of  pulmonary  phthisis  is  sadly  familiar.  Ordinarily  there  is  a 
red  face  in  the  first  stage  of  acute  alcoholism  and  the  apoplectic 
form  of  intracranial  hemorrhage.  The  face  is  usually  flushed 'in 
hysterical  convulsions  and  frequently  in  the  comatose  form  of  the 
same  disease.  Large  fibroid  tumours  and  ovarian  cystomata  are  not 
uncommonly  associated  with  a  florid  face.  A  heart  which  has  hyper- 
trophied  to  a  greater  extent  than  is  demanded  by  its  work  at  a  given 
time  may  produce  more  or  less  permanent  flushing  of  the  face. 

Evanescent  or  transient  flushing  of  the  face  is  a  manifestation  of 
irregular  vasomotor  action,  which  may  be  due  to  a  variety  of  per- 
turbing influences.  In  many  cases  such  flushings  are  simply  evi- 
dences of  a  more  or  less  marked  congenital  instability  of  the  nervous 
system,  and  when  exhibited  under  mental  excitement  by  children 
and  young  adults,  particularly  young  girls,  are  not  of  diagnostic 
value.  Care  should  be  taken  in  such  cases  that  a  face  flushed  by  the 
slight  agitation  of  an  interview  with  the  physician  does  not  disguise 
the  presence  of  a  decided  anaemia  {chlorosis  rubra).  It  is  not  unusual, 
after  the  first  excitement  has  subsided,  to  see  the  familiar  pallor 
replace  the  red  upon  the  cheeks  and  lips.  In  addition  to  anaemia, 
transient  flushings  are  associated  with  conditions  of  fatigue,  espe- 
cially neurasthenia  and  exophthalmic  goitre,  sometimes  with  consti- 
pation, gastric  catarrh,  and  gastric  neuroses.  Alternate  redness  and 
pallor  of  the  face  is  quite  common  in  cerebral  meningitis,  and  is 
occasionally  witnessed  in  typhoid  fever.  The  vasomotor  condition 
which  above  all  others  is  made  the  subject  of  bitter  complaint  is  the 
flushing,  accompanied  by  a  sensation  of  heat  and  by  sweating,  which 
attends  the  menopause. 

VI.  Skin  of  Face. — This  shares  in  the  eruptions  of  the  exanthem- 
ata and  generalized  diseases  of  the  skin.  It  is  especially  the  seat 
of  milium  and  acne.  Ecchymoses  of  the  face,  if  not  due  to  trauma- 
tism, may  be  the  result  of  the  rupture  of  small  subcutaneous  vessels 
from  violent  coughing,  as  in  pertussis,  or  are  manifestations  of  pur- 
pura. 


COLOUR— AND  LOSS— OF   HAIR  165 

VII.  The  Hair. — This  is  to  a  very  slight  extent  an  index  to  the  gen- 
eral robustness  and  vigour  of  the  individual.  Thick,  coarse  hair  is 
at  times  associated  with  rude  strength  of  constitution,  and  scanty, 
fine-textured  hair  with  a  delicate  habit  of  body ;  but  there  are  many 
instances  in  which  this  is  not  the  case.  There  is  some  diagnostic 
value  in  an  observation  of  the  colour  and  scantiness  of  the  hair. 

(a)  Colour  of  the  Hair. — The  physiological  loss  of  the  pigment 
of  the  hair  (grayness)  begins  in  the  average  individual  at  forty  to 
forty-five  years  of  age,  and  slowly  increases  as  the  years  pass.  Early 
grayness  is  frequently  a  sign  of  premature  old  age,  and  is  associated 
with  degenerative  arterial  changes,  but  is  compatible  with  good 
health  and  otherwise  normal  tissues.  It  is  sometimes  an  hereditary 
peculiarity.  Cases  of  sudden  whitening  of  the  hair  as  the  result  of 
extreme  terror  or  anxiety  have  been  reported.  In  a  case  of  Addi- 
son's disease  the  hair,  previously  a  pronounced  blonde,  became  as 
black  and  coarse  as  that  of  a  Xorth  American  Indian.  Circum- 
scribed gray  spots  may  be  due  to  trophic  changes  produced  by  neu- 
ralgia or  other  disease  affecting  the  fifth  nerve. 

The  fact,  if  it  is  apparent,  that  the  hair  is  dyed,  may  be  an  im- 
portant clew  in  the  diagnosis  of  chronic  lead  poisoning,  as  this  metal 
enters  into  the  composition  of  various  hair  dyes  and  washes.  Hy- 
drogen dioxide  bleaches,  pyrogallic  acid  darkens,  the  hair.  The  hair 
of  those  who  work  in  copper  may  acquire  a  greenish  colour,  while 
that  of  cobalt  miners  and  indigo  handlers  may  exhibit  a  bluish  tint. 

{b)  Loss  of  Hair. — This  may  be  general  or  circumscribed. 

General  or  diffused  baldness,  when  not  preceded  by  disease,  is 
physiological,  usually  antedating  grayness  as  an  evidence  of  age,  and 
its  appearance  at  an  early  period  is  a  somewhat  frequent  hereditary 
trait.  Rapid  loss  of  hair  is  a  common  occurrence  after  acute  febrile 
diseases,  more  particularly  typhoid  fever,  gout,  and  erysipelas.  Fall- 
ing out  of  the  hair,  either  general  or  circumscribed,  is  one  of 
the  symptoms  of  syphilis.  In  chronic  hydrocephalus  the  hair  is 
almost  invariably  thin.  Frequent  and  severe  neuralgias  of  the 
fifth  nerve  are  sometimes  followed  by  loss  of  hair.  In  anaemia 
and  phthisis  pulmonalis,  and  usually  in  myxoedema,  the  hair  may 
become  scanty. 

Circumscribed  areas  or  patches  of  baldness  may  be  due  to  ring- 
worm (tinea  tonsurans)  or  alopecia  areata.  Scars  upon  the  scalp 
are  usually  destitute  of  hair.  A  marked  bald  patch  upon  the  back 
of  an  infant's  head  is  suggestive  of  rickets,  because  of  the  decided 
tendency  in  this  disease  to  a  constant  rolling  of  the  head  upon  the 
pillow.  This  condition  is  seen  to  a  slighter  extent  in  almost  all 
infants. 

13 


166  THE  EVIDENCES  OP  DISEASE 

yill.  Edema  or  Swellings  of  the  Face.— («)  The  face  shares  in  the 
condition  of  general  dropsy  or  anasarca,  especially  that  which  is  due 
to  renal  disease.  Puffiness  or  edema  of  the  face  as  a  whole  may  be 
due  to  emphysema  (toward  the  close),  pneumothorax,  chronic  inter- 
stitial pneumonia,  and  mediastinal  tumours.  In  pertussis  it  may  be 
present  from  the  frequent  interference  with  the  return  circulation 
caused  by  the  violent  expiratory  efforts  during  paroxysms  of  cough. 
The  face  is  more  or  less  characteristically  swollen  in  erysipelas,  measles, 
variola,  dengue,  and  trichinosis.  The  enlargement  of  the  face  in 
myxoedema  is  due  to  a  thickened  condition  of  the  skin  and  subcu- 
taneous tissues,  which  resembles  edema  but  does  not  pit  on  pressure. 

(b)  Localized  edematous  and  usually  fugitive  swellings  of  the 
face  may  be  due  to  urticaria  or  angioneurotic  edema,  or  may  occur 
as  an  intercurrent  symptom  of  exophthalmic  goitre. 

(c)  Swelling  and  puffiness  of  the  forehead  may  occur  in  glanders 
or  thrombosis  of  the  superior  longitudinal  sinus. 

{d)  Swelling  over  the  upper  jaw  may  be  due  to  alveolar  abscess, 
phosphorus  necrosis,  or  disease  of  the  antrum. 

(e)  Swelling  of  the  lower  jaw  may  be  accounted  for  by  alveolar 
abscess  or  actinomycosis. 

(/)  A  swelling  in  front  of  the  ear,  extending  downward  behind 
the  angle  of  the  jaw,  at  first  unilateral  but  later  appearing  also  on 
the  other  side,  is  due  to  parotitis,  usually  epidemic  (mumps).  Ow- 
ing to  the  position  of  the  gland,  the  lower  portion  of  the  ear  is  rather 
characteristically  pushed  outward. 

(g)  A  tender  edematous  swelling  over  the  mastoid  process  may  be 
due  to  involvement  of  the  mastoid  cells  in  the  course  of  an  otitis 
media,  or  to  thrombosis  of  the  lateral  sinus. 

(h)  The  cheeks  are  sometimes  swollen  as  a  result  of  the  gingival 
conditions  in  scurvy,  and  in  gangrenous  stomatitis  {cancrum  oris) 
there  is  a  great  and  brawny  infiltration  of  the  cheeks  and  lips.  Furun- 
cles and  anthrax  (malignant  pustule)  may  also  be  the  cause  of  in- 
flammatory swellings  seated  upon  some  portion  of  the  face. 

IX.  Abnormal  Movements  of  the  Head,  (a)  Nodding  Spasm. — A 
rhythmic  nodding  movement  of  the  head  may  be  a  form  of  habit 
spasm  or  of  epilepsy  in  children.  In  the  latter  case  it  is  accompanied 
by  a  momentary  loss  of  consciousness.  Like  other  spasmodic  affec- 
tions, it  may  be  indicative  of  rachitis.  It  may  occur  in  hysteria, 
either  alone  or  as  a  part  of  the  hysterical  salaam  convulsion  (rhyth- 
mic or  hysterical  chorea). 

{h)  Spasmodic  Torticollis  {clonic). — A  spasmodic  jerking  of  the 
head,  recurring  every  few  minutes,  in  which  the  head  is  brought 
toward  one  shoulder,  and  at  the  same  time  the  face  is  rotated  to  the 


FIXITY  OP  HEAD— FACIAL  SPASM  167 

opposite  side  and  the  chin  raised,  is  the  clonic  form  of  spasmodic 
torticollis.  The  shoulder  may  be  simultaneously  jerked  upward  to 
meet  the  head.  The  movements  of  the  head  in  chorea  are  by  con- 
trast extremely  irregular  and  bizarre,  and  the  facial  muscles  are 
affected  before  those  of  the  neck. 

X.  Abnormal  Fixity  of  the  Head.— («)  Inahility  or  disincU?ia- 
tion  to  move  the  head,  especially  if  the  patient  is  prone  to  support  it 
by  the  hands,  may  be  due  to  tuberculous  disease  of  the  cervical  ver- 
tebrae, and  if  associated  with  dysphagia  it  points  to  disease  of  the 
articulation  between  the  atlas  and  occiput. 

(b)  Retraction  of  the  Head. — Drawing  back  and  fixation  of  the 
head  by  contraction  of  the  posterior  cervical  muscles,  so  that  the 
occiput  bores  into  the  pillow,  is  a  symptom  of  all  forms  of  cerebral 
and  cerebro-spinal  meningitis,  particularly  when  affecting  the  basal 
meninges.  It  is  also  seen  in  tetanus  and  strychnine  poisoning  as  a 
part  of  the  general  tonic  spasm.  In  nervous  infants  a  transient  re- 
traction of  the  head  accompanies  a  fit  of  crying  from  temper  or  pain, 
especially  the  pain  caused  by  acute  indigestion. 

(c)  Other  causes  of  abnormal  fixity  are  occipito-cervical  myalgia, 
post-pharyngeal  abscess,  congenital  and  spasmodic  (tonic)  torticollis, 
rheumatism  (acute,  chronic,  gonorrhceal),  arthritis  deformans,  swol- 
len and  painful  cervical  glands,  contracted  cicatrices  (especially  from' 
burns),  and  sprain  of  the  cervical  muscles  or  other  traumatism  of  the 
neck. 

XI.  Facial  Spasm. — Spasmodic  contraction  of  the  facial  muscles 
may  be  tonic  (continuous)  or  clonic  (intermittent),  unilateral  or  bi- 
lateral, and  involving  one  or  all  of  the  muscles  which  are  innervated 
by  the  facial  nerve.  In  order  to  form  an  opinion  of  the  cause  of 
spasmodic  affections  of  the  face,  it  is  advisable  to  take  into  considera- 
tion age,  sex,  and  possible  neuropathic  diathesis,  and  to  ascertain  the 
presence  or  absence  of  disease  of  the  eyes,  teeth,  skin,  and  possibly 
of  uterine  disease  and  intestinal  parasites.  In  some  cases  the  facial 
symptoms  constitute  a  comparatively  insignificant  part  of  a  disease 
of  the  nervous  system. 

The  diseases  or  conditions  which  may  be  indicated  by  facial  spasm 
are  mimic  spasm,  habit  spasm,  convulsive  tic,  blepharospasm,  nicti- 
tating spasm,  exophthalmic  goitre,  chorea,  epilepsy,  tetanus,  menin- 
gitis, hysteria,  spasm  following  paralysis,  irritation  at  the  root  of  the 
facial  nerve  and  lesion  of  its  cortical  centre. 

{a)  Mimic  Spasm. — A  more  or  less  constant  twitching  of  one  side 
of  the  face  with  partial  closing  of  the  eye,  occurring  in  an  adult,  is 
mimic  spasm.  It  is  usually  bilateral,  and  ordinarily  does  not  begin 
until  adult  age. 


168  THE  EVIDENCES  OF  DISEASE 

(b)  Habit  Spasm. — If  in  a  neurotic  child,  usually  a  girl  from  seven 
to  fourteen  years  of  age,  there  is  a  sudden  wink  of  the  eye  or  a  rapid 
drawing  of  the  mouth  to  one  side,  or  a  sniff,  occurring  at  irregular 
intervals  and  greatly  intensified  in  severity  by  emotional  causes,  it 
is  habit  spasm. 

(c)  Convulsive  Tic. — In  an  hereditarily  neurotic  child,  irregular 
movements  of  the  facial  muscles,  and  frequently  those  of  the  arm, 
if  accompanied  by  an  explosive  ejaculatory  utterance  of  profane  or 
obscene  words  {coprolalia).,  or  the  involuntary  repetition  of  a  word 
(echolalia),  or  the  mimicking  of  an  action  [echokinesis),  is  convulsive 
tic  or  Gilles  de  la  Tourette's  disease. 

(fZ)  Blepharospasm. — A  tonic  (persistent)  closure  of  the  eye  is 
ordinarily  due  to  some  ocular  disease  causing  photophobia  and 
spasmodic  contraction  of  the  orbicularis  palpebrarum.  Very  seldom 
it  is  a  symptom  of  hysteria. 

(e)  Winking  Spasm. — Eapid  clonic  contractions  of  the  orbicularis 
palpebrarum  (winking  or  nictitating  spasm)  is,  in  the  absence  of  ocu- 
lar disease,  either  habit  spasm  or  hysteria. 

(/)  Exophthalmic  Goitre. — A  clonic  spasm  of  the  levator  palpe- 
brae  superioris  resulting  in  successive  rapid  liftings  of  the  upper 
eyelids  is  an  occasional  symptom  (Abadie's  sign)  of  exophthalmic 
goitre. 

{g)  Chorea. — The  facial  muscles  are  more  or  less  affected  by  irreg- 
ular jerking  movements  in  chorea ;  but  the  diagnosis  is  made  by  the 
associated  symptoms. 

{h)  Epilepsy.,  Meningitis.,  Tetanus. — In  epilepsy  there  are  tonic 
followed  by  clonic  spasms  of  the  facial  muscles,  but  the  simultaneous 
presence  of  general  convulsions  will  establish  the  diagnosis  unless  it 
happens  to  be  a  variety  of  petit  mal.  In  the  latter  case  the  diagnosis 
of  epilepsy  may  be  determined  by  the  occurrence  of  a  momentary  loss 
of  consciousness,  biting  of  the  tongue,  or  the  presence  of  a  prelimi- 
nary aura.  In  meningitis  and  tetanus  the  facial  spasm  is  usually 
tonic,  and  is  overshadowed  by  the  associated  symptoms. 

{i)  Hysteria. — The  facial  spasm  of  hysteria  is  usually  tonic,  less 
commonly  clonic,  and  requires  for  the  diagnosis  of  its  character  a 
careful  search  for  corroborative  symptoms. 

( ; )  Spasm  following  Paralysis. — Facial  spasm  or  contracture, 
generally  tonic  and  sometimes  permanent,  may  follow  facial  paraly- 
sis. The  latter,  in  the  vast  majority  of  cases,  is  unilateral.  If  the 
paralysis  is  hysterical  the  tonic  contraction  affects  the  muscles  of  the 
non-paralyzed  side  of  the  face  ;  if  due  to  other  causes,  the  contrac- 
ture ordinarily  takes  place  in  the  paralyzed  muscles  during  or  subse- 
quent to  the  recovery  of  their  power. 


FACIAL  SPASM— FACIAL  PARALYSIS  169 

(k)  Irritation  at  Root  of  Facial. — Clonic  unilateral  spasm  or 
twitching  of  one  or  more  of  the  facial  muscles  may  be  caused  by  irri- 
tation of  the  facial  at  its  emergence  by  the  pressure  of  a  tumour  of 
the  base  of  the  brain,  or  an  aneurism  of  the  vertebral  artery.  The 
diagnosis  is  usually  made  joos^  mortem. 

(I)  I'ic  Douloureux. — Spasmodic  movements  of  the  face  may  occur 
in  this  disease,  but  simply  as  incident  to  the  pain.  Movements  of  the 
eyes  and  facial  muscles  frequently  complicate  nodding  spasm  {q.  v.). 

XII.  Facial  Paralysis. — Paralysis  of  the  muscles  of  the  face  is 
almost  always  unilateral,  very  rarely  bilateral. 

In  unilateral  facial  paralysis  the  affected  side  of  the  face  has  a 
smooth,  expressionless  appearance,  due  to  the  obliteration  of  the 
wrinkles  which  normally  give  it  character.  The  mouth  is  drawn  to 
the  sound  side.  There  is  an  inability  to  pucker  the  lips  as  in  whis- 
tling, and  labial  sounds  are  bunglingly  articulated.  In  eating,  food 
collects  between  the  teeth  and  the  cheek.  During  sleep  the  cheek 
flaps  with  inspiration  and  expiration  because  of  the  paralysis  of  the 
buccinators,  and  the  nostril  of  the  paralyzed  side  does  not  dilate 
upon  forced  inspiration. 

If  the  paralysis  is  of  peripheral  origin,  involving  the  facial  nerve 
only  and  not  constituting  a  part  of  a  hemiplegia,  the  eye  can  not  be 
completely  closed,  and  the  forehead  can  not  be  wrinkled,  owing  to 
paralysis  of  the  orbicularis  palpebrarum  and  the  occipito-frontalis. 
The  tongue,  if  protruded,  does  not  in  reality  deviate  from  the  middle 
line,  as  may  be  determined  by  watching  its  relation  to  the  central 
upper  incisors,  the  genio-hyo-glossus  not  having  been  affected.  The 
apparent  deviation  is  due  to  the  pulling  of  the  mouth  to  the  sound 
side. 

If  the  paralysis  is  of  central  origin^  the  upper  branch  of  the  facial 
is  but  slightly  affected,  the  power  of  closing  the  eye  and  wrinkling 
the  forehead  is  largely  retained,  and  the  tongue  deviates  toward  the 
paralyzed  side,  as  the  genio-hyo-glossus  usually  loses  its  power  and  its 
healthy  fellow  is  unopposed. 

The  best  test  of  facial  paralysis  is  to  request  the  patient  to  close  the  eyes 
tightly  and  to  raise  the  upper  lip  so  as  to  expose  the  teeth.  If  complete  facial 
paralysis  is  present,  the  eye  will  not  close,  the  eyeball  rolls  upward,  and  the 
difference  between  the  two  sides  of  the  face  becomes  very  noticeable.  This 
device  should  always  be  employed,  as  otherwise,  in  the  case  of  children  or 
plump,  smooth-faced  adults,  a  slight  facial  paralysis  may  escape  detection. 
Moreover,  in  the  course  of  time  secondary  contractures  may  occur  in  the  para- 
lyzed muscles  which  will  restore  the  wrinkles,  and,  unless  the  other  muscles  are 
exerted,  may  deceive  the  observer  into  mistaking  the  affected  side  for  the 
sound  one. 


170 


THE  EVIDENCES  OF  DISEASE 


Having  determined  the  presence  of  unilateral  facial  paralysis,  it 
is  desirable,  if  possible,  to  determine  its  cause.  The  facial  nerve 
supplies  all  the  muscles  of  the  face,  except  those  of  mastication, 
which  are  innervated  by  the  motor  branch  of  the  fifth  and  the  stape- 
dius, stylo-hyoid,  buccinator,  and  platysma  myoides. 

Paralysis  of  the  facial  nerve  (Fig.  26)  may  be  central  (supra- 
nuclear), due  to  a  lesion  affecting  the  cortical  centre  of  the  fibres 


Leg 
Arm 


1.  LESION  caus- 
ing facial 
monoplegia 


a.  LESION  upper 
section  pons  = 
ord.  hemiplegia 

3.  LESION  lower 
section  pons  = 
crossed  paraly- 
sis. Face  same 
side ;  arm,  leg- 
.  opposite  side 
Decussation  of 
motor  fibres  tc 
arms  and  legs 


Int.  capsule,  post,  limb 

Decussation  fac.  fibres 

Fac.  nerve  entering  int.  audit,  meatus- 

niculate  ganglion 

4.  LESION  =  lost  taste  in  ant. 
§  tongue — perhaps  abnor- 
mally acute  hearing 
To  stapedius 

Chorda  tympani 

Stylo-mastoid  foramen 


-Upper  branch  of 
facial  (orbicula) 
risand  frontalis 

-Lower  branch  to 
remaining  mus- 
cles of  expres- 
sion 


Causes 

OF  Peripheral  Paralysis  affecting  Nerve. 

Causes  AFFEcriNa 
Centre,  or    Fi- 

Bet. pons  and 
int.  meatus. 

At  and  beyond 

bres  TO  Nucleus. 

In  pons. 

In  aqueduct. 

stylo-mastoid 
foramen. 

Hemorrhage. 

Hemorrhage. 

Tumours. 

Inflammation 

Injury. 

Embolism. 

Tumour. 

Gummata. 

or  necrosis  of 

Parotid     swell- 

Thrombosis. 

Softening. 

Basal  meningi- 

bone   due    to 

ing. 

Softening. 

Diphtheria. 

tis  and  endar- 

disease of  ear. 

Multiple  neuri- 

Tumours. 

Bulbar  paraly- 

teritis. 

Fracture      pe- 

tis. 

Abscess. 

sis. 

Practxire  at 

trous   portion 

Peripheral  neu- 

Locomotor 

base. 

of  bone. 

ritis  (rheumat- 

ataxia. 

ic). 

Fia.  26. — Showing  tlie  varieties  and  causes  of  paralysis  of  the  facial  nerve. 


which  run  from  it  to  the  nucleus ;  or  nuclear^  a  lesion  involving  the 
nucleus  itself;  or  infranuclear^  caused  by  disease  or  injury  of  the 
nerve  after  it  leaves  the  nucleus,  either  while  it  pursues  its  course 
through  the  pons,  or  while  in  the  bony  canal,  or  after  emerging  from 
the  stylo-mastoid  foramen  and  penetrating  the  substance  of  the 
parotid  gland  on  the  way  to  its  final  distribution. 


CAUSES  OF  FACIAL  PARALYSIS  171 

The  first  essential  in  determining  the  cause  of  a  given  case  of 
facial  paralysis  is  to  ascertain  whether  it  is  of  central  or  peripheral 
origin.  With  rare  exceptions,  if  the  lesion  is  central,  the  eye  can  be 
closed  and  the  forehead  wrinkled,  especially  under  the  influence  of 
emotion.  Moreover,  the  normal  response  to  the  faradic  and  galvanic 
currents  is  preserved,  and  the  reaction  of  degeneration  does  not 
appear,  because  the  nucleus  still  exerts  its  trophic  influence  upon  the 
paralyzed  muscles.  On  the  other  hand,  if  the  lesion  is  peripheral, 
affecting  the  nucleus  or  the  nerve  trunk,  the  orbicularis  and  frontalis 
are  powerless,  the  response  to  faradism  disappears,  and  the  galvanic 
excitability  (q.  v.)  is  qualitatively  altered.  The  muscles  degenerate 
because  they  are  cut  off  from  the  trophic  stimulus  of  the  nucleus. 

(a)  The  Central  Causes  of  Facial  Paralysis. — In  the  great  major- 
ity of  cases  facial  paralysis  of  central  origin  is  associated  with  hemi- 
plegia, and,  like  the  latter,  is  due  to  intracranial  hemorrhage,  em- 
bolism, or  thrombosis,  with  softening  (less  frequently  tumour  and 
abscess),  affecting  the  cortex  or  the  facial  fibres  as  they  pass  down  in 
the  corona  radiata  or  the  internal  capsule.  The  facial  paralysis  is 
on  the  same  side  as  that  of  the  arm  and  leg,  because  the  fibres  from 
the  cortex  to  the  nucleus  decussate  before  entering  the  nucleus,  and 
the  facial  muscles  consequently  bear  the  same  relation  to  the  cortex 
as  do  the  muscles  supplied  by  the  spinal  nerves.  The  determination 
as  to  which  of  the  central  lesions  is  causing  the  paralysis  must  be 
made  by  the  history  and  associated  symptoms.  If  there  is  facial  palsy, 
presenting  the  characters  of  a  central  paralysis  and  not  associated 
with  hemiplegia,  it  is  due  to  a  lesion  of  the  face  centre  in  the  cortex. 

(b)  Nuclear  and  Peripheral  Causes  of  Facial  Paralysis.— {1)  Nu- 
cleus alone. — Lesions  affecting  the  nucleus  alone  are  not  common 
but  may  occur  as  a  result  of  hemorrhage,  tumour,  and  chronic  sof- 
tening, or  in  the  course  of  diphtheria,  anterior  poliomyelitis,  and 
bulbar  paralysis. 

(2)  Crossed  paralysis.— A  special  form  of  motor  disturbance  is 
crossed  paralysis — palsy  of  the  face  on  one  side  and  of  the  arm  and 
leg  on  the  opposite  side,  the  facial  paralysis  being  in  this  case  on  the 
same  side  as  the  lesion.  If  this  condition  is  present,  it  is  indicative 
of  a  lesion  in  the  lower  part  of  the  pons,  involving  the  nerve  between 
its  nucleus  and  the  point  upon  the  side  of  the  pons  from  which  it 
emerges.  In  this  form  of  paralysis  the  location  of  the  lesion  is  very 
definitely  in  the  lower  portion  of  the  pons,  for,  if  it  is  in  the  upper 
portion,  the  facial  paralysis  will  be  upon  the  same  side  as  that  of  the 
arm  and  leg  (ordinary  hemiplegia),  because  in  this  case  the  facial 
fibres,  like  those  of  the  arm  and  leg,  are  invaded  above  their  point  of 
decussation. 


172 


THE  EVIDENCES  OF  DISEASE 


(3)  At  its  point  of  emergence  from  the  pons  (Figs.  27  and  28) 
the  nerve  may  be  involved  by  tumours,  gummata,  basal  meningitis, 
or  endarteritis  of  syphilitic  origin  and  fracture  of  the  base.  Syph- 
ilis is  the  most  important  factor  in  these  basal  lesions,  which  are 


1 


Fig.  27. — The  base  of  the  brain.    Eedrawu  froiu  Gray. 

always  accompanied  by  evidences  of  involvement  of  other  cranial 
nerves  (Dana). 

(4)  During  its  course  through  the  bony  canal  (aqueduct  of  Fallo- 
pius),  the  nerve  may  be  paralyzed  by  fracture  of  the  petrous  portion 
of  the  temporal  bone,  or  by  inflammation  or  caries  of  the  same,  due 
to  otitis  media. 

(5)  At  or  after  its  emergence  from  the  stylo-mastoid  foramen  the 
nerve  may  be  injured  by  blows ;  by  accidental  cutting  during  the. 


CAUSES  OF   FACIAL   PARALYSIS 


173 


removal  of  enlarged  cervical  glands,  parotid  or  other  tumours ;  and 
at  birth  by  direct  pressure  of  the  forceps.  In  the  latter  instance  it 
should  be  remembered  that  the  paralysis  may  be  due  to  intracranial 
hemorrhage,  but  in  this  case  other  paralyses  usually  coexist.     The 


f  lo.  28. — Points  of  exit  of  the  cranial  nerves  from  the  skull.     Redrawn  from  Henle. 


nerve  may  also  be  so  pressed  upon  by  swelling  of  the  parotid  gland 
that  it  loses  its  function. 

(6)  Paralysis   of  the  facial   may  be   present  as  a  part  of  mul- 


174  THE  EVIDENCES  OF  DISEASE 

tiple   neuritis,  locomotor  ataxia   (lesion   affecting   the   pons),   and 
hysteria. 

(7)  As  the  most  common  cause  of  central  facial  paralysis  is  either 
hemorrhage  or  tumour,  so  the  majority  of  cases  of  peripheral  facial 
paralysis  are  due  to  exposure  to  cold  and  consequent  diffuse  rheu- 
matic neuritis  of  the  facial  nerve  (Bell's  palsy,  q.  v.).  The  neuritis 
may  in  one  instance  affect  mainly  the  peripheral  terminations  of  the 
nerve,  in  another  that  portion  lying  in  the  Fallopian  canal. 

(8)  To  determine  the  particular  form  of  disease  which  is  respon- 
sible for  the  paralysis  requires  a  review  of  the  history  and  accom- 
panying symptoms  which  may  point  to  the  conditions  mentioned  as 
possible  causes — e.  g.,  sudden  hemiplegia  and  unconsciousness  in 
an  old  person  with  atheromatous  arteries ;  or  vertigo,  vomiting,  con- 
vulsions, and  paralysis  of  other  cranial  nerves  in  tumour  of  the 
brain. 

The  location  of  a  peripheral  lesion  may  be  ascertained  within  certain  limits 
by  testing  the  sense  of  taste  in  the  anterior  two  thirds  of  the  tongue.  If  the 
sense  of  taste  is  partly  or  entirely  lost,  the  lesion  must  be  between  the  geniculate 
ganglion  of  the  nerve  and  the  point  where  the  chorda  tympani  is  given  off.  If 
it  is  not  lost,  the  lesion  is  either  central  to  the  genu  or  peripheral  to  the  chorda. 
In  the  greater  number  of  cases  it  is  peripheral. 

The  hearing  power  of  the  ear  on  the  paralyzed  side  may  be  abnormally 
acute  or  less  than  normal.  If  abnormally  sensitive,  it  indicates  that  the  lesion 
extends  into  the  Fallopian  canal  and  affects  the  nerve  to  the  stapedius,  para- 
lyzing it  and  allowing  the  unopposed  tensor  tympani  to  tighten  the  drum 
membrane.     If  the  hearing  is  impaired,  it  is  usually  due  to  otitis  media. 

(c)  Bilateral  or  Double  Facial  Paralysis  {Facial  Diplegia).— This 
is  of  very  rare  occurrence,  and  when  present  is  caused  by  bilateral 
and  symmetrical  cortical  lesions :  tumour  or  gummatous  disease  at 
the  base  of  the  brain,  disease  of  the  pons — viz.,  a  lesion  at  the  point  of 
decussation  of  the  face  fibres,  disease  of  the  basilar  artery,  acute  and 
chronic  bulbar  paralysis,  diphtheritic  multiple  neuritis,  and  double 
mastoiditis  of  otitic  origin. 

XIII.  Miscellaneous  Affections  of  the  Head  and  Face.— (r?)  Syph- 
ilitic or  Tuberculous  Ulceration. — Indurated  grayish  spots  upon  the 
face  which  break  down,  giving  rise  to  deep,  scooped-out  ulcers  with 
hard,  thickened  borders,  and  leaving  smooth,  white,  circular  cicatri- 
ces, are  ulcerated  subcutaneous  gummata.  It  is  sometimes  difficult 
to  distinguish  an  ulcerating  gumma  from  a  tuberculous  ulcer,  but  in 
the  latter  the  ulcer  is  more  shallow,  the  edges  are  flat  and  soft,  and 
the  scar  reddish  or  purple.  If  the  diagnosis  is  uncertain,  an  attempt 
may  be  made  to  find  the  tubercle  bacillus  or  the  therapeutic  test  may 
be  applied. 


HEAD  AND  FACE— EAR  175 

(b)  Herpes  Zoster. — One  or  more  groups  of  small  vesicles  seated 
upon  an  inflamed  base,  attended  by  a  burning  or  neuralgic  pain,  and 
occurring  along  the  course  of  one  or  more  branches  of  the  fifth  nerve, 
is  herpes  zoster. 

(c)  Distended  Veins. — Distended  or  enlarged  veins  upon  the  scalp 
may  be  due  to  tumours  of  the  neck,  thrombosis  of  the  lateral  sinus, 
or  meningitis.  They  are  especially  prominent  in  chronic  hydro- 
cephalus. 

{d)  Erysipelas  of  the  Face  and  Head. — Redness  beginning  over 
the  bridge  of  the  nose  or  at  the  site  of  an  abrasion,  spreading  rapidly 
over  the  face  and  scalp,  the  advancing  edge  being  well  defined,  causing 
great  oedema  of  the  face,  eyelids,  ears,  and  scalp,  which  sadly  alters 
the  patient's  appearance,  and  attended  with  sudden,  usually  high, 
fever,  is  erysipelas  {Streptococcus  pyogenes). 

(e)  Excessive  Sweating  of  the  head  in  a  child  is  suggestive  of 
rachitis  {q.  v.).,  although  it  is  observed  to  a  considerable  extent  in 
many  children  who  are  not  rachitic. 


SECTION    XV 
THE  EAR 

I.  Pain. — (a)  Otitis  Media. — By  far  the  most  frequent  cause  of 
severe  pain  in  the  ear  (earache)  is  an  otitis  media  secondary  to  scarlet 
fever,  epidemic  influenza,  acute  simple  rhino-pharyngitis  or  tonsilitis, 
measles,  diphtheria,  and  typhoid  fever.  It  is  most  common  in  chil- 
dren and  may  explain  an  obscure  infantile  illness. 

{h)  Other  Causes  of  Earache. — Pain  in  the  ear  may  be  also  due  to 
decaying  teeth,  alveolar  abscess,  mastoid  disease,  abscess  of  the  meatus, 
foreign  body  in  the  ear,  neuralgia,  rheumatism  of  temporo-maxillary 
articulation,  and,  if  in  the  right  ear,  aneurism  of  the  innominate. 
Ear  pain  is  sometimes  due  to  ulcer  or  cancer  of  the  tongue. 

II.  Colour.  — (a)  Waxy. — The  external  ear,  when  abnormally  white, 
waxy,  or  transparent,  may  be  simply  a  manifestation  of  the  general 
loss  of  colour  incident  to  the  various  forms  of  anaemia,  leucaemia, 
myxoedema,  and  other  conditions  in  which  pallor  {q.  ■y.)  is  a  symptom. 

{h)  Blue. — A  livid  or  bluish  tint  of  the  external  ear  is  usually  in- 
dicative of  general  cyanosis  and  its  causes  {q.  v.).  A  frost-bitten  ear 
is  at  first  blue,  but  when  frozen  is  waxy  white. 

(c)  Ecchymosis  loith  Swelling. — A  swollen  black  and  blue  pinna 
may  be  due  to  injury,  but  may  also  be  an  example  of  that  curious 
trophoneurosis,  hcematoma  auris  of  the  insane. 


176  THE  EVIDENCES  OF  DISEASE 

III.  Shape. — (a)  Stigmata  of  Degeneration. — Ears  unusually  promi- 
nent, long,  or  misplaced,  with  absence  of  helix,  antihelix,  or  lobule, 
are  marks  of  degeneration  or  imperfect  physical  development. 

(b)  Tophi. — Small  hard  nodules,  found  usually  on  the  borders  of 
the  ear,  are  chalky  masses  of  sodium  urate  of  gouty  origin  and  may 
be  so  numerous  as  to  cause  deformity. 

(c)  Abscess  of  Meatus,  etc. — If  the  external  ear  is  swollen  so  that 
it  stands  out  from  the  head,  and  if  on  inspection  the  meatus  is  found 
to  be  inflamed  and  almost  closed,  with  absence  of  tinnitus  and  ver- 
tigo, it  is  an  abscess  of  the  external  meatus.  The  calibre  of  the 
meatus  may  also  be  lessened  by  periostitis,  exostoses,  and  sebaceous 
cysts. 

IV.  Discharges. — («)  Blood. — A  fracture  of  the  base  of  the  skull 
may  cause  an  aural  hemorrhage,  followed  by  the  escape  of  a  consider- 
able amount  of  clear  cerebro-spinal  fluid  from  the  subarachnoid 
space.  Kupture  of  the  tympanic  membrane,  either  as  a  result  of 
injury  or  consequent  upon  an  otitis  media,  may  be  responsible  for  a 
discharge  of  blood — in  the  latter  case  mixed  with  pus.  Hemorrhage 
from  the  ear,  especially  in  the  newborn,  may  be  an  evidence  of 
haemophilia. 

{b)  Pus. — A  flow  of  pus — otorrhcea — may  be  either  acute  or 
chronic,  and,  while  it  may  be  due  to  a  polypus  or  abscess  of  the  ex- 
ternal meatus,  it  is,  in  the  great  majority  of  cases,  an  evidence  of 
otitis  media  with  or  without  complications.  A  slight  moisture  may 
be  indicative  of  eczema  or  impacted  cerumen  in  the  meatus. 

Y.  Hearing. — (a)  Tinnitus. — Subjective  sounds  heard  in  the  ear 
{tinnitus  aurium),  or  with  much  less  frequency  vaguely  located  in 
the  head  {tinnitus  cerebri),  are  of  varying  intensity  and  character. 
Asa  rule,  the  sound  is  heard  on  one  side  only.  It  is  a  very  common 
symptom,  and  may  be  due  to  so  many  conditions  that  in  a  given  case 
it  is  often  difficult  and  sometimes  impossible  to  determine  its 
etiology. 

The  character  of  the  sounds  may  be  of  service  in  ascertaining 
their  cause  (Dana),  although  too  much  reliance  must  not  be  placed 
upon  this  as  a  diagnostic  factor. 

If  they  are  of  a  boiling,  bubbling,  gurgling,  singing,  or  whistling 
quality,  their  origin  is  likely  to  be  found  in  rhino-pharyngeal  catarrh 
with  involvement  of  the  Eustachian  tube  and  middle  ear,  or  some 
source  of  irritation  in  the  external  meatus.  If  the  sound  is  of  a 
constant  rushing  or  knocking  character,  it  may  be  due  to  congestion, 
inflammation,  or  hemorrhage  of  the  labyrinth.  If  the  tinnitus  is 
like  a  systolic  bruit,  synchronous  with  the  heart  beat,  and  is  stopped 
by  carotid  compression,  it  is  presumably  due  to  vasomotor  paralysis,. 


TINNITUS  AURIUM— DEAFNESS  1Y7 

aneurism,  or  inflammation  of  the  middle  ear.  If  the  sound  is  of  a 
ringing  or  roaring  description,  it  is  probably  caused  by  chronic 
middle-ear  catarrh,  tympanic  disease,  syphilis,  brain  tumours,  or 
meningitis. 

If  the  noise  is  referred  to  the  head  {tinnitus  cerebri)  rather  than 
the  ear,  and  neither  deafness  nor  aural  disease  be  present,  it  is  in  all 
likelihood  caused  by  arteriosclerosis  or  meningitis.  If  the  tinnitus 
is  of  a  complicated  character — viz.,  musical  sounds  or  words — it  is 
indicative  of  some  central  lesion. 

It  is  helpful  to  bear  in  mind  that  the  most  frequent  causes  of  tin- 
nitus aurium  are :  neurasthenia  and  the  neuropathic  diathesis,  with 
vasomotor  irregularity ;  diseases  of  the  ear,  as  impacted  cerumen, 
otitis  with  fluid  in  the  middle  ear  and  obstruction  of  the  Eustachian 
tube ;  blood  diseases,  as  anaemia  (with  coincident  cerebral  anaemia) 
and  leucaemia ;  toxaemic  states,  as  in  gout,  nephritis,  alcoholism,  and 
the  overuse  of  tobacco ;  the  arteriosclerosis  of  old  people ;  and  dis- 
turbances of  the  digestion. 

Other  and  less  frequent  causes  are  as  follows  : 

Hypertrophy  of  the  heart  and  aneurism  of  the  cerebral,  basilar,  or 
vertebral  arteries  may  cause  a  pulsating  tinnitus.  Tinnitus  may  con- 
stitute the  premonitory  aura  of  an  epileptic  seizure  or  initiate  an 
attack  of  catalepsy.  It  is  one  of  the  multiform  manifestations  of 
hysteria.  Xoises  in  the  ear,  due  perhaps  to  local  disease,  may  be  the 
basis  of  aural  hallucinations  in  delirium  tremens  and  insanity.  Asso- 
ciated with  vertigo  and  deafness  it  is  one  of  the  prominent  symptoms 
in  Meniere's  disease.  An  attack  of  migraine  is  frequently  preceded 
or  accompanied  by  sudden  loud  noises,  perhaps  like  a  pistol  shot. 
Buzzing  or  ringing  in  the  ears  may  precede  an  attack  of  intracranial 
hemorrhage  or  thrombosis.  Tinnitus  is  a  rare  occurrence  in  organic 
disease  involving  the  auditory  nucleus  or  tract,  e.  g.,  tumour.  It  is 
not  uncommon  as  a  tinnitus  cerebri  in  meningitis,  especially  chronic 
pachymeningitis  following  sunstroke,  chronic  alcoholism,  or  blows 
upon  the  head.  Tinnitus  with  deafness  may  be  due  to  the  adminis- 
tration of  the  cinchona  alkaloids,  as  well  as  salicylic  acid  and  its  com- 
pounds. Ergot  in  considerable  doses  may  give  rise  to  ringing  in 
the  ears  because  of  its  probable  action  in  producing  cerebral  anaemia. 
Various  subjective  sounds,  due  to  toxaemia,  circulatory  disturbances, 
or  aural  disease,  may  be  present  in  some  of  the  infections,  particu- 
larly cholera,  malarial,  typhoid,  and  typhus  fevers. 

(b)  Deafness. — In  the  majority  of  cases  deafness  depends  upon 
disease  of  the  tympanum,  middle  ear,  or  Eustachian  tube.  It  may, 
however,  be  due  to  disease  of  the  auditory  nerve,  its  nucleus,  or  its 
cortical  centre,  in  which  case  it  is  spoken  of  as  "  nervous  deafness." 


178  THE  EVIDENCES  OP  DISEASE 

The  distinction  between  ordinary  deafness  and  the  nervous  form 
is  made  by  testing  with  the  watch  or  the  tuning  fork. 

If  the  ticking  of  the  watch  or  the  vibrations  of  the  tuning  fork 
are  heard  faintly  or  not  at  all  when  held  at  varying  distances  from 
the  ear  (aerial  conduction),  but  become  distinctly  audible  when  the 
watch  or  the  handle  of  the  fork  is  placed  in  contact  with  the  skull 
or  mastoid  process  (bone  conduction),  the  deafness  is  of  the  ordinary 
variety  and  due  to  aural  disease.  If,  on  the  other  hand,  watch  and 
fork  are  heard  indistinctly  or  not  at  all,  both  in  contact  and  at  a  dis- 
tance, the  deafness  is  due  to  some  lesion  of  the  nerve  or  its  connec- 
tions. In  the  first  case  the  nerve  is  normal  and  can  appreciate 
vibrations  brought  by  the  bone,  while,  through  some  fault  in  the 
mechanism,  aerial  vibrations  are  not  transmitted  to  the  nerve  end- 
ings. In  the  second  case  the  nerve  is  at  fault  and  can  not  appreciate 
vibrations,  no  matter  how  well  they  may  be  conducted. 

Nervous  Deafness. — The  presence  of  nervous  deafness  having 
been  determined,  its  possible  causes  must  be  remembered.  The 
lesions  producing  it  may  affect  the  cortical  centre,  the  nucleus  and 
root  of  the  nerve,  or  its  terminations  in  the  labyrinth. 

The  eighth  nerve  has  a  double  function.  The  cochlear  branch  is 
the  nerve  of  hearing;  the  vestibular  branch,  which  supplies  the 
semicircular  canals,  is  the  space  sense  nerve.  The  cortical  centre 
for  the  auditory  nerve  is  situated  in  the  1st  and  2d  temporal  convo- 
lutions. 

(1)  Cortical  lesions. — As  a  clinical  curiosity  nervous  deafness  of 
both  ears  may  be  caused  by  bilateral  lesions  of  the  cortical  centres. 
Disease  of  the  left  cortical  centre  produces  word  deafness — inability 
to  understand  the  meaning  of  words,  although  the  sounds  may  be 
heard.  A  lesion  of  the  right  cortical  centre  may  give  rise  to  defect- 
ive hearing  in  the  left  ear.  Loss  of  hearing  due  to  hysteria  is  of 
cortical  origin.  Headache,  mental  strain,  and  "nervousness"  may 
produce  a  temporary  diminution  of  auditory  acuity,  although  the 
variation  from  these  causes  is  usually  in  the  direction  of  hyperacusis, 
or,  more  properly,  dysacusis,  when  ordinary  sounds  act  as  irritants. 

A  lesion  of  the  corpora  quadrigemina,  or  the  internal  capsule, 
may  involve  the  fibres  leading  to  the  nucleus  and  thus  impair  the 
power  of  audition.  The  particular  lesions  which  may  occur  here  are 
tumour,  abscess,  hemorrhage,  or  cortical  meningitis. 

(2)  Lesions  of  the  nucleus  and  the  root  of  the  nerve. — Disease  of 
the  nucleus  itself  is  rare,  but  at  the  base  of  the  brain  (Figs.  27  and 
28)  the  nerve  may  be  compressed  or  injured  by  tumours,  hemorrhage, 
fracture  of  the  base,  violent  blows  upon  the  head  without  fracture, 
and  meningitis      Of  these  causes  the  more  frequent  are  syphilitic 


NERVOUS  AND  NON-NERVOUS  DEAFNESS  179 

meningitis  in  the  adult,  and  epidemic  cerebro-spinal  meningitis  in 
children.  In  the  latter  the  deafness  may  be  permanent  and,  if  in 
au  infant,  deaf-mutism  may  result.  The  nerve  may  undergo  primary 
degeneration  in  locomotor  ataxia. 

(3)  Labyrinthine  disease. — In  the  great  majority  of  cases  nervous 
deafness  is  due  to  a  lesion,  either  primary  or  an  extension  of  middle- 
ear  disease,  affecting  the  terminations  of  the  nerve  in  the  internal 
ear — the  end  organ.  There  may  be  syphilitic  disease ;  inflammation, 
hemorrhage,  or  tumour  of  the  labyrinth;  tuberculous  disease  or 
injury  of  the  petrous  bone ;  and  atrophy  of  the  nerve  endings  in 
locomotor  ataxia.  Quinine,  salicylic  acid,  or  the  salicylates  may  be 
responsible  for  the  deafness  by  causing  labyrinthine  hypersemia. 
Meniere's  disease,  as  limited  by  some,  is  due  to  a  lesion  of  the 
labyrinth.  The  constant  noise  and  jarring  incident  to  certain  occu- 
pations (railway  engineers,  boiler  makers)  may  produce  nervous  deaf- 
ness. Loud  reports  or  explosions  have  a  similar  effect,  usually 
temporary  unless  the  concussion  is  sufficiently  violent  to  inflict  a 
traumatism.  Some  of  the  fevers,  notably  typhoid  and  typhus  fevers, 
the  septicaemic  form  of  pneumonia,  and  diphtheria,  are  attended 
with  marked  impairment  of  hearing  without  middle-ear  disease. 

The  determination  of  the  special  lesion  in  nervous  deafness  must 
be  made  from  a  comparison  of  the  associated  signs  and  symptoms, 
viz.,  those  of  tumour  or  abscess  of  the  brain,  intracranial  hemorrhage, 
or  basal  meningitis,  affecting  the  cortex,  nucleus,  or  nerve  root, 
together  with  a  careful  examination  of  the  ear  in  labyrinthine  dis- 
ease. Sudden  total  deafness  is  very  suggestive  of  syphilis  of  the 
internal  ear.  Hysterical  deafness  is  to  be  distinguished  by  its  affect- 
ing one  ear  only ;  by  its  suddenness  of  onset,  usually  following  strong 
emotion  or  shock;  by  its  incompleteness,  the  failure  concerning 
mainly  high  and  low  notes ;  by  the  equal  diminution  in  air  and  bone 
conduction  ;  by  the  presence  of  hysterical  stigmata  {q.  v.),  and  per- 
haps by  a  return  of  hearing  as  sudden  as  its  loss. 

Non-nervous  Deafness.— Ot  all  cases  of  deafness  by  far  the  great- 
est number  are  due  not  to  affection  of  the  nerve,  but  to  some  defect 
in  the  auditory  mechanism  for  conveying  vibrations  to  the  end- 
organ. 

The  diseases  and  conditions  of  the  ear  which  will  usually  be 
found  responsible  for  loss  or  impairment  of  the  power  of  hearing  are 
middle-ear  inflammation  resulting  from  simple  or  specific  infectious 
rhino-pharyngitis,  postnasal  adenoids,  enlarged  faucial  tonsils,  nasal 
polypi,  and  nasal  stenosis  from  any  cause.  Wax  in  the  meatus,  aural 
polypi,  parotitis,  or  other  inflammations  or  growths  may  produce 
deafness  by  closing  the  external  meatus. 


180  THE  EVIDENCES  OP  DISEASE 

(c)  Hyperacusis. — An  extraordinary  acuteness  of  the  sense  of 
hearing  {hyperacusis)  may  be  symptomatic  of  hysteria,  facial  paral- 
ysis with  loss  of  power  in  the  stapedius  muscle,  and  hypnosis. 

Allied  to  hyperacusis  is  dysacusis — the  causing  of  unpleasant 
sensations  by  ordinary  sounds — which  may  be  significant  of  the  cere- 
bral congestion  of  fevers,  or  an  irritable  condition  of  the  nervous 
system  during  convalescence  from  febrile  diseases  or  in  debilitated 
persons.  It  is  a  rather  frequent  complaint  in  hysteria,  neurasthenia, 
hypochondriasis,  migraine,  and  severe  headaches.  It  may  be  present 
in  epilepsy,  meningitis,  and  tetanus. 


SECTION   XYI 

THE  EYE 

The  signs  and  symptoms  referable  to  the  eye  are  of  importance, 
not  only  with  reference  to  the  disorders  of  the  nervous  system  but 
also  in  connection  with  diseases  of  other  organs.  These  signs  and 
symptoms  will  be  enumerated  in  the  usual  order  of  a  clinical  exam- 
ination. 

I.    THE    EYELID 

{a)  Swelling,  Puffiness. — The  eyelids,  particularly  the  lower,  are 
swollen  in  general  anasarca,  and  are  usually  the  earliest  seat  of 
oedema  of  renal  origin.  Anaemia  is  not  infrequently  attended  by 
swelling  of  the  lids.  A  bloated  appearance  of  the  eyes,  possibly 
with  ecchymoses,  is  common  in  the  later  stages  of  a  severe  pertussis. 
The  effect  of  full  doses  of  arsenic  in  causing  pufiiness  of  the  lids  is 
familiar.  Angioneurotic  oedema  may  be  seen  in  this  locality,  and  is 
perhaps  analogous  to  the  oedema  of  the  lids  and  forehead  which 
infrequently  occurs  in  neurotic  adolescents. 

Because  of  the  anatomical  connection  between  the  vessels  of  the 
face  and  those  of  the  cranial  cavity  (Figs.  29  and  30),  cerebral  throm- 
bosis may  give  rise  to  a  swelling  of  one  or  both  eyelids,  with  some 
protrusion  of  the  eyeball,  the  puffiness  subsequently  extending  to 
the  face. 

Erysipelas  and  glanders,  the  former  especially,  may  be  the  cause 
of  swelling  so  great  as  to  prevent  opening  of  the  eye.  Severe  coryza, 
hay  fever,  and  iodism  may  induce  noticeable  swelling  of  the  lids. 
So,  also,  the  lids  are  swollen  in  measles,  variola,  and  occasionally  in 
varicella. 

{h)  Hordeolum. — A  minute,  painful  abscess  at  the  edge  of  the  eye- 
lid is  a  sty  or  hordeolum.     If  occurring  in  successive  series,  they  may 


AFFECTIONS  OF  EYELID 


181 


be  indicative  of  the  overuse  of  defective  eyes,  or  more  frequently  of 
digestive  or  genital  disorders.  If  small,  single,  and  superficial,  they 
are  of  purely  local  origin.  They  must  be  differentiated  from  chala- 
zion (cyst  of  a  Meibomian  gland),  a  slow-growing  tumour  which  may 
become  inflamed  and  suppurate. 


.^(Communication  through  parietal  foramer\ 


External 
Jugular  vein 


Fig.  29. — Diagram  showing  the  communications  (indicated  in  the  figure  by  black  dots) 
existing  between  tlie  superior  longitudinal  and  lateral  sinuses  and  the  external  veins. 
Redrawn  from  Leube. 


A  cystic  swelling,  of  some  standing,  toward  the  inner  canthus,  is 
a  mucocele  (chronic  dacryocystitis),  which  may  become  inflamed 
and  suppurate.  And  there  may  be  an  acute  inflammation  of  the 
lachrymal  sac  following  measles,  scarlet  fever,  ophthalmia,  or  other 
diseases  in  which  there  is  conjunctival  inflammation. 

(c)  Blepharitis. — If  the  edges  of  the  eyelids  are  reddened,  thick, 
inflamed,  and  crusted  with  secretions,  possibly  showing  minute  ulcers 
or  pustules,  the  condition  is  a  blepharitis  resulting  from  a  previous 
ophthalmia  or  an  attack  of  measles.  It  is  usually  indicative  of  anae- 
mia and  a  catarrhal,  perhaps  tuberculous,  diathesis. 

{d)  Verruca. — Warts  upon  the  eyelids  are  not  common,  and  are 
only  of  importance  in  old  people  because  of  the  possibility  of  com- 
mencing epithelioma. 
14 


182 


THE  EVIDENCES  OF  DISEASE 


(e)  Ulcers.     1.  Epithelioma. — In  an  elderly  person  a  shallow,  flat 
ulcer  on  the  nasal  side  of  the  lower  lid,  usually  concealed  by  a  scab, 


External  jugular 
vein 


Communication  with  veins 
at  back  of  neck 

Fig.  30. — Diagram  showing  the  communications  (indicated  in  the  figure  by  black  dots) 
between  the  lateral  and  cavernous  sinuses  and  the  external  veins.  Kedrawn  from 
Leube. 


EYELIDS— COATS  OF  EYEBALL  183 

and  having  lasted  for  several  years,  is  quite  certainly  an  epitheli- 
omatous  ulcer. 

2.  Syphilis. — The  initial  lesion  of  syphilis  may  occur  on  the  eye- 
lid in  the  shape  of  a  small,  moist,  slightly  ulcerated  surface,  with 
considerable  induration  and  swelling.  The  diagnosis  can  usually  be 
made  with  certainty  only  by  the  secondary  symptoms.  A  very  rare 
lesion  is  an  ulcer  in  the  tertiary  stage  of  syphilis,  deeper,  more 
inflamed,  and  punched  out  in  appearance  than  in  epithelioma,  which 
is  practically  the  only  disease  with  which  it  may  be  confounded. 

(/)  Tophi. — As  in  the  ear,  so  may  small  nodules  of  sodium  urate 
form  in  the  eyelids,  significant  of  the  gouty  diathesis. 

{g)  Colour  of  the  Lids.  1.  Xanthelasma. — One  or  more  soft  and 
very  slightly  elevated  yellow  patches  on  the  eyelids  of  elderly  people, 
varying  in  size  from  a  mere  point  to  the  size  of  a  finger  nail,  and 
situated  near  the  inner  angle  of  the  eye  (if  unilateral,  usually  on  the 
left),  is  xanthelasma. 

2.  Duskiness. — A  darkening  or  duskiness  of  the  lids  and  under 
the  eyes  is  seen  in  some  women  during  menstruation  and  early  in 
pregnancy,  also  in  menorrhagia  and  long-continued  leucorrhoea. 
Duskiness  may  be  very  prominent  in  the  anaemia  and  pallor  of  bru- 
nettes, or  after  fatigue,  mental  excitement,  loss  of  sleep,  or  severe 
pain,  and  in  exhausting  diseases.  Dark  circles  round  the  eyes  con- 
stitute a  time-honoured,  if  not  always  reliable,  symptom  of  self- 
abuse. 

{h)  Blepharospasm. — (See  Index.) 

{i)  Lagophthalmos. — The  unnaturally  open  eye  may  be  due  to  the 
contraction  of  a  scar,  to  loss  of  power  in  the  orbicularis  palpebrarum, 
facial  paralysis,  or  exophthalmic  goitre.  In  the  latter  disease  it  is 
conjoined  with  protrusion  of  the  eyeball  (proptosis)  and  inability  to 
follow  with  the  upper  lid  a  downward  movement  of  the  eyeball 
(vonGraefe's  sign). 

Incomplete  closure  of  the  lids  during  sleep  is  a  common  symp- 
tom of  exhausting  diseases,  particularly  in  children.  As  the  eye- 
balls are  normally  turned  upward  while  sleeping,  the  sclerotic  is  thus 
exposed,  giving  a  ghastly  expression  to  the  face.  A  similar  rolling 
up  of  the  eye  and  imperfect  closing  of  the  lids  is  frequently  seen  in 
hysterical  individuals. 

(/)  Ptosis.— Dvoo^mg  of  the  upper  eyelid  (see  Index). 

II.  THE  CONJUNCTIVA,  SCLEROTIC,  AND  CORNEA 

{a)  Colour.  1.  Yellow  Sclerotic— ^een  in  jaundice,  and  may  be 
due  to  fatty  deposits,  triangular  in  shape,  apex  at  the  cornea,  and 
running  laterally  toward  the  angles  of  the  eye. 


ig4  THE  EVIDENCES  OP  DISEASE 

2.  Bluish-white  or  Pearly  Sclerotic. — This  is  found  in  the  anaem- 
ias,  in  phthisis,  in  nephritis,  and,  by  contrast  with  the  discoloured 
face,  in  Addison's  disease. 

3.  hiflamed  or  Injected  Conjunctiva. — This  may  be  caused  by 
gonorrheal  infection  or  by  the  bacillus  of  diphtheria,  in  which  case 
it  is  attended  with  a  profuse  purulent  discharge  or  the  formation  of 
pseudo-membrane.  A  certain  amount  of  conjunctivitis  is  present  in 
measles,  hay  fever,  coryza,  and  influenza  of  the  catarrhal  type. 
Typhus  fever  presents  a  brilliantly  injected  conjunctiva,  as  does  yel- 
low fever  to  a  lesser  degree.  Meningitis,  either  simple  or  tubercu- 
lous, is  a  not  infrequent  cause  of  inflammation  and  discharge,  per- 
haps unilateral.  Facial  paralysis,  by  causing  undue  exposure  of  the 
eyeball,  may  give  rise  to  redness  and  inflammation. 

Neuralgia  of  the  fifth  nerve  and  glaucoma  produce  conjunctival 
congestion  ;  so  also  do  full  doses  of  arsenic  or  potassium  iodide,  espe- 
cially if  there  is  an  idiosyncrasy.  Ulcers  of  the  cornea  are  attended 
with  reddening  of  the  eye.  The  possible  presence  of  a  foreign  body 
should  be  remembered. 

Subconjunctival  hemorrhage  or  ecchymosis  may,  after  the  receipt 
of  an  injury,  indicate  a  fracture  of  the  base  anteriorly,  the  blood 
passing  forward  into  the  orbit.  The  non-surgical  causes  are  the  vio- 
lent straining  which  may  occur  in  pertussis,  severe  vomiting,  obsti- 
nate constipation,  or  heavy  lifting.  Subconjunctival  ecchymosis 
may  also  occur  in  the  epileptic  seizure  and  in  asthma  or  severe  dysp- 
noea. They  may  be  hemorrhagic  infarcts  and  significant  of  ulcera- 
tive endocarditis. 

{h)  Dryness  and  Moisture  of  the  Eye. — The  eye  may  become  dry 
and  glazed  in  collapse  or  the  typhoid  status,  as  well  as  in  disease 
attended  by  lagophthalmos. 

Lachrymation — an  increased  secretion  of  watery  fluid — usually 
accompanies  irritation  or  inflammation  of  the  conjunctiva,  and 
accordingly  is  present  in  measles,  influenza,  pertussis,  and  typhus 
fever  in  the  early  stages,  hay  fever,  asthma,  coryza,  trifacial  neu- 
ralgia, facial  paralysis,  iodism,  and  foreign  bodies  in  the  eye.  The 
moist  eye  of  the  chronic  alcoholic  is  familiar.  Aside  from  lachry- 
mation, the  tears  may  overflow  the  edge  of  the  lids  {epiphora) 
because  of  displacement  of  the  puncta  lachrymalis  or  obstruction 
between  the  punctum  and  nasal  opening  of  the  duct. 

(c)  The  Cornea. — 1.  Arcus  Senilis. — Fothergill  made  a  distinc- 
tion between  the  true  and  the  false  arcus  senilis.  The  true  arcus  is 
an  ill-defined,  grayish,  partial  or  complete  ring  at  the  circumference 
of  the  cornea,  the  cornea  itself  being  somewhat  hazy.  ^Tien  pres- 
ent it  is  an  indication  of  beginning  or  well-marked  arteriosclerosis, 


CORNEA- PUPIL  185 

atheroma,  gout,  chronic  nephritis,  and  the  degeneration  of  old  age. 
The  false  arcus  is  a  sharply  delineated  ring  of  a  clear  yellow  or  yel- 
lowish-white colour,  due  to  a  deposit  of  fat,  and  is  not  of  special 
diagnostic  significance. 

2.  Keratitis. — Interstitial  keratitis  is  the  only  variety  which  is  of 
general  medical  interest,  because  of  its  usual  cause — syphilis.  The 
cornea  has  the  appearance  of  ground  glass,  with  small  clearer  spots 
here  and  there  through  which  the  pupil  may  be  indistinctly  seen. 
It  is  usually  symmetrical,  and  occurs  between  5  and  15  years  of  age. 
Confirmatory  signs  should  be  looked  for  in  the  lips,  teeth,  nasal 
bones,  and  general  appearance. 

It  is  not  to  be  forgotten  that  a  hazy  or  steamy  cornea,  with  severe 
pain  around  a  reddened  eye,  possibly  with  nausea  and  vomiting,  and 
a  tense  globe,  are  the  symptoms  of  glaucoma. 

3.  Ulcers  of  Cornea. — A  reddened,  painful,  photophobic  eye,  with 
a  clear  cornea,  which  on  close  inspection  shows  a  slight  loss  of  sub- 
stance at  one  point,  is  an  example  of  a  corneal  ulcer.  This  may  be 
found  in  connection  with  exophthalmic  goitre,  and  is  due  to  the  con- 
stant exposure  of  the  eye  consequent  upon  the  inability  of  the  lids 
to  cover  the  protruding  eyeballs. 

The  unilateral  inflammation  of  the  eye  in  meningitis  may  lead  to 
a  corneal  ulcer.  In  disease  of  the  first  division  of  the  fifth  nerve, 
with  resulting  anaesthesia  of  the  cornea  and  conjunctiva,  the  cornea 
may  undergo  intractable  ulceration,  due  probably  to  trophic  altera- 
tions, although  latterly  the  importance  of  the  trophic  element  has 

been  denied. 

III.    THE    PUPIL 

The  points  to  be  observed  about  the  pupil  are  its  state  of  dilata- 
tion or  contraction,  inequality  (anisocoria),  response  to  light,  response 
to  accommodation,  and  the  skin  reflex. 

I.  Physiological  Conditions. — {a)  Diameter  of  the  Pupil. — This, 
under  ordinary  circumstances,  is  4  millimetres,  and  may  be  measured 
by  holding  a  properly  graduated  rule  close  to  the  eye.  Commonly 
the  observer  is  able  to  detect  any  important  abnormality  (both  small, 
both  large,  unequal)  in  this  respect  without  artificial  aid. 

{h)  Eespotise  to  Light. — The  responsiveness  of  the  pupil  to  light 
is  determined  for  each  eye  separately  by  asking  the  patient  to  look 
at  the  light  from  a  window.  Still  keeping  the  eyes  in  the  same 
direction,  the  hands  of  the  physician  are  placed  over  and  close  to, 
but  not  touching,  the  eyes.  One  hand  is  then  suddenly  removed  and 
the  behaviour  of  the  pupil  noted.  Normally  the  pupil  contracts  on 
exposure  to  light — the  direct  reflex.  This  hand  being  replaced,  the 
other  pupil  is  tested  in  a  similar  manner.     In  normal  eyes  the  pupil 


186  THE  EVIDENCES  OF  DISEASE 

of  the  covered  eye  will  also  contract — the  ifidirect  reflex.  If  particu- 
lar care  in  this  examination  is  desirable,  artificial  light  in  a  dark 
room  should  be  employed.  While  the  patient  with  eye  covered  looks 
toward  the  darkest  part  of  the  room,  the  light  is  brought  suddenly 
before  the  uncoyered  eye,  at  a  distance  of  3  or  4  feet,  so  that  the 
pupillary  accommodation  reflex  may  be  eliminated. 

(c)  Response  to  Accommodation. — As  the  pupil  grows  smaller  when 
the  eyes  converge  and  the  ciliary  muscle  contracts  in  the  act  of  ac- 
commodation for  near  objects,  this  function  should  also  be  examined. 
Let  the  examiner  place  his  finger  tip  12  or  15  inches  from  the  eye,  nearly 
in  a  line  with  some  object  at  least  20  feet  away,  and  direct  the  patient 
to  look  first  at  the  finger  and  then  at  the  distant  object  until  it  is 
decided  whether  or  not  the  pupil  contracts  when  looking  at  the  finger. 

{d)  Skin  Reflex. — The  pupil  also  dilates  if  the  skin  of  the  neck  is 
pinched  or  pricked,  because  by  so  doing  the  cervical  sympathetic  is 
irritated. 

{e)  Physiology  of  the  Iris. — Contraction  of  the  iris  is  effected  by 
circular  or  sphincter  fibres  which  are  controlled  by  a  reflex  nervous 
mechanism  (Fig.  31),  while  dilatation  is  secured  by  a  set  of  nerve 
fibres  which  oppose  the  action  of  the  oculomotorius  upon  the  circu- 
lar muscles  of  the  iris. 

The  balance  of  the  pupil  is  preserved  by  the  constant  action  of 
these  nerve  mechanisms,  which  keep  the  radial  and  circular  muscle 
fibres  of  the  iris  in  tonic  antagonistic  contraction.  Irritation  of  the 
sympathetic  or  dilator  mechanism,  as  by  pinching  the  neck,  overcomes 
the  constricting  mechanism  and  the  pupil  grows  larger.  Paralysis  of 
the  sympathetic  allows  the  oculomotorius  to  act  unopposed  and  the 
pupil  contracts.  Similarly  stimulation  of  the  oculomotor  mechanism 
will  cause  contraction,  while  paralysis  produces  dilatation  of  the  pupil. 

II.  Pathological  Conditloiis.— There  may  be,  therefore,  three  va- 
rieties of  paralysis  of  the  iris,  or  iridoplegia  (with  pupils  small  or  of 
a  medium  size),  as  follows : 

Loss  of  response  to  light — reflex  iridoplegia. 

Loss  of  response  to  accommodation — accommodative  iridoplegia. 

Loss  of  response  to  irritation  of  the  skin  of  the  W(^c^•— absent  skin 
reflex. 

The  abnormalities  of  the  iris  and  pupil,  together  with  their  diag- 
nostic indications,  may  be  stated  as  follows  : 

(a)  Iris  and  Pupillary  Outline. — Inflammation  of  the  iris  may 
be  indicative  of  gout,  rheumatism,  or  syphilis.  If  iritis  is  present, 
the  iris,  normally  blue  or  gray,  becomes  of  a  greenish,  muddy  hue, 
the  pupil  responds  sluggishly  to  light  and,  if  the  disease  is  uni- 
lateral, is  smaller  than  the  other,  because  of  the  iritic  congestion  and 


IRIS  AND  PUPIL 


187 


consequent  swelling.  There  is  a  narrow  zone  of  pinkish  hyperasmia 
around  the  edge  of  the  cornea.  If  the  iris  is  brown  or  black,  little 
change  of  colour  occurs.  AVhile  one  iris  may  normally  differ  in 
colour  from  the  other,  if  one  is  green  and  the  other  blue,  the  exist- 
ence of  an  iritis  should  be  strongly  suspected.     Kheumatic  iritis  is 


Fig.  31. — Nervous  mechanism  of  the  iris. 

Path  of  sensory  stimulation  through  optic  tract. 

^ Path  of  motor  impulse  through  third  nerve  to  sphincter  fibres,  causing  contraction 

of  pupil. 
Solid  black  =  path  of  impulses  from  point  near  nucleus  of  third  nerve  and  ciho-spinal 

centre  through  sympathetic  to  dilator  fibres,  causing  dilatation  of  pupil. 

usually  unilateral  and  is  prone  to  relapse  ;  so  also  is  the  rarer  gouty 
iritis.  Syphilitic  iritis  occurs  only  during  the  secondary  stage  of  the 
disease,  is  commonly  bilateral,  and  rarely  relapses. 

An  irregular  outline  of  the  pupil  is  due  to  iritis  and  subsequent 
adhesions  between  the  posterior  surface  of  the  iris  and  the  anterior 


188  THE  EVIDENCES  OF   DISEASE 

surface  of  the  lens  (posterior  synechias).    A  very  small  pupil  is  rarely 
quite  circular  in  shape. 

(b)  Anisocoria. — Inequality  of  the  pupils  may  be  present  in 
healthy  persons  and  in  those  whose  eyes  refract  unequally.  For  the 
special  pathological  relations  of  unequal  pupils  see  paragraphs  (/), 
(1)  and  ig),  (1)  following. 

(c)  Hippus. — A  rapid  contraction  and  dilatation  of  the  pupil  on 
sudden  exposure  to  light  is  normal  in  some  healthy  individuals.  It 
is  also  seen  in  the  early  stage  of  acute  meningitis,  in  disseminated 
sclerosis,  in  hysteria,  and  has  been  claimed  to  be  somewhat  charac- 
teristic in  epileptics.  In  Cheyne-Stokes'  respiration  the  pupils  may 
be  dilated  during  the  period  of  rapid  breathing  and  contracted  in 
the  apnceic  interval.  A  considerable  percentage  of  phthisical  pa- 
tients present  rapid,  transient,  unsymmetrical  dilatation  of  the 
pupils  (Eampoldi,  Destree),  presumably  due  to  irritation  of  the  upper 
thoracic  ganglion  by  tuberculous  glands.  This  statement  has  been 
partly  verified  in  my  experience. 

{d)  Argyll- Robertson  Pupil. — If  the  pupil  does  not  respond  to 
light  and  shade,  but  does  to  accommodation,  it  constitutes  the  Argyll- 
Eobertson  pupil,  a  condition  most  frequently  present  as  a  symptom 
of  locomotor  ataxia,  and  due  to  sclerotic  changes  in  Meynert's  fibres, 
or  in  that  portion  of  the  third  nerve  nucleus  which  presides  over  the 
light  reflex,  the  portion  which  regulates  the  accommodative  contrac- 
tion not  being  involved.  The  pupil  in  this  condition  is  usually  con- 
tracted (spinal  miosis),  because  the  lesions  in  the  cervical  cord  inter- 
fere with  the  dilating  mechanism.  Late  in  the  disease  the  accom- 
modation reflex  also  may  be  lost.  A  similar  pupillary  condition  is 
seen  as  a  symptom  of  intracranial  syphilis  and  progressive  paresis 
of  the  insane. 

(e)  Accommodative  Iridoplegia  with  Preserved  Light  Reflex. — This 
condition  is  the  opposite  of  the  Argyll-Robertson  pupil.  It  is  of 
infrequent  occurrence  and  may  denote  a  lesion  affecting  a  portion  of 
the  oculo-motor  nucleus  in  which  lie  the  cells  causing  accommoda- 
tive reaction.  It  may  also,  but  not  always,  exist  with  the  cycloplegia 
(paralysis  of  the  ciliary  muscle)  which  occurs  after  diphtheria. 

(/)  Dilated  Pupils. — Dilatation  of  the  pupils  (mydriasis)  may  be 
due  to  irritation  of  the  dilating  mechanism  overcoming  the  con- 
tractors, or  paralysis  of  the  contractors  allowing  unopposed  dilata- 
tion. 

(1)  Unilateral  Dilatation. — One  pupil  may  be  dilated  as  the  result 
of  disease  of  the  optic  nerve,  as  in  optic  atrophy ;  or  lessened  trans- 
parency of  the  media,  as  in  cataract  and  glaucoma.  If  the  pupil  of 
the  diseased  eye  does  not  react  directly  to  light,  but  does  react  when 


THE  PUPIL  189 

the  light  is  thrown  into  the  sound  eye  (consensual  or  indirect  reac- 
tion), it  shows  that  the  disease  is  in  the  optic  nerve  or  tract  and  that 
the  oculo-motor  nerve  of  the  diseased  side,  its  nucleus,  and  nuclear 
connections  with  the  corpora  quadrigemina,  and  through  the  latter 
with  the  opposite  optic  tract,  are  not  involved.  Unilateral  dilatation 
may  be  due  to  irritation  of  the  cervical  sympathetic  by  a  tumour  of 
the  neck,  by  aneurism  of  the  aorta,  or  aneurism  of  the  innominate 
(pupil  of  the  right  eye).  One  pupil  is  dilated  in  paralysis  of  one 
third  nerve  {q.  v.). 

Unilateral  dilatation,  unless  due  to  the  local  use  of  mydriatics, 
requires  a  thorough  examination  before  excluding  serious  organic 
disease. 

(2)  Bilateral  Dilatation. — Double  atrophy,  amaurosis  or  blindness 
from  any  cause,  will  obviously  give  rise  to  dilatation  and  failure  of 
the  light  reflex.  Mydriasis  may  result  from  cerebral  angemia  and 
poorly  filled  blood  vessels,  largely  because  the  centres  lack  the 
stimulus  of  the  blood-supply,  as  in  anaemia,  syncope,  shock,  nausea, 
and  aortic  regurgitation.  The  pupils  are  also  dilated  in  neuras- 
thenia, hysteria,  and  strong  emotion;  severe  dyspnoea  and  asphyxia; 
cerebral  hemorrhage,  thrombosis,  tumour  and  abscess ;  the  later 
stages  of  meningitis  and  diphtheritic  paralysis,  from  lesions  of  the 
oculo-motor  nerve  or  nucleus ;  and  in  melancholia,  trance,  and  the 
coma  following  an  epileptic  convulsion. 

The  drugs  which  have  a  mydriatic  action,  local  or  constitutional, 
are  aconite,  alcohol,  atropine,  chloral,  chloroform,  cocaine,  conium, 
duboisine,  hyoscyamus,  nitrous  oxide,  stramonium,  strychnine,  and 
tobacco. 

When  both  pupils  are  dilated  the  eye  has  a  peculiarly  brilliant 
expression,  which  may  be  particularly  noticeable  in  mania,  in  fevers 
attended  with  active  delirium,  exophthalmic  goitre,  and  poisoning 
with  belladonna. 

{g)  Contracted  Pupils. — Contraction  of  the  pupils  (miosis)  may 
be  due  to  irritation  of  the  oculo-motor  system  or  to  paralysis  of  the 
dilators.  Congestion  of  the  vessels  of  the  iris  by  causing  an  increase 
in  bulk  of  the  latter  will  produce  the  same  effect. 

(1)  Unilateral  Contraction. — Small  size  of  one  pupil  may  be  con- 
genital, but,  like  aniscoria  (unequal  pupils)  in  general,  should  be 
looked  upon  as  a  likely  indication  of  more  or  less  serious  trouble. 

The  pressure  of  an  aortic  aneurism,  if  sufficiently  great  to  paralyze 
the  sympathetic  (dilator)  fibres  in  the  upper  thorax,  may  explain 
unilateral  miosis.  The  same  symptom  may  be  caused  by  locomotor 
ataxia,  general  paresis  of  the  insane  and  other  lesions  which  may  at 
times  be  largely  unilateral,  affecting  the  cervical  cord.     Unilateral 


190  THE  EVIDENCES  OF  DISEASE 

cerebral  lesions  so  placed,  and  of  such  a  character  as  to  irritate  the 
oculo-motor  centre,  may  cause  unsymmetrical  miosis. 

(2)  Bilateral  Contraction. — A  certain  degree  of  miosis  and  slug- 
gish contraction  of  the  pupil  is  normal  in  old  age,  and  the  pupils  are 
contracted  during  sleep  in  a  healthy  individual. 

Congestion  of  the  iris,  such  as  occurs  in  the  injected  eye  of 
typhus  fever,  causes  miosis ;  so  also  with  mitral  insufficiency  and 
other  conditions  producing  venous  congestion.  The  pupils  are  con- 
tracted in  retinitis  and  when  the  condition  of  photophobia  exists. 

Bilateral  disease  of  the  cervical  cord  and  the  cervical  spine,  by 
paralyzing  the  sympathetic  dilator  fibres,  may  allow  miosis.  Sym- 
metrical miosis  may  thus  be  significant  of  locomotor  ataxia  in  par- 
ticular, disseminated  sclerosis,  general  paresis,  spinal  meningitis, 
tumour  or  hemorrhage  of  the  cord,  bulbar  paralysis,  hemorrhage  into 
the  pons,  and  tuberculous  disease  of  the  cervical  vertebrae.  Irritating 
lesions  of  the  brain,  by  stimulating  the  third  nerve  centre,  will  cause 
miosis,  notably  cerebral  meningitis,  cerebral  or  dural  hemorrhage, 
and  tumour  or  abscess  of  the  brain.  It  is  present  in  the  early  stage 
of  sunstroke,  and  is  also  a  symptom  of  the  urgemic  state. 

Certain  drugs  have  a  very  characteristic  action  in  contracting  the 
pupil,  particularly  opium  and  its  alkaloids.  Others  are  eserine,  pilo- 
carpine, and  chloral  during  its  primary  action. 

(h)  Absent  Skin  Reflex. — If  the  pupil  does  not  dilate  on  pinching 
or  pricking  the  skin  of  the  neck,  or  using  the  faradic  brush  in  the 
same  region,  it  may  be  due  to  the  atrophy  of  the  iris  in  a  glaucom- 
atous eye  or  to  posterior  synechiae  following  iritis.  It  is  not  infre- 
quent in  general  paresis. 

IV.    THE   EYEBALL 

The  symptoms  which  may  be  observed  in  examining  the  eyeball 
relate  to  pain  in  and  around  the  eye,  its  protrusion  or  recession,  its 
position  and  its  degree  of  mobility. 

I.  Fain. — Pain  in  and  around  the  eye  is  most  frequently  due  to 
trigeminal  neuralgia  or  migraine.  With  reference  to  prompt  treat- 
ment, the  pain  of  acute  glaucoma  should  never  be  mistaken  for 
either  of  these.  The  presence  of  dimmed  vision,  a  reddened  eye, 
hazy  cornea,  dilated  pupil,  and  greatly  increased  tension,  perhaps 
with  nausea  and  vomiting,  will  declare  the  case  to  be  one  of  glau- 
coma. Inflammatory  diseases  of  the  iris  or  conjunctiva  and  foreign 
bodies  may  explain  a  painful  eye. 

Photophobia  is  a  form  of  eye  pain  excited  by  exposure  to  light. 
It  is  present  to  varying  degrees  in  the  conjuctivitis  of  measles,  epi- 
demic influenza,  the  early  stage  of  pertussis  and  severe  coryza,  or  the 


THE  EYEBALL  191 

formation  of  the  vesicles  of  variola  and  varicella  upon  the  cornea. 
Ocular  or  retinal  hyperaesthesia  is  a  form  of  photophobia  not  depend- 
ent upon  local  inflammatory  disease  of  the  eye,  and  is  usually,  although 
not  always,  due  to  functional  disturbance  of  the  optic  tract  and 
nerve  or  the  cortical  centres  for  vision.  It  is  a  frequent  symptom 
in  neurasthenia,  hysteria,  migraine,  and  at  times  the  hypnotic  state, 
and  is  not  unusual  in  the  acute  indigestions  of  children.  It  may 
be  present  in  cinchonism  and  in  the  early  stages  of  typhus  fever  and 
meningitis.  It  has  occurred  in  albuminuric  retinitis  and  aortic 
insufficiency  (osler). 

II.  Protrusion  of  the  Eyeball. — Exoplithalmos  or  protrusion 
of  the  eyeball,  when  bilateral,  has  as  its  most  common  explanation 
exophthalmic  goitre.  The  eyes  may  protrude  in  spasmodic  asthma 
or  other  conditions  attended  by  severe  dyspnoea.  Thrombosis  of 
the  superior  longitudinal  sinus  may  be  attended  with  some  exoph- 
thalmos. A  patient  now  under  observation  has  a  marked  exoph- 
thalmos, apparently  as  a  result  of  enormous  cardiac  hypertrophy  due 
to  aortic  and  mitral  insufficiency.  There  may  be  a  moderate  proptosis 
in  paralysis  of  the  ocular  muscles.  It  should  be  remembered  that 
undue  exposure  of  the  sclerotic  will  give  an  impression  that  the  eyes 
are  protuberant. 

Swellings  or  tumours  may  displace  the  eyeballs  forward,  usually 
on  one  side,  perhaps  on  both  sides,  as  in  great  enlargement  of  the 
lachrymal  gland  and  aneurism,  exostosis,  or  cancer  of  the  orbit,  or 
tumours  of  the  upper  maxilla.  One  or  both  eyes  may  be  pushed 
downward  and  forward  by  subperiosteal  hemorrhages  into  the  upper 
portion  of  the  orbit,  which  may  be  present  as  one  of  the  lesions  of 
scurvy. 

III.  Recession  of  the  Eyeball. — Enoplithdlmos^  or  sinking  of 
the  eyeballs  into  the  orbit,  if  bilateral  may  be  due  to  absorption  of  the 
cushion  fat  of  the  orbital  cavity  such  as  takes  place  in  phthisis  pul- 
monalis,  marasmus,  diabetes,  typhoid  and  other  continued  fevers, 
the  cancerous  cachexia,  and  wasting  diseases  in  general.  It  may 
also  be  present  in  consequence  of  a  rapid  and  exhausting  drain  upon 
the  blood,  as  in  cholera,  severe  diarrhoea  and  large  hemorrhages,  or 
a  deficient  orbital  blood  supply  in  collapse. 

Unilateral  enophthalmos  may  be  indicative  of  a  lesion  of  the  cer- 
vical sympathetic  or  the  intracranial  sympathetic  ganglia  and  plex- 
uses interfering  with  nutrition  and  causing  atrophy  of  the  orbital 
connective  tissues  or  paralysis  of  Midler's  orbital  muscle.  In  high 
degrees  of  hypermetropia,  a  condition  in  which  the  antero-posterior 
diameter  of  the  eye  is  abnormally  short,  the  eyes  may  have  a  sunken 
appearance. 


192  THE  EVIDENCES  OF  DISEASE 

IV.  Position  of  the  Eyeball. — Xormally  during  sleep  the  eyes 
are  turned  upward,  so  that  the  cornea  is  well  protected.  The  same 
position  may  obtain  during  hysterical  coma  or  convulsions,  and  in  an 
epileptic  seizure.  In  ptosis  (paralysis  of  the  levator  palpebrae)  and 
in  chronic  hydrocephalus,  where  the  bulging  forehead  prevents  the 
proper  raising  of  the  upper  lid,  the  eyes  look  doivmvard  and  the  head 
must  be  tipped  back  in  order  to  see  an  object  on  or  above  a  hori- 
zontal plane.  If  both  eyes  are  turned  toward  the  same  side  it  consti- 
tutes conjugate  lateral  deviation  {q.  v.). 

V.  Disturbances  of  Ocular  Mobility. — The  functions  of  the 
nerves  and  muscles  of  the  eye  are  suflSciently  obvious  from  a  study  of 
the  diagram  (Fig.  32),  lack  of  space  forbidding  a  detailed  description. 
A  special  word  of  explanation  is  here  given  with  reference  to  the 
normal  conjugate  lateral  movements  of  the  eyes — i.  e.,  the  turning 
of  both  eyes  to  one  side  in  order  to  see  an  object  placed  laterally. 
In  order  to  accomplish  this,  it  is  obligatory  that  the  internal  rectus 
of  one  eye  and  the  external  rectus  of  the  other  should  act  consenta- 
neously. The  co-ordinate  action  of  the  two,  although  supplied  by 
separate  nerves  on  opposite  sides,  is  accomplished  by  the  communi- 
cating fibres  (posterior  longitudinal  bundle)  which  run  from  the 
nucleus  of  the  sixth  nerve  on  one  side  to  the  nucleus  of  the  third 
nerve  on  the  other  side.  An  impulse  travelling  from  the  left  cortex 
is  received  by  the  sixth  nucleus  on  the  right  side,  which  being  ex- 
cited immediately  forwards  the  impulse,  not  only  along  its  own  nerve 
to  the  right  external  rectus,  but  also  along  the  communicating  fibres 
to  the  nucleus  of  the  third  nerve  on  the  left  side,  and  it,  in  turn, 
transmits  it  to  the  left  internal  rectus.  The  right  external  rectus 
and  the  left  internal  rectus  simultaneously  contract,  thus  turning 
both  eyes  to  the  right. 

Symptoms  Indicative  of  Disturbances  of  the  Ocular  Muscles. 
(1)  Ptosis. — Drooping  of  the  upper  eyelid  with  an  inability  to  raise 
it  (ptosis)  is  due  to  paralysis  of  the  levator  palpebrae.  As  the  levator 
palpebrae  is  innervated  by  the  second  portion  of  the  oculo-motor 
nucleus,  ptosis  is  dependent  upon  some  interference  with  the  func- 
tion of  the  third  nerve,  its  nucleus,  or  its  cortical  centre.  It 
may  exist  alone,  but  is  ordinarily  combined  with  paralysis  of  the 
third  nerve.  The  pathological  possibilities  of  this  symptom  are  as 
follows : 

If  bilateral,  in  a  woman,  and  associated  with  spasm  of  the  orbicu- 
laris upon  attempting  to  raise  the  eyes,  and  presenting  other  symp- 
toms of  the  causative  affection,  it  is  probably  of  hysterical  origin. 
If  existing  from  birth,  and  the  patient  is  unable  to  roll  the  eyes 
upward,  it  is  due  to  congenital  defect  or  absence  of  the  levator  mus- 


PTOSIS— STRABISMUS  193 

cle.  Transient  double  ptosis,  slight  or  marked,  may  occur  in  the 
morning  upon  waking,  in  anaemic,  neurotic,  or  overworked  women ; 
and  as  a  result  of  the  administration  of  conium  or  gelsemium.  Dou- 
ble ptosis  may  be  caused  by  idiopathic  muscular  atrophy  if  the  facial 
muscles  and  the  levator  palpebrae  are  affected.  Drooping  of  one  lid 
and  contracted  pupil,  with  heat,  redness,  and  CEdema  of  the  skin  on 
the  same  side  constitutes  pseudo-ptosis,  and  is  caused  by  a  paralyzing 
lesion  of  the  sympathetic  nerve.  It  has  also  been  attributed  to  dis- 
ease of  the  corpus  striatum.  The  ptosis  in  this  case  is  referable  to 
the  paralysis  of  the  muscular  fibres  of  Miiller  which  exist  in  the  con- 
nective tissue  of  the  orbit  and,  when  active,  assist  in  the  retraction  of 
the  lid.  Very  seldom  a  unilateral  ptosis,  following  a  slight  apoplectic 
attack,  is  referable  to  a  cortical  lesion,  without  involvement  of  the 
other  branches  of  the  third  nerve.  In  severe  neuralgia  of  the  fifth 
nerve,  and  in  tetanus,  ptosis  may  exist,  possibly  because  of  trans- 
ferred irritation  from  the  fifth  nerve  acting  as  an  inhibitory  agent 
upon  the  oculo-motor  nucleus. 

Aside  from  the  conditions  which  have  just  been  recapitulated, 
ptosis  is  usually  associated  with  paralysis  of  other  ocular  muscles 
due  to  definite  lesions  or  functional  affections  of  the  third  nerve — 
i.  e.,  it  is  simply  one  of  several  symptoms  indicating  oculo-motor 
paralysis  (5'. «'.). 

(2)  Strabismus. — Squint  or  strabismus  is  an  inability  to  bring  the 
visual  axis  of  both  eyes  to  bear  at  the  same  instant  upon  one  point, 
the  visual  axis  of  one  eye  constantly  deviating,  as  a  rule  horizontally, 
sometimes  vertically,  from  the  object  inspected. 

If  the  squinting  eye  turns  toward  the  temple,  it  is  a  divergent  or  external 
strabismus;  if  toward  the  nose,  it  is  a  convergent  or  internal  strabismus. 
Vertical  squint  may  be  upward  or  downward.  By  asking  the  patient  to  look 
at  the  tip  of  the  examiner's  finger,  it  is  usually  easy  to  decide  as  to  which  eye 
squints  (the  sound  eye  fixing  itself  upon  the  finger),  and  whether  the  squint  is 
convergent,  divergent,  upward,  or  downward.  If  the  strabismus  be  slight 
and  uncertainty  arises,  the  finger  should  be  held  directly  in  front  of  the  face, 
at  about  18  inches  distance,  and  the  patient  asked  to  gaze  at  it.  The 
apparently  normal  eye  should  then  be  covered  by  a  card.  The  uncovered  eye, 
if  it  be  the  squinting  one,  will  immediately  alter  its  position  so  as  to  fix  itself 
upon  the  finger,  thus  demonstrating  that  it  had  not  before  been  properly  directed. 

Strabismus,  with  reference  to  its  origin,  may  be  of  two  kinds,  concomitant 
and  paralytic.  The  latter  form  is  that  which  is  of  importance  in  internal 
medicine. 

In  concomitnnt  strabismus  the  squinting  eye  will  retain  its  mobility,  moving 
readily  in  every  direction  concomitantly  with  its  companion,  the  degree  of 
strabismus  remaining  substantially  the  same.  The  principal  causes  of  con- 
comitant strabismus,  which  need  but  a  simple  mention,  are  overaction  of  cer- 


194  THE  EVIDENCES  OF   DISEASE 

tain  muscles  consequent  upon  refractive  errors,  and  imperfect  vision  of  an  eye 
with  resulting  disease  of  the  muscles. 

In  paralytic  strabismus  the  squinting  eye  loses,  to  a  greater  or  less  degree, 
its  power  of  movement — i.  e.,  its  range  of  motion  is  restricted  as  compared 
with  the  sound  eye.  It  is  due  to  a  loss  of  power  in  one  or  more  of  tlie  external 
ocular  muscles.  If,  for  instance,  the  internal  rectus  of  the  left  eye  is  paralyzed, 
and  the  patient  attempts  to  keep  the  eyes  fixed  upon  the  finger  as  it  is  passed 
slowly  from  his  left  to  his  right,  it  will  be  seen,  as  the  finger  passes  the  middle 
line,  that  the  left  eye  lags  behind  the  right  and  a  divergent  squint  develops, 
becoming  more  marked  the  further  the  finger  moves  to  the  right.  At  the  same 
time  double  vision,  or  diplopia,  becomes  manifest  to  the  patient.  Further- 
more, in  the  same  instance,  if  while  the  patient  is  looking  at  the  finger  held  to 
his  right,  the  sound  right  eye  is  screened  by  a  card  and  an  attempt  is  made  to 
fix  the  object  with  the  left  eye,  the  right  eye  behind  the  card  will  be  seen  to 
deviate  still  further  to  the  right.  This  is  termed  the  secondary  deviation,  and 
is  dependent  upon  the  physiological  law  that  when  two  muscles  are  acting 
toward  the  same  end  and  one  of  them  lacks  power,  if  an  increased  impulse  is 
sent  to  the  weaker,  the  stronger  one  shares  the  additional  stimulus  and  con- 
tracts more  vigorously.  As  paralytic  squint  is  simply  a  symptom  of  paralysis 
or  weakness  of  the  ocular  muscles,  its  diagnostic  indications  are  considered 
elsewhere  (Index — Paralysis,  Causes  of  Ocular). 

Closely  connected  with  and  dependent  upon  paralysis  of  the 
ocular  muscles  and  strabismus  is  the  subjective  symptom — 

(3)  Diplopia. — Double  vision  depends  upon  the  fact  that  unless 
the  visual  axes  are  correctly  adjusted,  each  to  the  other,  the  images 
of  the  objects  do  not  fall  upon  identical  points  in  each  retina. 
Under  normal  conditions  each  image  falls  upon  the  macula  lutea  of 
each  retina,  combining  to  form  a  single  image  in  the  sensorium. 

If  the  proper  relation  of  the  visual  axes  is  altered  by  a  wrong  position  of  an 
eye,  due  to  defective  action  of  the  ocular  muscles,  and  the  images  are  received 
upon  dissimilar  retinal  parts,  the  images  are  perceived  by  the  mind  as  of 
separate  origin— i.  e.,  double.  The  image  perceived  by  the  sound  eye  is  the 
true  image,  that  perceived  by  the  deviated  eye  is  the  false  image.  It  should 
be  remembered  that  diplopia  may  be  present,  but  not  manifest,  unless  the  eyes 
are  turned  in  such  a  direction  as  to  require  action  by  the  paralyzed  muscle  or 
muscles.  Thus,  in  the  case  already  described  (paralysis  of  the  left  internal 
rectus),  as  illustrating  paralytic  squint,  diplopia  may  not  be  present  if  the  eyes 
are  turned  to  the  left,  as  the  palsied  muscle  is  not  called  upon  to  contract ;  but 
if  the  eyes  are  required  to  turn  to  the  right,  the  deficient  activity  of  the  mus- 
cle causes  strabismus,  and  consequent  diplopia. 

Aside  from  the  double  vision  which  is  produced  by  the  action  of 
alcohol,  belladonna,  conium,  gelsemium,  and  sjoigelia  upon  the 
ocular  nerves,  diplopia,  like  strabismus,  is  a  symptom  of  paralysis  of 
the  ocular  muscles,  and  its  diagnostic  significance  will  be  discussed 


DIPLOPIA— CONJUGATE  DEVIATION  195 

in  connection  with  the  latter.  Any  lesion  of  the  brain,  cord,  or  basal 
meninges  (inflammation,  hemorrhage,  tumour,  softening,  sclerosis) 
which  causes  paralysis  of  one  or  more  of  the  external  ocular  muscles 
may  be  attended  with  diplopia. 

Double  sight  with  one  eye  (uniocular  diplopia)  may  occur  in 
cataract  and  astigmatism,  due  to  irregular  refraction,  and  in  brain 
tumour  as  a  psychical  aberration. 

(4)  Erroneous  Projection  and  Ocular  Vertigo. — Our  judgment  of 
the  relation  of  external  objects  to  our  own  body  is  largely  based  upon 
the  position  of  the  eyeballs,  and  a  knowledge  of  the  latter  comes 
through  the  degree  of  innervation  required  by  its  muscles.  If  the  eye 
looks  forward,  any  object  seen  by  it  is  recognised  as  being  directly 
in  front  of  us.  If  the  eye  is  turned  to  the  left,  an  object  seen  is 
recognised  as  lying  to  our  left  side.  The  relative  position  of  the 
two  objects  with  regard  to  each  other,  and  also  with  regard  to  the 
body,  is  judged  by  the  effort  which  requires  to  be  made  in  turning 
the  eye  from  one  object  to  another  and  the  resulting  range  of 
motion  of  the  eyeball.  If  a  muscle  is  weak,  the  movement  of  the  eye 
does  not  correspond  in  extent  to  the  effort  made  in  innervating  it, 
and  a  mistaken  judgment  as  to  the  position  of  the  body  with  refer- 
ence to  surrounding  objects  will  result.  As  the  balance  of  the  body 
is  largely  preserved  by  a  perception  of  its  relation  to  its  environment, 
if  the  perception  is  uncertain  or  incorrect,  dizziness  (ocular  vertigo) 
will  ensue.  In  order  to  detect  it,  the  sound  eye  must  be  covered  or 
closed,  as  it  is  rarely  present  if  both  eyes  are  open,  or  if  the  affected 
eye  is  shut. 

5.  Conjugate  Deviation. — If  both  eyes  are  turned  strongly  and 
persistently  toward  one  side,  either  right  or  left,  the  condition  is 
termed  conjugate  deviation.  This  condition  may  be  due  either  to 
spasm  or  paralysis  of  the  internal  rectus  of  one  side  and  the  external 
rectus  of  the  other  side,  and  the  eyes  may  be  turned  toward  the 
lesion  or  away  from  it,  depending  upon  its  location  and  whether  it 
is  irritative  (causing  spasm)  or  destructive  (causing  paralysis).  This 
symptom  depends  upon  the  normally  associated  action  of  the  inter- 
nal rectus  of  one  side  and  the  external  rectus  of  the  other  in  effect- 
ing horizontal  co-ordinated  motion  of  both  eyes  to  the  right  or  left, 
as  explained  upon  page  192.  Referring  to  Fig.  32,  the  lesions  which 
cause  this  symptom  are  as  follows : 

If  there  is  conjugate  deviation  to  the  right,  it  indicates  : 

{A )  An  irritating  lesion,  as  at  B,  involving  the  left  cortical  cen- 
tre, or  the  fibres  leading  from  it  through  the  corona  radiata  or  inter- 
nal capsule ;  or,  as  at  C,  affecting  the  fibres  from  the  cortex  in  the 
right  side  of  the  pons  after  decussation,  whereby  the  nucleus  of  the 


196 


THE  EVIDENCES  OF   DISEASE 


right  sixth  nerve  and  by  it  the  nucleus  of  the  left  third  nerve  are 
both  stimulated  and  the  right  external  and  left  internal  recti  are 
made  to  contract,  thus  turning  the  eye  to  the  right. 


Nucleus  of  VI  Nerve 


Nucleus  of  IV  Nerve 


Nocieus  of  III  Nerve 


III,  IV,  and  VI  Nerves 
Pass.through  Sph- 
enoidal Fissure 


Cortex 


^- — Rect.  Ext.    ^  Communicating  Fibres 
Between  Nucleus  of 
VI  Nerve  and  Nucleus 
of  III  Nerve. 


FiQ.  32. — Diagram  showing  the  ocular  muscles  and  their  nerve  supply. 


{B)  A  destructive  lesion  of  the  corresponding  right  cortical  cen- 
tre or  its  efferent  fibres,  or  of  the  same  fibres  in  the  left  side  of  the 
pons,  causing  paralysis  of  the  left  externus  and  right  internus,  allow- 
ing unopposed  action  of  the  right  externus  and  left  internus,  turning 
the  eyes  also  to  the  right. 


CONJUGATE  DEVIATION— NYSTAGMUS  197 

If  there  is  conjugate  deviation  to  the  left^'it  indicates  by  a  similar 
mechanism : 

{A)  An  irritating  lesion  of  the  right  cortex  or  cortical  fibres,  or 
the  same  fibres  in  the  left  side  of  the  pons,  or 

{B)  A  destructive  lesion  as  at  A  (left  cortical  or  cerebral),  or  at 
O  (right  side  of  pons). 

The  lesions  producing  conjugate  deviation  are,  in  particular, 
cerebral  hemorrhage,  tumour,  or  meningitis.  If  the  lesion  is  a  left- 
side hemorrhage  at  A  and  causes  right  hemiplegia,  the  eyes  look 
toward  the  lesion ;  but  if  the  lesion  is  or  becomes  irritant  and  spasms 
or  convulsions  occur,  the  eyes  turn  away  from  the  lesion.  On  the 
other  hand,  if  right  hemiplegia  is  present  as  the  result  of  a  destruc- 
tive tumour  in  the  pons  at  D,  the  eyes  look  away  from  the  lesion ; 
but  if  it  is  or  becomes  irritant,  and  spasms  and  convulsions  take 
place,  the  eyes  look  toward  the  lesion. 

The  determination  as  to  the  nature  of  the  lesion  must  be  made 
by  the  associated  symptoms  of  brain  tumour,  meningitis,  apoplexy, 
sclerosis,  or  abscess. 

6.  Nystagmus. — A  rapid  involuntary  oscillation  or  slow  move- 
ment of  both  eyeballs,  usually  from  side  to  side  (lateral  nystagmus), 
sometimes  vertical  or  rotatory.  It  is  a  clonic  bilateral  spasm  of 
the  ocular  muscles,  due  to  some  irritation,  either  functional  or  or- 
ganic, affecting  the  ocular  muscle  centres.  If  very  slight,  it  may  be 
intensified  by  directing  the  patient  to  look  steadily  at  an  object  held 
well  to  one  side  or  the  other ;  or  if  the  nystagmus  be  vertical  or 
rotatory,  by  directing  the  eye  upward  or  downward,  or  circumduct- 
ing the  eye  by  moving  the  object. 

Rarely  nystagmus  is  congenital  from  the  irritation  of  hereditarily 
defective  vision,  or  from  cataract  or  refractive  errors.  It  is  present 
in  many  cases  of  blindness  or  defective  sight  caused  by  optic  atrophy, 
amaurosis,  and  corneal  opacities.  It  may  be  found  in  albinos.  It 
is  frequently  seen  in  epileptic  or  other  convulsions,  and  may  form 
a  part  of  the  symptomatology  of  neurasthenia,  hysteria,  chorea,  and 
some  cases  of  insanity.  There  is  a  "miner's  nystagmus,"  a  mani- 
festation of  irritable  weakness  of  certain  of  the  ocular  muscles 
arising  from  the  strain  put  upon  them  by  looking  obliquely  up- 
ward while  lying  upon  the  side  and  using  the  pick  in  a  narrow 
vein  of  coal. 

The  most  important  diagnostic  associations  of  nystagmus,  how- 
ever, are  with  Friedreich's  ataxia,  disseminated  (insular)  sclerosis, 
and  brain  tumour,  especially  growths  involving  the  cerebellum,  pons, 
or  crus.  Acute  basal  meningitis  is  apt  to  present  it.  Occasionally 
it  is  seen  in  the  terminal  stage  of  locomotor  ataxia  and  in  chronic 
15 


198  THE  EVIDENCES  OF  DISEASE 

hydrocephalus.     Its  cause,  in  a  given  case,  must  be  determined  by 
the  associated  symptoms. 

7.  Irregular  or  Spasmodic  Movements  of  the  Eyes. — Xon-rhythmi- 
cal,  irregular  movements  of  the  eyes  may  occur  in  connection  with 
special  ocular  paralyses  or  insufficiencies  and  errors  of  refraction. 
Meniere's  disease,  when  due  to  lesions  of  the  labyrinth,  is  sometimes 
accompanied  by  forced  movements  of  the  eyes.  Chronic  hydro- 
cephalus and  meningitis  (basal  irritation)  may  give  rise  to  irregular 
spasmodic  movements  of  the  eyeballs.  In  hysteria  the  internal  rec- 
tus and  levator  palpebrae  may  be  tonically  contracted,  the  eyes  being 
opened,  convergently  squinted  and  uprolled.  Divergent  squint  is 
said  not  to  exist  in  hysteria  (Gowebs). 

8.  Loss  of  Power  of  Accommodation. — Paralysis  of  the  ciliary 
muscle  (cycloplegia)  is  responsible  for  loss  of  the  power  of  accommo- 
dation. In  this  condition  distant  objects  can  be  clearly  seen  but 
near  objects  are  indistinct.  It  must  not  be  confused  with  reflex 
iridoplegia  (loss  of  the  pupillary  light  reflex)  or  accommodative  iri- 
doplegia  (loss  of  the  pupillary  contraction  for  near  vision).  The 
first  and  last  both  depend  upon  the  integrity  of  the  same  portion  of 
the  oculo-motor  nucleus.  Cycloplegia  is  one  of  the  symptoms  of 
complete  third-nerve  paralysis,  is  a  common  symptom  in  diphtheritic 
paralysis,  and  is  also  seen  in  multiple  sclerosis. 

(c)  Diagnosis  and  Causes  of  Ocular  Paralysis.— Paralysis  of  one 
or  more  ocular  muscles  is  termed  ophthalmoplegia. 

Ophthalmoplegia  interna  concerns  the  internal  muscles,  viz.,  the 
ciliary  muscle,  and  the  circular  fibres  of  the  iris ;  externa.,  all  the  other 
(or  external)  ocular  muscles ;  total.,  both  external  and  internal ;  par- 
tial., a  limited  number  of  ocular  muscles.  There  may  be  much  vari- 
ation in  the  number  of  muscles  involved  as  well  as  differences  in  the 
completeness  of  the  paralysis. 

In  the  majority  of  cases  the  external  eye  muscles  can  be  ade- 
quately tested  by  asking  the  patient  to  follow  the  finger  moved  in 
different  directions,  and  the  intraocular  muscles  by  examining  for 
the  light  reflex  of  the  pupil  and  asking  the  examined  to  read  small 
print.  If  a  more  careful  investigation  is  needed,  as  with  the  slighter 
degrees  of  paralysis  and  the  ocular  asthenopias,  the  patient  should 
be  referred  to  a  competent  ophthalmologist. 

1.  Paralysis  of  the  Third  Nerve.— If  there  is  ptosis,  slight  exoph- 
thalmos, external  strabismus,  diplopia,  and  a  dilated  pupil  which 
reacts  neither  to  light  nor  to  accommodation,  and  if  when  an  object 
is  moved  in  various  directions  the  eye  fails  to  follow  it  in  an  upward, 
inward,  or  downward  direction,  but  will  move  outward  and  a  little 
downward  by  means  of  the  external  rectus  and  inferior  oblique,  there 


CAUSES  OF  OCULAR  PARALYSIS  199 

is  complete  oculo-motor  paralysis.  In  many  cases  some  of  the  muscles 
escape,  the  levator  and  superior  rectus  or  the  iris  and  ciliary  muscle 
being  alone  affected,  or  ptosis  existing  with  a  dilated  pupil. 

The  signs  indicating  paralysis  of  the  various  single  muscles  inner- 
vated by  the  third  nerve,  excepting  the  ciliary  muscle  and  the  iris, 
are  : 

For  the  rectus  superior. — The  affected  eye  lags  behind  its  sound  fellow  in 
following  the  object  of  regard  above  the  horizontal  line,  the  divergence  increas- 
ing the  higher  the  object  is  raised,  and  there  is  at  the  same  time  slight  diver- 
gent strabismus  from  the  action  of  the  inferior  oblique  if  the  latter  is  unaffected. 

For  the  rectus  internus. — If  the  moving  object  is  brought  horizontally 
across  toward  the  sound  eye,  the  diseased  eye  will  fail  to  follow  it  beyond  the 
middle  line,  or  will  do  so  with  a  wavering,  irregular  motion  due  to  the  action 
of  the  superior  and  inferior  recti,  if  the  latter  are  healthy. 

For  the  inferior  rectus. — If  the  point  of  fixation  is  carried  below  the  hori- 
zontal line,  the  affected  eye  fails  to  follow  it,  and  there  may  be  slight  conver- 
gent strabismus  from  the  action  of  the  superior  oblique. 

For  the  inferior  oblique. — Paralysis  of  this  muscle  alone  is  extremely  infre- 
quent and  is  difficult  to  detect.  On  looking  at  an  object  above  the  horizontal 
line  there  is  diplopia,  with  slight  deviation  of  the  eye  downward  and  inward. 

The  most  frequent  causes  of  oculo-motor  paralysis  are  cold  and 
syphilis,  the  former  producing  a  rheumatic  peripheral  neuritis ;  the 
latter  giving  rise  to  a  basal  meningitis  or  a  gummatous  growth  in- 
volving the  roots  of  the  nerve. 

Partial  paralysis  may  be  due  to  a  cortical  lesion  affecting  the  infe- 
rior parietal  lobule.  By  producing  anaemia  or  hyperaemia  of  the 
nucleus,  undue  exposure  to  light,  migraine  and  the  excessive  use  of 
alcohol,  morphine  and  tobacco  may  cause  a  temporary  paralysis. 
There  is  a  rare  form  of  complete  oculo-motor  paralysis,  affecting 
women,  recurring  at  intervals  of  one  or  several  months,  and  coming 
on  suddenly  with  headache  and  vomiting  or  a  well-marked  migraine. 

As  organic  disease  of  the  third-nerve  nucleus  is  usually  associated 
with  disease  of  the  fourth  and  sixth  nuclei  an  oculo-motor  paralysis, 
without  loss  of  power  of  the  external  rectus  and  superior  oblique,  is, 
as  a  rule,  functional. 

While  the  nerve  is  penetrating  the  crus  it  may  be  involved  by 
tumour  or  other  lesion  of  the  crus,  in  which  case  there  will  be  partial 
or  complete  third-nerve  paralysis  conjoined  with  hemiplegia  on  the 
opposite  side  of  tlie  body,  a  combination  characteristic  of  unilateral 
disease  of  the  crus.  If  in  addition  there  are  unilateral  paralysis  and 
atropliy  of  the  tongue,  the  lesion  is  localized  in  the  inner  and  inferior 
aspect  of  the  crus  involving  the  cerebral  fibres  passing  to  the  nucleus 
X)f  the  hypoglossal  or  motor  nerve  of  the  tongue. 


200 


THE   EVIDENCES  OP   DISEASE 


Ptosis  occurring  on  one  side,  disappearing  and  then  appearing  on 
the  other  side  (alternating),  is  usually  due  to  variable  syphilitic 
lesions  in  the  neighbourhood  of  the  nucleus. 

At  and  after  its  emergence  from  the  pons  (Fig.  27)  on  its  way  to 
the  sphenoidal  fissure,  the  third  nerve  may  be  involved  by  basilar 
meningitis,  frequently  of  syphilitic  origin,  or  by  gummatous  deposits 
or  tumours.  The  lesions  of  locomotor  ataxia  which  cause  ptosis  may 
be  in  the  same  locality.  If  due  to  disease  at  the  base,  the  oculo-mo- 
tor  paralysis  is  usually  bilateral  and  apt  to  be  accompanied  by  inter- 
ference with  the  function  of  the  other  cranial  nerves.  Third-nerve 
paralysis  may  also  be  one  of  the  symptoms  of  primary  muscular 
atrophy  and  upper  bulbar  palsy. 

Oculo-motor  paralysis  may  be  indicative  of  pressure  in  the  cav- 
ernous sinus  (Fig.  33),  or  inflammation  at  the  sphenoidal  fissure 
(Fig.  32),  or  injury  (fracture)  in  either  locality. 


Lining  membrane  of  sinus 


Dura  mater  lining 
pituitary 


Sixth  nerve 


Third  nerve 


Fourth  nerve 


First  division  of 
fifth  nerve 


Internal  carotid 
Fig.  33. — Plan  showing  the  relative  position  of  the  structures  in  tlie  right  cavernous  sinus, 
viewed  from  behind.     Redrawn  from  Gray. 

If  loss  of  accommodation,  loss  of  light  reflex,  and  external  squint 
succeed  an  attack  of  diphtheria  it  is  usually  indicative  of  a  neuritis 
of  the  third  nerve.  Neuritis  of  this  nerve  may  also  occur  in  the 
course  of  locomotor  ataxia.  Finally,  tumours  of  the  orbit  may  be 
responsible  for  this  form  of  ocular  paralysis. 

2.  Fourth-nerve  Paralysis. — The  fourth  nerve  supplies  the  supe- 
rior oblique,  and  paralysis  of  this  muscle  is  somewhat  difficult  of 
detection.  If  paralyzed,  when  the  fixing  object  is  moved  downward 
below  the  horizontal  line  the  diseased  eye  fails  to  follow  it,  there  is 
slight  convergent  strabismus,  and  the  patient  has  double  vision  while 
looking  down.  The  diplopia  is  an  extremely  annoying  symptom,  as 
the  eye  is  so  constantly  employed  in  writing,  reading,  and  walking, 
all  of  these  occupations  requiring  down-turning  of  the  eye.  The 
head  is  apt  to  be  carried  forward  and  toward  the  sound  side. 

Isolated  paralysis  of  this  nerve  is  very  infrequent.     When  pres- 


OCULAR  PARALYSIS  AND  INSUFFICIENCY  201 

ent  it  may  be  indicative  of  pressure  upon  its  trunk  as  it  winds 
around  the  outer  surface  of  the  crus  to  reach  the  antero-lateral  edge 
of  the  pons  (Fig.  37).  The  pressure  may  be  due  to  the  exudation  of 
basilar  meningitis,  tumour  or  aneurism  at  the  termination  of  the 
basilar  artery  bearing  against  the  crus.  If  the  symptoms  of  cerebellar 
disease  coexist  with  fourth-nerve  palsy,  it  is  indicative  of  a  lesion  of 
the  anterior  part  of  the  cerebellar  hemisphere  on  the  same  side  (Starr). 
There  may  be  paralysis  of  this  nerve,  presumably  due  to  a  peripheral 
neuritis  as  the  result  of  epidemic  influenza,  rheumatism  (cold),  gout, 
and  diabetes,  as  well  as  alcoholism  and  lead  poisoning.  It  may  be  a 
transient  symptom  of  neurasthenia. 

3.  Sixth,  involving  Associated  Action  of  the  Third  Nerve. — A 
lesion  of  the  nucleus  of  the  sixth  nerve,  as  at  E,  Fig.  32,  may  cause 
conjugate  deviation  of  the  paralytic  form,  the  mechanism  of  which 
has  been  previously  explained. 

4.  Third,  Fourth,  and  Sixth  Nerves. — Total  ophthalmoplegia  may 
be  indicative  of  disease  in  the  cavernous  sinus  or  the  sphenoidal 
fissure  (Figs.  32  and  33),  especially  if  there  is  anaesthesia  of  the  peri- 
pheral distribution  of  the  ophthalmic  division  of  the  trifacial  nerve 
(skin  of  forehead,  upper  eyelid  and  nose).  The  branches  of  this  divi- 
sion accompany  the  ocular  nerves  through  the  sphenoidal  foramen, 
and  it  may  be  involved  in  morbid  processes  in  these  localities — i.  e., 
syphilitic  or  other  periostitis,  gumma  or  other  tumour,  aneurism  or 
arterio-venous  aneurism  of  the  internal  carotid,  or  thrombosis  of  the 
cavernous  sinus. 

Ophthalmoplegia,  external,  internal  or  total,  may  be  a  symptom 
of  acute  or  chronic  polioencephalitis  superior  (upper  bulbar  palsy, 
nuclear  palsy). 

When  paralysis  of  all  the  ocular  muscles  is  associated  with  facial 
paralysis  without  hemiplegia,  it  is  probably  due  to  a  basal  lesion,  as 
the  facial,  like  the  ocular  nerves,  is  liable. to  involvement  by  disease 
at  the  base. 

{d)  Asthenopia  and  Insufficiencies  of  the  Ocular  Muscles.— If  com- 
plaint is  made  that  close  use  of  the  eye,  such  as  that  involved  in 
writing,  reading,  or  sewing,  causes  them  to  feel  strained,  hot,  and 
uncomfortable,  and  perhaps  gives  rise  to  headache  in  the  forehead, 
vertex,  or  occiput,  the  source  of  the  trouble  may  be  found  in  a  weak- 
ness of  the  ocular  muscles,  particularly  the  recti.  If  this  weakness 
exists  the  patient  can  not  keep  the  visual  axes  of  the  eyes  in  proper 
relation  without  an  effort,  either  conscious  or  unconscious. 

If  normal  strength  of  the  ocular  muscles  is  present  it  is  called 
orthophoria.  If  some  of  the  muscles  are  weak  it  is  termed  hetero- 
plioria.     The  varieties  of  heterophoria  are :  esophoria,  weakness  of 


202  THE  EVIDENCES  OF  DISEASE 

the  externi,  causing  a  tendency  to  convergence  of  the  visual  axes ; 
exophoria^  a  tendency  to  divergence  of  the  visual  axes  from  weakness 
of  the  interni ;  hyperphoria^  a  tendency  of  the  visual  axis  of  an  eye 
to  deviate  upward.  None  of  these  deviations  are  sufficiently  obvious 
to  constitute  strabismus.  As  all  errors  of  refraction  should  be  cor- 
rected before  making  the  special  tests,  it  is  always  advisable  to  have 
the  examination  made  by  a  competent  ophthalmologist. 

"While  the  immense  importance  of  muscular  asthenopia  in  causing 
various  forms  of  nervous  disease  has  been  vigorously  urged  by  cer- 
tain writers,  the  consensus  of  ojDinion  among  the  masters  of  ophthal- 
mology and  neurology  appears  to  be  that  its  etiological  influence  has 
been  greatly  overrated.  According  to  the  more  conservative  view  it 
is  not  a  factor  in  causing  chorea,  hysteria,  or  epilepsy  ;  but  in  neuro- 
pathic individuals  it  may  intensify  or  render  more  frequent  attacks 
of  migraine,  trigeminal  neuralgia,  occipital  and  cervical  headaches, 
vertigo,  and  perhaps  choreiform  movements  of  the  upper  facial  mus- 
cles. It  is  probable  that  correction  of  refractive  errors  will  relieve 
the  troublesome  symptoms  more  effectually  than  tenotomies. 

V.  VISION 

The  disorders  of  vision  which  are  of  diagnostic  importance  are 
hemianopia,  alterations  in  the  colour  fields,  amblyopia,  and  amau- 
rosis. 

I.  Minor  Disorders. — If  objects  seen  have  a  yellow  tint,  it 
may  be  due  to  jaundice  or  the  administration  of  santonin.  In 
exhausted  neuropathic  women  or  children,  overuse  of  the  eyes  may 
cause  everything  to  turn  red.  The  small,  beaded,  semitransparent 
threads  or  dots  (muscae  volitantes),  seen  in  looking  at  some  clear 
expanse  of  light,  are  of  small  diagnostic  importance,  but  they  appear 
to  be  most  abundant  in  cerebral  anaemia  or  hyperaemia,  hysteria, 
functional  disorders  of  the  stomach  and  liver,  and  cardiac  hyper- 
trophy. Flashes  or  small  luminous  points  of  light  before  the  eyes 
occur  most  commonly  in  acute  indigestion,  and  may  constitute  the 
aura  of  epilepsy.  Migraine  may  be  preceded  by  scotomata  resem- 
bling a  cloud,  the  edges  of  which  are  brilliantly  lighted  or  col- 
oured, the  "  flittering  scotoma  "  of  German  writers.  It  is  said  that 
such  appearances  occasionally  precede  an  attack  of  intracranial  hem- 
orrhage or  thrombosis,  and  may  be  present  in  hypochondriasis,  insan- 
ity, delirium  tremens,  typhus  fever,  and  meningitis. 

II.  Alterations  in  the  Field  of  Vision.— The  alterations  in 
the  size  and  shape  of  the  visual  fields  which  are  of  more  or  less 
value  in  diagnosis  are :  (a)  hemianopia,  (S)  contraction  of  the  visual 
fields  for  light,  and  (c)  contraction  of  the  colour  fields.     In  con- 


HEMIANOPIA  203 

nection  with  hemianopia,  blindness  due  to  disease  of  the  optic  nerve 
or  its  central  connections  will  be  considered. 

(«)  Hemianopia. — The  condition  variously  termed  hemiopia,  hemi- 
anopia, or  hemianopsia  is  that  in  which  there  is  blindness  of  one 
half  of  the  field  of  vision.  It  is  due  to  functional  or  organic  disease 
affecting  the  optic  nerve  or  its  central  connections.  The  optic- 
nerve  mechanism  is  shown  in  Fig.  34. 

Hemianopia,  or  blindness  of  one  half  of  the  visual  field,  is  of  dif- 
ferent varieties,  and,  together  with  the  qualifying  terms  employed, 
refers  to  the  field  of  vision  from  the  point  of  view  of  the  patient — 
not  to  the  retina.  Thus,  right  temporal  hemianopia  means  that  the 
outer  or  temporal  half  of  the  field  of  vision  of  the  right  eye  is  blind, 
so  that  if  the  eye  is  fixed  upon  a  point  directly  in  front  objects  to 
the  right  of  the  point  of  fixation  will  not  be  perceived.  But  it  must 
be  remembered  that  blindness  of  the  temporal  half  of  the  field  of 
vision  is  due  to  loss  of  function  of  the  inner  or  nasal  half  of  the 
retina,  because  of  the  crossing  of  the  light  rays  in  the  media,  and  so 
with  other  varieties. 

If  the  hemianopia  affects  both  visual  fields,  it  is  bilateral ;  if  cor- 
responding halves  (both  right  or  both  left),  it  is  homonymous  or  lateral. 
If  both  temporal  or  both  inner  fields  are  implicated,  it  is  heteronymous. 
Furthermore,  the  inner  fields  are  termed  nasal ;  the  outer,  temporal. 
Very  rarely  the  upper  or  lower  halves  of  the  visual  field  are  effaced, 
and  it  is  then  called  superior  or  inferior  (sometimes  altitudinal) 
hemianopia.  Hemianopia  may  be  partial,  only  a  portion  of  the  half 
field  being  blank.  The  unaffected  half  may  retain  its  normal  dimen- 
sions or,  as  in  some  cases,  be  reduced  in  size. 

To  determine  the  presence  of  hemianopia  each  eye  must  be  tested 
separately,  the  resting  eye  having  been  covered  by  a  card.  The 
patient,  being  placed  with  his  back  to  the  light,  is  told  to  fix  the  un- 
covered eye  upon  that  part  of  the  physician's  face  (placed  about  two 
feet  away)  which  is  most  nearly  on  the  horizontal  plane  of  the  eye. 
The  finger  or  a  bit  of  white  paper  is  then  brought,  first  from  one 
side,  then  from  the  other,  to  the  median  line.  If  the  patient  can  not 
see  the  paper  until  it  has  passed  nearly  or  quite  to  the  line  of  fixation, 
hemianopia  exists.  The  vertical  extent  of  the  field  is  tested  in  a 
similar  manner  by  bringing  the  object  from  above  downward  and 
below  upward.  To  get  an  accurate  outline  of  the  visual  and  colour 
fields,  it  is  necessary  to  employ  the  perimeter. 

Hemianopia  in  the  majority  of  cases  is  due  to  organic  disease  of 
the  brain,  such  as  hemorrhage,  softening,  inflammation,  or  tumour, 
but  may  be  of  functional  origin  in  connection  with  gout,  lithaemia, 
migraine,  and  occasionally  hysteria.     It  is  of  considerable  value  in 


204 


THE  EVIDENCES  OF   DISEASE 


localizing  certain  lesions  but  the  determination  of  the  nature  of  the 
causative  lesion  depends  upon  the  associated  symptoms.  The  diag- 
nostic indications  of  the  various  forms  of  hemianopia  are  as  follows ; 


Fig.  34. — Diagram  showing  optic  tracts,  visual  fields,  and  lesions  causing  hemianopia. 


HEMIANOPIA  205 

Unilateral  Nasal  Hemianopia. — Blindness  of  the  nasal  half  of  the 
field,  an  extremely  rare  occurrence,  indicates  a  very  limited  lesion  at 
the  outer  angle  of  the  chiasm,  as  at  A  (Fig.  34,  to  which  subsequent 
references  apply). 

Binasal  Hemianopia. — Also  rare  is  blindness  of  the  nasal  half  of 
both  fields,  requiring  for  its  manifestation  two  symmetric  lesions,  as 
at  ^1,  on  both  outer  angles  of  the  chiasm,  or  the  outer  sides  of  both 
optic  nerves. 

Bitemporal  Hemianopia. — Blindness  of  the  temporal  halves  of 
both  fields  is  produced  by  a  lesion  involving  the  anterior  angle  or 
central  portion  of  the  chiasm,  as  at  B. 

The  disease  (affecting  the  chiasm)  which  is  most  frequently  re- 
sponsible for  the  three  preceding  varieties  of  hemianopia  is  tumour 
or  enlargement  (as  in  acromegaly)  of  the  pituitary  body,  with  which 
may  be  associated  diabetes,  proptosis,  and  a  flow  of  fluid  from  the 
nostril.  Other  causes  are  tubercles,  tumours,  cysts,  basilar  menin- 
gitis, periostitis,  exostosis,  fracture  of  the  body  of  the  sphenoid  bone, 
and  gumma.  The  latter  may  give  rise  to  evanescent  recurring  hemi- 
anopia. When  the  chiasm  is  affected  the  lesion  is  apt  to  be  progress- 
ive, and  gradually  involves  both  crossed  and  uncrossed  fibres,  thus 
causing  total  blindness  of  one  or  both  eyes,  according  to  the  extent 
of  the  destruction.  Lesions  of  the  chiasm  may  be  attended  by  symp- 
toms indicating  involvement  of  the  olfactory,  the  fifth,  and  the 
ocular-muscle  nerves — viz.,  anosmia,  anaesthesia  of  conjunctiva  and 
cornea,  and  ocular  paralysis. 

Bight  or  Left  Lateral  {Homonymous)  Hemianopia. — Blindness  of 
the  right  or  left  half  of  both  fields  is  significant  of  a  lesion  situated 
at  some  point  between  the  chiasm  and  the  cortical  centre  in  the 
occipital  lobe — viz.,  the  optic  tract,  the  pulvinar  or  posterior  gray 
mass  of  the  thalamus,  the  anterior  corpora  quadrigemina,  the  fibres 
passing  from  the  thalamus  and  corpora  to  the  occipital  lobe  either  in 
the  internal  capsule  or  the  optic  radiations,  or  the  cortical  centre 
itself. 

The  situation  of  the  various  lesions  which  cause  homonymous 
hemianopia  is  of  course  on  the  opposite  side  from  the  defective  half 
of  the  visual  fields.  Thus,  C,  7),  E,  and  F  represent  lesions  on  the 
right  side  of  the  brain  causing  left  hemianopia.  It  should  be  noted 
with  reference  to  right  hemianopia  that  there  is  much  difficulty  in 
reading,  because  the  words  lying  to  the  right  of  the  point  of  fixation 
are  invisible. 

To  determine  if  the  lesion  lies  between  the  chiasm  and  the  cor- 
pora, AVernicke's  pupil  symptom,  "hemianopic  pupillary  inaction," 
may  be  of  service  if  it  can  be  obtained.     A  beam  of  light  must  be 


206  THE  EVIDENCES  OF  DISEASE 

thrown  upon  the  blind  half  of  the  retina,  and  the  resulting  contrac- 
tion or  non-contraction  of  the  pupil  noted.  If  the  pupil  does  not 
react  (pupillary  inaction)  it  shows  that  the  reflex  arc,  retina  to  cor- 
pora, corpora  to  third  nerve,  to  iris,  is  injured,  and  that  the  lesion 
must  lie  anterior  to  the  corpora  in  the  optic  tract.  On  the  other 
hand,  if  the  pupil  does  react,  the  reflex  arc  is  intact,  and  the  lesion 
lies  posterior  to  the  corpora  in  the  internal  capsule,  optic  radiations, 
or  cuneus.  Pupillary  inaction,  if  found,  is  a  valuable  localizing 
symptom,  but  it  is  obviously  hard  to  determine  it  because  of  the 
difficulty  in  causing  the  ray  of  light  to  impinge  only  on  the  blind 
half  of  the  retina  without  stimulating  the  seeing  half. 

The  diseases  which  may  affect  the  optic  tract  are  neoplasm,  syph- 
ilitic meningitis,  gummata  and  tuberculous  meningitis.  In  these 
cases  the  crus  may  be  implicated,  causing  hemiplegia,  or,  as  the  result 
of  basal  lesions,  ocular-muscle  paralyses.  The  absence  of  any  form 
of  aphasia  in  right  hemiplegia  is  against  a  central  lesion  and  in 
favour  of  an  affection  of  the  tract. 

As  in  the  majority  of  cases  of  hemianopia  there  is  organic  disease 
of  the  brain,  hemiplegia  and  hemianaesthesia  on  the  same  side  with 
the  hemianopia  are  not  uncommon  associated  symptoms ;  and,  in 
left-side  lesions,  aphasia.  If  athetosis  coexists  with  lateral  hemian- 
opia it  is  significant  of  a  lesion  involving  only  the  posterior  gray 
mass  of  the  optic  thalamus,  the  pulvinar.  If  the  hemianopia  in- 
volves a  quadrant  and  not  a  semicircle,  or  is  otherwise  incomplete, 
and  if  mind  blindness  or  word  blindness  coexists,  the  lesion  is  usually 
cortical.  Dimness  of  vision  in  one  eye,  and  a  marked  contraction 
in  the  visual  field  of  the  other,  together  with  mind  blindness  (seeing 
but  not  recognising  objects),  is  a  combination  indicative  of  a  lesion 
of  the  angular  gyrus. 

Hemianopia  in  rare  instances  may  be  due  to  hysteria,  in  which 
case  the  conjunctiva  is  usually  anaesthetic  and  hemianaesthesia  is  pres- 
ent. But  by  far  the  most  common  alterations  of  vision  in  hysteria 
are  contraction  of  the  visual  fields  and  changes  in  the  colour  sense. 

Altitudinal  Hemianopia. — Blindness  of  the  upper  or  lower  half 
of  the  visual  field  may  be  caused  by  a  lesion  affecting  the  upper  or 
lower  portions  of  the  chiasm  and  is  usually  associated  with  optic 
neuritis. 

Unilateral  superior  or  inferior  hemianopia  may  be  due  to  a  lesion 
respectively  of  the  lower  or  upper  portion  of  the  cuneus,  and  if  the 
lesions  happen  to  be  symmetrical  and  bilateral — a  clinical  curiosity 
— the  hemianopia  will  be  double. 

Total  blindness  of  one  eye  may  be  due  to  a  lesion  of  one  optic 
nerve  (Fig.  34),  or  disease  of  one  occipital  lobe,  and  if  in  addition 


CONTRACTION  OF  VISUAL  FIELDS— AMAUROSIS 


207 


there  is  hemianopia  of  the  opposite  eye,  it  may  be  due  to  disease 
of  the  decussating  fibres  in  the  centre  of  the  chiasm  together  with 
the  direct  fibres  of  one  lateral  angle.  Total  blindness  of  both  eyes 
will  be  caused  by  disease  affecting  the  entire  chiasm,  or  bilateral 
lesions  of  the  cuneus.  It  is  presupposed  that  no  disease  of  the 
retina  or  other  ocular  structures  suflBcient  to  account  for  the  loss  of 
sight  is  present. 

(b)  Contraction  of  the  Visual  Fields  for  Light. — In  ordSr  to  deter- 
mine the  presence  of  this  symptom  one  invokes  the  aid  of  the  oculist 
and  his  perimeter,  as  it  can  not  be  ascertained  by  any  less  accurate 
test.  Leaving  out  of  consideration  glaucoma,  optic  atrophy,  or  other 
organic  disease,  by  far  the  most  important  indications  of  a  nearly 
uniform  contraction  of  the  visual  fields  relate  to  the  presence  of 
hysteria  and  traumatic  neuroses.  As  a  rule,  one  field  presents  a 
greater  contraction  than  the  other.  In  neurasthenia,  while  there 
may  not  be  a  true  concentric  limitation  of  the  visual  field,  yet  the 
fatigue  of  continued  testing  will  sometimes  develop  a  decided  tem- 
porary diminution  in  its  size. 

(c)  Contraction  of  the  Visual  Fields  for  Colour.— The  colour 
fields  are  tested  by  the  perimeter,  using  bits  of  coloured  paper. 
Passing  from  the  circumference  to  the  centre  of  the  field,  the  percep- 
tion of  white  objects  is  found 

to  have  the  widest  extent.  A 
little  nearer  blue  is  perceived, 
then  red,  then  green  (Fig.  35). 

Limitation  of  the  colour  fields 
is  a  common  symptom  in  hys- 
teria and  traumatic  neuroses. 
Sometimes  a  transposition  of  the 
normal  fields  for  different  col- 
ours will  occur,  one  taking  the 
place  usually  occupied  by  an- 
other. A  central  blank  or  sco- 
toma for  red  or  green  is  a  con- 
stant symptom  of  tobacco  or 
other  toxic  amblyopia,  usually 
due  to  a  retrobulbar  neuritis.  Like  vision  in  general,  the  colour 
perception  may  be  much  reduced  or  abolished  by  optic  neuritis  or 
atrophy. 

III.  Amblyopia,  Amaurosis.— Amblyopia  is  dimness  of  vision 
or  partial  blindness,  while  amaurosis  signifies  a  total  loss  of  sight, 
mthout  appreciable  lesmis.  The  causes  producing  these  forms  of 
partial  or  total  blindness  are,  as  a  rule,  of  a  functional  character, 


Fig.  35. — Visual  colour  field  of  right  eye. 


208  THE  EVIDENCES  OF  DISEASE 

affecting  either  the  centres  or  the  retina  or,  if  organic,  do  not  pro- 
duce noticeable  alterations  in  the  appearance  of  the  latter. 

The  loss  of  vision  is  usually  sudden,  bilateral,  and,  in  most  cases, 
temporary.  The  most  frequent  causes  are  uraemia,  diabetes,  tobacco, 
and  certain  drugs,  large  hemorrhages,  migraine,  and  hysteria.  "When 
occurring  in  uraemia  it  ordinarily  follows  coma  or  convulsions,  is 
sudden  and  usually  lasts  but  one  or  two  days.  It  may  supervene  in 
a  similar  manner  in  diabetes,  and  in  all  cases  of  amblyopia  the  urine 
should  be  examined  for  sugar.  In  tobacco  amblyopia  the  onset  is 
slow,  the  loss  of  sight  is  most  marked  in  the  centre  of  the  visual 
field,  and  on  testing  the  colour  field  a  central  blank  or  scotoma  for 
red  and  green  is  found  to  exist.  Quinine  and  the  salicylates  may 
cause  sudden  amaurosis,  and  it  sometimes  occurs  in  alcoholism. 
Severe  hemorrhages,  particularly  those  from  the  stomach,  may  be 
responsible  for  a  sudden  failure  of  sight.  Migraine  may  exhibit  as 
one  of  its  symptoms  a  fugitive  blindness,  perhaps  of  only  one  half 
the  visual  field  (hemianopia).  The  amaurosis  of  hysteria  is  associated 
with  emotional  states  and  other  characteristic  symptoms,  and  no 
matter  how  complete  the  apparent  loss  of  sight  may  be,  the  pupillary 
reflex,  both  direct  and  consensual,  is  retained. 

Other  and  less  frequent  causes  are  blows  upon  the  eye  or  the 
head  without  visible  injury,  shock  from  lightning  or  the  dynamo 
current,  and  poisoning  from  lead.  In  cases  in  which  strabismus  or 
a  high  degree  of  astigmatism  with  hypermetropia  has  existed  from 
an  early  age,  one  eye  may  be  accidentally  discovered  to  possess  very 
little  power  of  vision. 

IV.  Ophthalmoscopic  Signs  of  Extraocular  Diseases. 
— Valuable  diagnostic  information  may  be  obtained  by  an  examina- 
tion of  the  interior  of  the  eye,  but  it  is  an  open  question  whether 
the  general  practitioner,  who  makes  an  occasional  ophthalmoscopic 
examination,  can  rely  upon  his  own  interpretation  of  what  he  sees. 
As  a  rule,  the  examination  should  be  made  by  a  specialist. 

The  conditions  of  general  diagnostic  value,  as  distinguished  from 
purely  local  ocular  diseases,  are  :  retinal  hemorrhage,  optic  neuritis, 
optic  atrophy,  pulsating  retinal  arteries,  embolism  or  thrombosis  of 
the  central  artery  and  tubercles  of  the  choroid. 

(a)  Retinal  Hemorrhage. — Apoplexy  of  the  retina  occurs  most 
commonly  in  elderly  people  with  degenerated  arteries.  Cardiac 
hypertrophy  from  valvular  disease  or  chronic  nephritis  may  be  the 
causative  condition.  So  also  may  the  gouty  diathesis  (Hutchinson) 
and  hemorrhagic  blood  states,  as  in  scurvy,  haemophilia,  purpura,  and 
grave  anaemias.  Retinal  extravasations  may  also  be  significant  of 
malarial  fever,  ulcerative  endocarditis,  pyaemia,  suddenly  suppressed 


OPTIC  NEURITIS  209 

menstruation,  the  menopause,  and  leucaemia,  although  in  the  latter  a 
retinitis  is  more  common, 

(b)  Optic  Neuritis. — Inflammation  of  the  optic  nerve,  with  con- 
gestion, hemorrhage,  and  exudation  into  its  substance,  may  affect 
the  nerve  posterior  to  the  globe,  retrobulbar  nenritis ;  the  nerve 
and  its  end,  papillitis  ;  the  retina,  retinitis.  In  course  of  time  there 
may  be  connective-tissue  proliferation  and  consequent  atrophy  of  the 
nerve  fibres,  giving  rise  to  secondary  (consecutive)  optic  atrophy. 

(1)  Betrobulbar  Neuritis. — In  this  form  of  inflammation  of  the 
optic  nerve  the  retina  itself  is  but  slightly  affected.  If  acute,  there 
is  pain  in  the  globes  with  rapid  loss  of  sight,  but  in  the  more  chronic 
forms  the  visual  defects  consist  of  scotomata  (blind  spots  in  the 
visual  field)  for  colour  or  light.  It  is  indicative  of  the  abuse  of  alco- 
hol or  tobacco  (amblyopia),  lead  poisoning,  diabetes,  and  syphilis, 
and  is  sometimes  due  to  rheumatic  inflammation. 

(2)  Papillitis. — Inflammation  of  the  papilla  is  in  reality  a  de- 
scending optic  neuritis  with  a  very  marked  swelling  of  the  papilla, 
the  "  choked  disk  "  of  earlier  writers.  It  is  the  extreme  grade  of 
papillitis  to  which  reference  is  had  in  the  following  paragraphs. 
Papillitis  of  a  much  less  intensity  is  present  as  a  part  of  retinitis  or 
neuro-retinitis.  The  vision  in  many  cases  remains  nearly  normal, 
while  in  others  there  may  be  limitation  of  the  visual  fields  or  scotom- 
ata for  light  and  colour. 

Papillitis  of  the  extreme  grade,  and  usually  affecting  both  eyes,  is 
of  great  value  as  a  symptom  of  brain  tumours,  occurring  as  it  does  in 
§  of  all  cases,  without  reference  to  the  size  of  the  growth.  It  does 
not  accompany  growths  in  the  medulla  (Hcghlings  Jackson),  is  not  very 
common  in  lesions  of  the  motor  cortex,  and  is  most  frequent  in  cere- 
bellar neoplasms.  Xext  in  frequency  it  is  symptomatic  of  tubercu- 
lous meningitis  (80  per  cent  of  all  cases),  and  it  may  also  be  present 
in  the  non-tuberculous  and  suppurative  forms  of  the  same  disease. 
It  is  also  found  in  a  considerable  proportion  of  cerebral  abscesses. 

(3)  Retinitis  and  Neuro-retinitis. — As  retinal  disease  is  usually 
secondary  to  some  extraocular  cause,  it  is  in  the  majority  of  cases  a 
bilateral  affection.  If  the  retina  is  chiefly  involved,  it  is  a  retinitis ; 
but  if  the  papilla,  as  usual,  presents  evidence  of  disease,  it  constitutes 
a  neuro-retinitis. 

The  varieties  and  diagnostic  significance  of  this  condition  are  as 
follows : 

Hemorrhagic  Xeuro-retinitis.— In  this  form  the  retinal  hemor- 
rhages are  abundant.  It  occurs  in  general  atheromatous  degenera- 
tion of  the  arteries,  in  cardiac  hypertrophy,  in  cardiac  valvular  dis- 
ease, especially  the  insuflBciencies,  and  in  aneurism.     It  may  also  bo  a 


210  THE  EVIDENCES  OF  DISEASE 

symptom  of  diabetes  and  chronic  nephritis,  and  sometimes  happens 
in  sudden  suppression  of  menstruation  or  chronic  discharges. 

Albuminuric  Neuro-retinitis. — It  occurs  in  from  15  to  20  per  cent 
of  all  cases  of  chronic  Bright's  disease,  most  commonly  with  the 
interstitial  variety.  The  papillitis  may  be  so  marked  that  it  is  diffi- 
cult to  determine  whether  it  is  of  renal  or  intracranial  origin. 

Syphilitic  Ketinitis  or  Choroido-retinitis. — In  inherited  syphilis 
retinitis  pigmentosa  may  occur.  As  a  secondary  symptom  of  acquired 
syphilis  both  retina  and  choroid  are  more  likely  to  be  affected.  Puru- 
lent choroiditis  may  be  a  symptom  of  pyaemia,  ulcerative  endocarditis, 
■cerebro-spinal  meningitis,  and  other  infective  diseases. 

Anaemic  Neuro-retinitis. — Inflammatory  and  hemorrhagic  altera- 
tions in  the  retina  and  papilla  may  be  due  to  large  hemorrhages,  per- 
nicious anaemia,  and  severe  chloro-anaemia. 

Leucaemic  Xeuro-retinitis. — In  25  to  30  per  cent  of  cases  of  leu- 
caemia retinitis  is  present. 

Finally,  neuro-retinitis  may  be  found  in  lead  poisoning,  diabetes, 
diphtheria  and  other  infectious  diseases,  the  malarial  cachexia,  chronic 
hydrocephalus,  and,  as  a  unilateral  symptom,  in  disease  of  the  bones 
of  the  orbit  or  erysipelatous  inflammation  of  the  orbital  tissues.  It 
may  exist  without  an  assignable  cause. 

(c)  Optic  Atrophy. — Atrophy  of  the  optic  nerve  may  be  primary 
or  secondary. 

(1)  Primary  Atrojihy^  not  preceded  by  papillitis  or  neuro-retini- 
tis, is  in  the  majority  of  cases  a  symptom  of  spinal-cord  disease,  espe- 
cially locomotor  ataxia.  Less  frequently  it  occurs  with  disseminated 
sclerosis,  lateral  sclerosis,  and  general  paralysis.  There  is  an  heredi- 
tary form  affecting  young  males.  Other  causes  are  large  hemorrhages, 
diabetes,  the  specific  fevers,  chronic  alcoholism,  and  lead  poisoning. 

(2)  Secondary  Atrophy. — Secondary  or  consecutive  atrophy  is 
usually  consequent  to  an  optic  neuritis,  the  causes  of  which  have 
been  previously  rehearsed.  Eetrobulbar  neuritis,  syphilitic  choroido- 
retinitis,  and  retinitis  pigmentosa  may  also  be  responsible  for  con- 
secutive atrophy.  In  some  cases  of  chronic  hydrocephalus  a  greatly 
distended  third  ventricle  may  press  upon  the  chiasm  and  produce 
similar  changes. 

{d)  Pulsation  of  the  Retinal  Arteries. — Visible  pulsation  may  be 
found  due  to  aortic  insufficiency,  great  cardiac  hypertrophy,  or  vaso- 
motor instability  as  in  exophthalmic  goitre  and  other  conditions  in 
which  there  is  abnormal  throbbing  of  tlie  arteries. 

{e)  Embolism  and  Thrombosis  of  the  Central  Artery.— Obstruc- 
tion or  thrombosis  of  the  central  artery  causes  a  sudden  loss  of  vision, 
commencing  at  the  circumference  of  the  visual  field  and  extending 


EXAMINATION  OF  THE  NOSE  211 

to  the  centre.  It  is  frequently  indicative  of  cardiac  or  vascular  dis- 
ease— viz.,  ulcerative  endocarditis,  valvular  disease,  particularly  mitral 
stenosis,  atheroma  of  the  large  arteries,  aneurism  of  the  aorta,  throm- 
bosis of  the  pulmonary  veins,  and  very  rarely  it  occurs  in  chorea. 
In  a  very  small  proportion  of  cases  the  sudden  loss  of  sight  in  chronic 
nephritis  is  said  to  be  due  to  this  accident. 

(/■)  Tubercles  in  the  Choroid. — These  are  significant  of  tubercu- 
lous meningitis  or  general  miliary  tuberculosis. 


SECTION  xvn 

THE  NOSE 

I.  Examination  of  the  Nose  and  Nasal  Chambers. — 

Having  a  good  light  (Argand,  Welsbach,  electric)  upon  the  right 
of  the  patient,  on  a  level  with  or  a  little  higher  than  his  mouth, 
desire  him  to  sit  nearly  erect  on  a  straight-backed  chair  in  such  a 
manner  that  he  is  supported  without  lolling  back.  The  observer  sits 
facing  the  patient,  knees  outside  if  a  man,  to  the  patient's  right  if  a 
woman.  A  forehead  mirror,  3  to  3|^  inches  in  diameter,  with  a  cen- 
tral opening,  should  be  employed.  As  a  rule,  it  is  better  to  wear  the 
mirror  in  front  of  the  left  eye,  as  the  otherwise  obscuring  glare  of 
the  light  is  thus  avoided. 

Having  directed  the  reflected  light  upon  the  nose,  note  its  shape, 
colour,  presence  of  excoriation,  fissure,  or  eruption.  Tilt  up  the  tip 
of  the  nose,  and  inspect  the  lower  portion  of  the  septum  as  to  sym- 
metry and  the  existence  of  ulcers  or  raw  surfaces.  Closing  first  one, 
then  the  other  nostril,  desire  the  patient  to  breathe  rather  deeply  in 
order  to  determine  their  patency  and  whether  or  not  the  alae  fall  in 
unduly  during  inspiration. 

Then  warm  and  introduce  a  nasal  speculum  (bivalve,  duckbill,  or 
wire).  The  first  of  the  intranasal  structures  to  be  seen,  provided  the 
patient's  head  is  not  retracted,  is  usually  the  rounded  end  of  the 
inferior  turbinate  body,  from  which  this  structure  may  be  followed 
backward  for  a  varying  distance.  Note  if  it  appears  swollen  and 
abnormally  large,  and  if  so  always  test  its  consistence  with  a  probe 
in  order  to  determine  whether  the  enlargement  is  bony,  firm,  or  a 
soft  vascular  tumidity.  Depress  the  head  slightly  so  as  to  see  the 
inferior  meatus,  where  foreign  bodies,  if  present,  are  usually  found ; 
then  tip  it  backward  in  order  to  bring'the  middle  turbinate  (which 
begins  considerably  farther  back  than   the   inferior)   and    middle 


212  THE  EVIDENCES  OF  DISEASE 

meatus  into  sight.  The  latter  is  the  usual  location  of  polypus  and 
the  place  where  the  thick  pus  of  antral,  frontal,  or  ethmoidal  disease 
is  found.  If  the  inferior  turbinal  is  so  large  that  it  interferes  with 
the  examination  of  the  parts  behind  and  above,  apply  a  pledget  of 
cotton  soaked  in  a  5  to  10  per  cent  solution  of  cocaine  or  suprarenal 
capsule  to  the  part,  which  will  speedily  reduce  the  swelling  so  far  as 
it  is  due  to  vascular  engorgement. 

Finally,  turn  the  patient's  head  slightly  from  side  to  side  in  order 
to  examine  the  septum  for  abnormal  deviations,  ridges,  spurs,  ulcera- 
tions, or  perforations.  It  should  be  borne  in  mind  that  the  septum 
is  rarely  evenly  placed  between  the  two  nostrils,  so  that,  as  a  rule, 
one  cavity  is  larger  than  the  other.  Test  all  projections  with  the 
probe  to  discover  their  consistence,  extent,  and  whether  opposing 
projections  are  in  firm  contact,  thus  causing  erosions  or  turbinal 
pressure.     The  superior  turbinate  can  not  be  seen. 

The  examination  thus  far  has  been  from  the  front^anterior 
rhinoscopy.  Inspection  from  the  back,  or  posterior  rhinoscopy, 
requires  the  use  of  a  small  (i  to  ^  inch  in  diameter)  laryngoscopic 
mirror.  The  tongue  depressor  (usually  indispensable)  should  be 
applied,  and  the  patient  instructed  by  precept  and  example  to 
breathe  quietly  through  the  nose.  Then,  having  warmed  the  mirror, 
introduce  it,  reflecting  surface  upward  and  parallel  to  the  tongue 
depressor,  until  the  soft  palate  is  approached,  when  it  should  be 
turned  so  that  it  passes  edgewise  between  the  uvula  and  the  left  ton- 
sil to  a  point  below  and  behind  the  soft  palate.  Having  again 
turned  the  mirror  so  that  the  reflecting  surface  looks  upward  and 
forward,  the  posterior  nares  should  be  brought  into  view.  The  sur- 
face to  be  examined  is  of  such  shape  and  extent  that  it  can  not  be 
seen  all  at  once.  The  mirror  must  be  turned  and  shifted  in  a  man- 
ner which  can  only  be  acquired  by  practice. 

The  most  striking  object  first  seen  is  the  posterior  edge  of  the 
septum  (Fig.  36),  sharp  and  yellowish  in  colour  below,  broadening 
and  becoming  more  distinctly  red  above.  To  either  side  may  be 
seen  two  bluish-red  or  gray-red  swellings — the  posterior  extremities 
of  the  middle  turbinates.  Below  are  the  inferior  turbinates,  of 
which  the  upper  halves  only  are  usually  seen ;  above  are  visible  the 
superior  turbinates. 

The  colour,  shape,  and  size  of  the  turbinates  and  the  presence  of 
pus  or  polypi  should  be  determined.  By  turning  the  mirror  to  one 
side  or  the  other,  keeping  it  low  down  with  its  back  resting  almost 
against  the  tonsil,  the  openings  of  the  Eustachian  tubes  may  be  seen 
as  rounded  red  prominences  with  central  yellowish  depressions. 
Posterior  to  these  are  the  fossae  of  Rosenmiiller.     Finally,  the  mirror 


THE  NOSE 


213 


Fig.  36. — Post-rhinoscopic  view  of  the  septum,  cboanse, 
Eustachian  tube  mouths,  soft  palate,  and  pharynx 
vault  (after  Heymann). 


should  be  turned  upward  in  order  to  observe  the  vault  of  the 
pharynx,  the  surface  of  which  normally  somewhat  resembles  that  of 
the  faucial  tonsil.  The  most  important  abnormality  here  is  the 
adenoid  or  lymphoid  growth  so  commonly  found  to  be  the  cause  of 
habitual  mouth-breath- 
ing in  children.  Digi- 
tal examination  of  the 
upper  pharynx  is  often 
required  to  determine 
the  exact  size  and  loca- 
tion of  the  growth,  and 
is  indispensable  in  chil- 
dren who  are  too  young 
to  be  under  control. 
The  child's  head  is  held 
either  by  an  assistant  or, 
better,  by  the  physician, 
who  sits  or  stands  by  the 
patient  and  embraces 
and  steadies  the  head 
with  his  left  arm.  The 
right  forefinger,  palmar  surface  up,  is  then  passed  in  at  the  angle  of 
the  mouth,  invaginating  the  cheek  between  the  teeth  of  the  patient 
to  prevent  biting.  The  finger,  having  been  carried  back,  hugging  the 
tonsil,  is  hooked  up  behind  the  palate  to  the  upper  pharynx,  where 
it  explores  the  pharyngeal  vault,  septum,  turbinates,  and  Eustachian 
prominences. 

Posterior  rhinoscopy  is  rarely  easy,  generally  difficult,  and  some- 
times impossible,  even  in  the  hands  of  the  expert. 

II.  Pain  in  or  around  the  Nose. — Burning  or  smarting  sen- 
sations usually  attend  coryza  or  other  acute  catarrhal  inflammations ; 
and  if  great  pain  in  the  nasal  chambers  is  present,  it  may  be  a  symp- 
tom of  a  syphilitic  lesion,  glanders,  or  impacted  foreign  body. 
Severe  pain  just  above  the  root  of  the  nose  is  due  to  inflammation  of 
the  frontal  sinus ;  in  the  nose  and  cheek,  of  the  antrum ;  referred  to 
the  nasal  cavities  and  ear,  of  the  Eustachian  tubes.  A  sensation  of 
dryness  is  a  common  complaint  in  the  early  and  late  stages  of  coryza 
and  a  persistent  and  annoying  symptom  of  atrophic  rhinitis. 

III.  Shape,  Colour,  and  Ulceration  of  Nose.— The  nose 
becomes  coarse  and  broad  in  cretinism  and  myxoedema.  A  depressed, 
sunken,  "  saddle  "  nose  may  be  due  to  a  previous  injury,  but  if  there 
is  no  history  of  traumatism,  syphilis  should  be  suspected.  The  nose 
is  broadened  or  distorted  and  displaced  by  growing  tumours  in  the 

16 


214  THE  EVIDENCES  OP  DISEASE 

nasal  cavities  or  the  adjacent  facial  bones.  A  nose  which  is  pinched 
and  insignificant  relatively  to  the  lower  part  of  the  face  may  be 
indicative  of  nasal  obstruction  and  consequent  mouth-breathing. 

A  chronic  redness  of  the  nose  due  to  dilated  capillaries,  perhaps 
also  with  some  papules,  may  be  significant  of  chronic  alcoholism,  or 
is  an  acne  rosacea  from  other  causes.  A  similar  redness  may  be 
caused  by  chronic  digestive  disorders,  amenorrhoea,  and,  exception- 
ally, by  chronic  hypertrophic  rhinitis.  Acute  redness  of  the  nose, 
with  pain  and  swelling,  especially  of  one  ala,  may  be  the  result  of  a 
small  pustule  or  boil,  to  be  seen  just  within  the  nares ;  or  may  be  a 
beginning  erysipelas.  In  the  latter  case  the  redness  rapidly  extends, 
and  there  is  a  marked  elevation  of  the  bodily  temperature. 

A  superficial  ulceration  of  the  wing  of  the  nose  in  a  young  person, 
usually  painless,  beginning  as  a  reddish  papule,  spreading  in  various 
directions,  and  healing  in  one  portion  while  breaking  down  in 
another,  is  probably  a  tuberculous  ulcer.  In  an  elderly  patient  a 
small,  hard,  scabbing  ulcer,  somewhat  painful,  gradually  extending, 
and  perhaps  with  glandular  involvement,  is  an  epithelioma.  In  all 
cases,  both  children  and  adults,  an  ulcer  of  the  margin  of  the  nose 
or  multiple  circular  ulcers  should  cause  a  careful  search  elsewhere 
for  evidences  of  syphilis. 

IV.  Sneezing. — This  is  a  spasmodic  expiration,  caused  usually 
by  direct,  rarely  by  reflex,  irritation  of  the  sensory  nerves  of  the 
nose,  and  occurs  as  an  early  symptom  of  coryza,  measles,  pertussis, 
asthma,  and  hay  fever.  Small  doses  of  the  iodides  in  susceptible 
individuals,  and  large  doses  in  many  others,  will  induce  it,  as  well  as 
the  inhalation  of  various  irritants  like  pepper,  snuff,  powdered  ipe- 
cac, euphorbium,  or  veratrum,  and  solutions  of  zinc  chloride.  It  has 
been  attributed  to  gout,  and  prolonged  paroxysms  of  sneezing  have 
been  asserted  to  be  of  hysterical  origin.  Syringing  or  manipulation 
of  the  external  auditory  canal  will  sometimes  provoke  a  reflex  sneeze. 

V.  Acting  Nares  ;  Eegurgitation  of  Fluids. — In  some  sen- 
sitive and  neurotic  individuals  the  nostrils  dilate  with  each  inspiration, 
especially  under  mental  excitement.  Aside  from  this,  acting  nares 
indicate  marked  dyspnoea  {q.  v.)  of  various  origin,  and  among  other 
conditions  are  very  noticeable  in  emphysema,  asthma,  pneumonia, 
obstructive  diseases  of  the  larynx,  and  the  broken  compensation  of 
cardiac  valvular  lesions.  It  is  a  particularly  useful  symptom  in  the 
form  of  pneumonia  in  children  which  begins  with  such  marked 
gastro-intestinal  symptoms  that  the  underlying  pulmonary  condition 
is  overlooked.  The  respiration  may  not  be  very  rapid,  but  the  dilat- 
ing nostrils  often  give  the  first  clew  to  the  real  nature  of  the  case. 

If  upon  attempting  to  swallow  fluids  a  portion  escapes  through 


NASAL  STENOSIS  AND  DISCHARGES  215 

the  nostrils,  one  of  three  conditions  is  usually  present — cleft  palate, 
diphtheritic  paralysis  of  the  soft  palate,  or  bulbar  paralysis. 

VI.  Nasal  Stenosis. — Difficulty  in  breathing  through  the  nos- 
trils, the  stenosis  coming  on  somewhat  rapidly,  may  be  symptomatic  of 
an  acute  coryza,  hay  fever,  nasal  diphtheria,  foreign  bodies  in  children 
(one  nostril),  or  the  prodromal  stage  of  variola,  typhus  fever,  or 
glanders.  A  more  chronic  and  slow-coming  nasal  obstruction  affect- 
ing one  or  both  sides  is  usually  referable  to  hypertrophic  rhinitis, 
postnasal  lymphoid  growths,  polypi,  or  a  deviated  septum.  If 
accompanied  by  "the  snuffles  "  in  infants,  hereditary  syphilis  should 
be  suspected. 

VII.  Discharges  from  the  Nose. — Xasal  discharges  may  be 
clinically  (a)  non-offensive,  watery,  mucous,  muco-purulent,  or  puru- 
lent ;  {b)  offensive ;  (c)  bloody  or  composed  of  blood  alone,  accord- 
ing to  the  nature  and  seat  of  the  causal  condition. 

(a)  A  watery  discharge,  in  some  cases  very  profuse,  marks  the 
beginning  of  acute  coryza,  hay  fever,  the  catarrhal  form  of  epidemic 
influenza,  pertussis,  measles,  iodism,  and  typhus  fever.  In  the  later 
stages  of  some  of  these  the  discharge  grows  thick  and  muco-purulent. 
Watery  fluid  may  flow  from  one  nostril  during  an  attack  of  trigemi- 
nal neuralgia.  An  occasional  watery  discharge,  with  a  persistent 
obstruction  of  one  or  both  nostrils,  may  be  due  to  nasal  polypi.  A 
recurring  flow  of  pus  from  one  nostril,  particularly  if  brought  on  by 
lying  upon  or  leaning  over  toward  the  side  opposite  to  that  which  is 
discharging,  is  probably  an  antral  abscess,  and  the  probability  is 
increased  if  bad  teeth  are  present.  In  children  the  possibility  of  a 
foreign  body  should  not  be  overlooked.  Finally,  irritating  gases  or 
powders  will  produce  a  smart  watery  flow. 

(b)  Offensive  discharges  may  be  significant  of  an  impacted  foreign 
body.  Coming  on  in  the  course  of  pharyngeal  diphtheria  and  irri- 
tating the  parts  with  which  it  comes  in  contact,  it  may  indicate  nasal 
infection  before  membrane  can  be  discovered  in  the  nasal  cavities. 
An  extremely  offensive  continuous  discharge  from  both  nostrils, 
which  may  be  accompanied  with  greenish-gray  crusts,  is  symptomatic 
of  atrophic  rhinitis  (ozcena)  due  to  syphilis,  caries  or  necrosis  of  the 
bones,  or  glanders.  It  may  be  a  sequel  of  scarlatina.  The  patient 
is  usually  unconscious  of  the  fetid  odour.  Cancer  or  lupus  affect- 
ing or  encroaching  upon  the  nasal  chambers  may  also  be  responsible 
for  discharges  possessing  an  unpleasant  smell. 

(c)  A  discharge  of  blood  from  the  nose  (epistaxis)  may  be  a  result 
either  of  local  or  general  causes.  It  is  usually  a  capillary  oozing 
and  upon  inspection  the  bleeding  area  is  seen  to  be  congested,  ecchy- 
motic,  or  superficially  ulcerated.     A  common  site  of  the  bleeding 


216  THE  EVIDENCES  OP  DISEASE 

spot  is  upon  the  cartilaginous  septum.  Less  frequently  it  arises 
from  the  posterior  end  of  the  middle  turbinated  body  or,  in  chil- 
dren with  adenoids,  from  the  vault  of  the  pharynx  or  at  times  from 
the  accessory  sinuses.  Careful  specular  inspection  under  a  good 
light,  clots  having  been  removed  by  swab  or  spray,  is  necessary  to 
determine  the  exact  location  of  the  hemorrhagic  point.  If  ejiistaxis 
occurs  during  sleep  the  blood  may  run  into  the  pharynx  and,  after 
having  been  swallowed,  may  be  vomited  or,  if  clinging  to  the  pharynx, 
be  hawked  up,  thus  simulating  haematemesis  or  haemoptysis.  Nose- 
bleed from  local  causes  is  usually  unilateral,  but  if  due  to  blood 
changes  or  general  diseases  is  apt  to  take  place  from  both  sides. 

Epistaxis  is  ordinarily  not  sufficiently  severe  to  produce  constitu- 
tional symptoms,  but  after  operations  on  the  nose  or  in  cases  of 
haemophilia  may  be  so  profuse  or  continue  so  long  as  to  seriously 
threaten  life,  although  an  actual  fatal  result  is  extremely  rare. 

1.  Nasal  Causes  of  Epistaxis. — Aside  from  traumatic  causes,  caries 
or  necrosis  of  the  nasal  bones,  ulceration  from  a  foreign  body  or  other 
causes,  polypus,  new  growths,  varicosities,  and  chronic  nasal  catarrh 
may  be  responsible  for  epistaxis.  Arteritis  and  alcoholism  may 
render  the  vessels  liable  to  rupture. 

2.  General  Causes  of  Epistaxis. — People  of  full  habit  may  have  a 
rather  frequently  recurring  nosebleed  which  appears  to  be  conserva- 
tive. Delicate  children  suffer  from  it,  especially  at  puberty  and  after 
exertion  under  a  hot  sun.  It  is  a  common  complaint  of  mountain 
climbers  at  considerable  altitudes,  and  inhalation  of  very  hot  or  very 
cold  air  may  induce  it.  In  suppressed  menstruation  it  may  be  vicari- 
ous. The  chronic  anaemias  are  frequently  attended  by  epistaxis,  and 
it  is  a  symptom  of  leucaemia,  purpura  haemorrhagica,  and  scurvy.  It 
is  the  most  ordinary  form  of  hemorrhage  in  haemophilia.  Less  com- 
monly it  may  be  the  result  of  cardiac  hypertrophy  and  valvular  dis- 
ease, enlarged  bronchial  glands,  pleurisy  with  large  effusion,  emphy- 
sema, and  the  strain  of  pertussis. 

It  is  a  symptom  of  diagnostic  value  in  the  prodromal  stage  of 
typhoid  fever,  and  is  an  occasional  event  in  other  infections,  as  ery- 
sipelas, malarial  fever,  measles,  scarlet  fever,  dengue,  relapsing  fever, 
pyaemia,  and  acute  yellow  atrophy  of  the  liver ;  also  in  phosphorus 
poisoning.  As  an  infrequent  happening  it  occurs  in  ascites,  peri- 
tonitis, appendicitis,  enlarged  spleen,  large  ovarian  cystomata,  uterine 
fibroids,  chronic  nephritis,  and  cerebral  thrombosis.  Finally,  it  may 
be  impossible  to  assign  a  cause  for  its  presence. 

VIII.  The  Sense  of  Smell. — The  olfactory  bulbs  and  the  irasso- 

#         elated  parts  are  in  reality  portions  of  the  brain.     The  peripheral 

nerves  arising  from  the  bulb  are  distributed  to  the  mucous  mem- 


ABNORMALITIES  IX  THE  SENSE  OP  SMELL  217 

brane  of  the  upper  portion  of  the  nasal  septum  and  the  superior 
and  middle  turbinates.  The  centre  for  the  sense  of  smell  is  said  to 
be  in  the  uncinate  convolution  (Ferrier). 

To  test  the  function  of  the  olfactory  nerve,  non-irritating  sub- 
stances must  be  used,  as  pungent  vapours  affect  mainly  the  trigeminal 
nerve.  Suitable  odorous  bodies  are  musk,  oil  of  cloves,  or  pepper- 
mint in  convenient  containers.  It  should  be  remembered  that  the 
perception  of  any  single  odour  is  lost  in  3  or  4  minutes,  but  is 
regained  by  1  minute  of  rest.  It  is  essential  that  the  odorous 
material  should  enter  the  nostrils  as  a  vapour  or  in  a  state  of  fine 
division,  and  the  act  of  smelling  is  usually  assisted  by  "  sniffing," 
which  is  a  modified  inspiration.  It  is  also  necessary  that  the  mucous 
membrane  should  be  moist  in  order  that  the  odorous  particles  shall 
enter  into  solution  on  the  surface  of  the  mucous  membrane. 

The  clinical  symptoms  relating  to  the  sense  of  smell  are  anosmia^ 
loss  of  the  sense  of  smell ;  hyperosmia^  increased  sensitiveness  of  the 
sense  of  smell ;  and  parosmia^  subjective  perversion  of  the  olfactory 
8ense. 

(«)  Anosmia. — The  loss  of  the  sense  of  smell  is,  in  the  majority  of 
instances,  due  to  local  disease  of  the  nasal  mucous  membrane — viz., 
chronic  rhinitis,  particularly  the  atrophic  variety,  and  polypi  or 
other  new  growths.  The  inhalation  of  irritating  vapours  or  extremely 
foul  odours  may  temporarily  or  permanently  abolish  the  sense  of 
smell.  Paralysis  of  the  trigeminal  wUl  impair  the  olfactory  power 
of  the  affected  side  because  of  the  deficient  secretion  and  conse- 
quent dryness  of  the  mucous  membrane  which  is  thus  induced. 
Loss  of  the  power  of  smell  may  be  a  symptom,  purely  neurotic,  of 
neurasthenia  and  hysteria. 

Less  frequently  the  sense  of  smell  is  abolished  because  of  injury 
or  lesion  of  the  olfactory  bulb  or  tract.  Falls  or  blows  upon  the 
head,  affecting  the  nerve  in  its  course,  may  have  as  their  only  symptom 
a  persistent  anosmia.  Caries  of  the  bones  supporting  the  tract  or 
bulb,  and  basal  meningitis  or  tumours  involving  the  nerve,  may  be 
instrumental  in  causing  olfactory  anaesthesia.  Possibly  from  atrophy 
of  the  nerves  anosmia  may  be  one  of  the  symptoms  of  locomotor 
ataxia.  It  is  sometimes  congenital  and  results  from  imperfect 
development  of  the  olfactory  nerve  tissue.  Partial  anosmia  may 
be  due  to  a  lesion  of  the  uncinate  gyrus  or  disease  of  one  hemi- 
sphere. 

{h)  Hyperosmia. — Hyperaesthesia  or  abnormal  sensitiveness  of  the 
sense  of  smell  is,  in  its  slighter  degrees,  not  an  uncommon  symptom 
in  neurotic  individuals.  More  rarely  the  sensitiveness  is  extreme 
and  is  symptomatic  of  hysteria  and  neurasthenia. 


218  THE  EVIDENCES  OP  DISEASE 

(c)  Parosmia. — Olfactory  sensations  without  a  physical  basis,  the 
apparent  odours  usually  being  unpleasant  or  offensive  {kakosmia)^ 
are  not  infrequent  as  hallucinations  in  the  psychoses.  A  bad  odour, 
like  that  of  burning  rags  or  feathers,  may  constitute  the  premonitory 
aura  of  epilepsy.  Very  rarely,  after  head  injuries,  ordinary  odours 
are  perverted,  so  that  a  usually  agreeable  perfume  is  perceived  as 
foul.  Finally,  subjective  kakosmia  has  been  associated  in  a  limited 
number  of  cases  with  tumour  of  the  hippocampus. 


SECTION  XVIII 
THE   MOUTH 

Undee  this  heading  will  be  given  the  diagnostic  evidence  which 
may  be  derived  from  an  examination  of  the  lips,  buccal  surfaces, 
gums,  teeth,  and  tongue. 

I.  The  Liips. — Thick  or  thin  lips  are  often  a  racial  character- 
istic, as  in  the  African  or  American  Indian.  Full  lips  in  white  races 
are  said  to  mark  a  phlegmatic  temperament  or  to  indicate  a  tend- 
ency to  the  worship  of  Bacchus  and  Venus ;  while  thin-lipped  indi- 
viduals are  apt  to  be  nervous  and  of  somewhat  acrid  temper.  The 
lips  are  thickened  and  coarse  in  myxcedema  and  cretinism. 

Their  colour  is  often  significant  of  anaemia  and  other  conditions 
in  which  the  skin  is  pallid,  and  the  first  evidence  of  cyanosis  is  often 
seen  in  them,  their  slight  blueness  attracting  attention  to  the  exist- 
ence of  cardiac  disease. 

If  the  lips  are  open,  and  particularly  if  they  are  dry  and  cyanosed, 
it  is  apt  to  be  indicative  of  dyspnoea,  due  to  disease  of  the  heart  or 
lungs,  especially  the  chronic  forms — e.  g.,  emphysema  or  failing  com- 
pensation in  valvular  lesions.  It  may  be  due  to  disease  within  the 
mouth,  stomatitis,  glossitis,  cancrum  oris,  phlegmonous  tonsilitis,  or 
some  form  of  nasal  stenosis.  If  the  lips  are  loose  and  pendulous  it 
is  suggestive  of  diphtheritic  paralysis  or  chronic  bulbar  palsy.  The 
open  mouth  is  seen  in  all  conditions  of  great  prostration,  and  in 
idiots  and  some  cases  of  insanity. 

Trembling  or  tioitchmg  of  the  lips  may  be  a  symptom  of  general 
paralysis  or  chronic  bulbar  palsy.  Convulsive  raising  of  the  upper 
lip  is  an  occasional  evidence  of  severe  abdominal  pain. 

Utiilateral  deviation  of  the  lips,  the  angle  of  the  mouth  being 
drawn  to  one  side  and  downward,  if  not  due  to  loss  of  teeth  on  the 
opposite  side  or  to  the  contraction  of  scars,  is  indicative  of  facial 


LIPS— BUCCAL  CAVITY  219 

paralysis,  the  latter  either  existing  alone  or  as  a  part  of  a  hemi- 
plegia. 

A  brawny,  hot  sivelUng  of  the  lip  may  be  a  small  abscess  or  a 
more  extensive  and  serious  carbuncular  inflammation.  The  lips  are 
swollen  as  a  part  of  the  disease  in  the  fortunately  rare  cancrum  oris, 
and  the  swelling  may  be  due  to  the  taking  of  corrosive  poisons,  in 
which  case  the  interior  of  the  mouth  will  also  be  swollen  and  red- 
dened. Bites  of  insects  may  explain  a  swelled  lip,  and  among  other 
causes  are  alveolar  abscess,  bitten  lip  in  epileptic  or  other  convul- 
sion, and  angeioneurotic  oedema. 

Foam  upoti  the  lips  is  a  common  symptom  during  an  epileptic 
seizure,  and  sometimes  in  the  later  stages  of  cerebral  apoplexy.  It 
should  be  borne  in  mind  that  a  bit  of  soap  in  the  mouth  is  employed 
by  malingerers  in  simulating  epileptic  convulsions. 

Miscellaneous  Affections  of  the  Lips. — Herpes. — Vesicles  upon  the 
lips  are  especially  common  in  malarial  fevers,  pneumonia,  and  acute 
coryza,  as  well  as  other  febrile  diseases. 

Fissures. — Cracks  or  fissures  (rhagades),  or  the  scars  resulting 
from  them,  if  occurring  in  infants  or  children,  must  be  regarded 
with  suspicion  as  suggestive  of  inherited  syphilis.  The  vertical 
crack  in  the  middle  of  the  lower  lip,  which  is  occasionally  seen,  is 
not  of  special  significance. 

Chancre. — A  single,  small  ulcer  upon  the  lip,  with  an  indurated 
base  and  accompanied  by  enlargement  of  the  submental  glands,  is 
likely,  if  in  a  young  person,  to  be  the  initial  lesion  of  syphilis. 

Mucous  PaM^s.— Flattened,  warty  outgrowths,  strictly  delimited, 
coated  with  a  gray  matter,  and  found  at  the  angles  of  the  mouth,  are 
the  mucous  patches  of  the  secondary  stage  of  syphilis. 

Epithelioma.— A.  somewhat  irregular  ulcer,  usually  upon  the  lower 
lip,  gradually  enlarging,  recurrently  scabbing  over  and  becoming 
denuded,  at  times  originating  from  a  wart,  is  probably  an  epithe- 
lioma, and,  if  of  some  standing,  the  glands  beneath  the  jaw  are 
enlarged.  The  occurrence  of  such  an  ulcer  in  a  middle-aged  or 
old  person,  its  progressive  increase  in  size  and  the  late  involve- 
ment of  the  glands,  will  differentiate  it  from  the  initial  lesion  of 
syphilis. 

11.  The  Buccal  Cavity.— The  Odour  of  the  Breath.— Varia- 
tions from  the  normal  in  this  respect  may  be  of  considerable  value 
in  diagnosis. 

In  hydrocyanic-acid  poisoning  the  breath  may  smell  of  peach 
kernels  or  bitter  almonds,  and  an  alliaceous  or  garlicky  odour  is 
present  in  phosphorus  poisoning,  provided  in  both  cases  that  too 
long  a  time  has  not   elapsed.     The  narcotic  odour  of  the  opium 


220  THE  EVIDENCES  OF  DISEASE 

preparations  may  explain  a  profound  stupor,  and  the  characteristic 
fumes  of  ether,  chloroform,  and  alcohol  are  sufficiently  familiar. 

Local  conditions  in  the  mouth  may  be  accountable  for  an  unpleas- 
ant or  foul  odour  of  the  breath,  as  in  those  to  whom  the  cult  of  the 
toothbrush  is  unknown.  If  sordes  have  collected  upon  the  teeth, 
the  breath  is  apt  to  be  stale  and  musty.  A  foul  odour  attends  in 
some  degree  all  forms  of  stomatitis  and  glossitis,  most  fetid  in  the 
mercurial  and  gangrenous  forms,  less  so  in  scurvy.  Caries  of  the 
teeth,  necrosis  of  the  jaw,  pharyngeal  or  tonsillar  diphtheria,  follicu- 
lar tonsilitis,  and  lacunar  concretions  are  local  conditions  which 
may  explain  the  existence  of  unpleasant  emanations. 

An  intensely  fetid  breath,  in  the  absence  of  other  sufficient  causes, 
may  be  due  to  gangrene  of  the  lung,  pulmonary  actinomycosis,  bron- 
chiectasis, and  pyothorax  or  pyopneumothorax  with  a  fistulous  open- 
ing into  a  bronchus. 

A  common  cause  of  bad  breath  is  some  form  of  gastritis,  espe- 
cially that  caused  by  chronic  alcoholism,  and  it  is  sometimes  due  to 
constipation.  In  children  with  gastric  disorders  it  is  often  merely  a 
sour  smell. 

A  hot,  "  feverish  "  breath  is  common  in  febrile  disorders,  and  the 
disagreeable  odour  is  most  noticeable  in  typhus  fever,  measles,  and 
scarlet  fever.  An  ammoniacal,  "  urinous  "  odour  is  not  uncommon 
in  the  more  severe  grades  of  uraemia.  A  heavy,  sweetish  odour,  like 
stale  beer  or  overripe  apples,  and  due  to  the  presence  of  acetone  or 
diacetic  acid,  is  perceived  in  bad  cases  of  diabetes  mellitns,  often 
preceding  or  accompanying  diabetic  coma.  Finally,  a  slight  cadav- 
eric smell  is  at  times  perceptible  in  the  breath  of  those  who  are  crit- 
ically ill. 

Puffing  Cheeks. — In  most  forms  of  coma  the  cheeks  are  lax  and 
puff  outward  with  each  expiration.  The  same  thing  is  seen  during 
sleep  in  toothless  elderly  persons.  Facial  paralysis,  alone  or  as  a 
part  of  a  hemiplegia,  is  the  usual  cause  of  outward  blowing  or  flap- 
ping of  one  cheek. 

PetecMsB :  Pigmented  Spots. — Small  extravasations  are  occasion- 
ally seen  upon  the  buccal  mucous  membrane  and,  when  present,  may 
be  caused  by  one  of  the  grave  anaemias,  haemophilia,  purpura  haemor- 
rhagica,  and  scurvy;  or  they  may  be  the  hemorrhagic  infarcts  of 
ulcerative  endocarditis. 

Brownish  or  yellowish  pigment  patches  on  the  buccal  and  palatal 
surfaces  and  the  inner  aspect  of  the  lips  are  significant  of  Addison's 
disease ;  and  the  mucous  membrane  may  exhibit  discoloured  pur- 
plish patches  in  those  saturated  with  silver  salts.  Oral  inflamma- 
tions in  the  coloured  races  may  be  followed  by  pigmentary  changes. 


THE  BUCCAL  CAVITY  221 

The  yellow  of  jaundice  and  the  bluish  tint  of  cyanosis  are  more  or 
less  obvious  in  the  oral  mucous  membrane. 

Exanthems,  Erythema,  Vesicles.— The  rash  of  measles  is  often 
seen  upon  the  pharjoigeal  and  palatal  surfaces  prior  to  its  appear- 
ance upon  the  skin,  and  Koplik  has  described,  as  absolutely  charac- 
teristic of  measles,  small  red  spots  with  a  minute  blue-white  centre 
upon  the  inner  surface  of  the  cheeks,  which  disappear  as  the  rash 
develops.  The  angry  redness  of  scarlet  fever  involving  the  entire 
oral  and  faucial  surfaces  is  very  striking.  A  slighter  redness  is  pres- 
ent in  simple  erythematous  stomatitis,  and  the  rare  occurrence  of  a 
salivary  calculus  with  the  accompanying  redness  should  be  remem- 
bered. Vesicles  when  present  may  be  the  beginning  of  an  aphthous 
stomatitis,  herpes,  or  the  eruption  of  varicella  or  smallpox. 

White  Spots,  Ulcers,  Sloughs. — Small  grayish  ulcers  with  red- 
dened margins,  which  have  begun  as  vesicles,  situated  upon  the 
inside  of  the  lips  and  cheeks  and  the  edges  of  the  tongue,  are  the 
lesions  of  aphthous  stomatitis,  the  common  "  canker  sores."  Small 
ulcers  on  the  hard  palate  in  infants  may  be  due  to  the  friction  of 
the  rubber  nipple  ;  or,  if  in  very  weak  newborn  infants,  situated  sym- 
metrically on  either  side  of  the  median  line  and  usually  increasing 
in  size,  constitute  a  form  of  oral  disease  reported  by  Parrot.  Ulcers 
on  the  buccal  mucous  membrane  are  also  seen  in  mercurial  stoma- 
titis and  the  sore  mouth  of  syphilis.  White,  curdlike  patches, 
beginning  on  the  tongue  and  spreading  to  the  inside  of  the  lips  and 
cheeks,  and,  if  detached,  leaving  a  normal  or  slightly  ulcerated 
surface,  form  the  disease  known  as  thrush  (parasitic  stomatitis). 
Deep  ulceration,  with  the  formation  of  sloughs,  may  be  caused  by 
corrosive  poisons,  gangrenous  stomatitis,  and  glanders.  A  case  of 
peliosis  rheumatica  is  reported  by  Hare,  in  which  sloughing  of  the 
chee~k  occurred. 

Dryness  of  the  Mouth. — The  secretion  of  saliva  may  be  checked 
by  various  causes.  That  drjmess  of  the  mouth  is  produced  by  fright 
or  excitement  is  a  fact  within  the  experience  of  most  individuals. 
So  also  with  the  dry  mouth  of  febrile  states.  One  of  the  unpleasant 
symptoms  of  mouth-breathing  is  the  stiff,  dry  tongue  of  the  morning 
awakening.  Persistent  dryness  of  the  mouth  is  often  significant  of 
diabetes  or  chronic  gastritis,  and  is  not  infrequently  present  in 
chronic  nephritis.  Finally,  a  dry  mouth  may  constitute  the  disease 
known  as  xerostomia  (Hutchinson). 

Salivation  and  Dribbling. — The  amount  of  saliva  which  is  secreted 
in  24  hours  is,  under  normal  circumstances,  from  2  to  3  pints.  Ptya- 
lism  or  hypersecretion  of  saliva,  in  which  this  amount  is  greatly 
exceeded,  may  occur  in  early  pregnancy  and  sometimes  attends  the 


222  THE   EVIDENCES  OF  DISEASE 

menstrual  period.  All  forms  of  stomatitis  may  cause  an  increase. 
The  pain  due  to  dental  causes,  alveolar  abscess,  or  trigeminal  neu- 
ralgia, and  the  process  of  dentition  itself,  will  induce  an  excessive 
formation  of  saliva.  It  occurs  infrequently  in  hysteria  and  other 
psychic  neuroses,  and  in  hydrophobia.  Ptyalism  is  sometimes  pres- 
ent in  the  early  stages  of  variola  and  typhus  fever,  and  has  occurred 
during  convalescence  from  typhoid  fever.  Thick  saliva  accumulates 
in  quinsy  and  mumps. 

Certain  chemical  substances  and  drugs  will  produce  an  increased 
flow  of  saliva — viz.,  acids,  aconite,  alkalies,  antimony,  cantharides ; 
copper,  gold,  iodine,  and  mercury  compounds;  muscarine,  pilocar- 
pine, and  tobacco.  Too  large  a  dose  of  mercury  or  an  unusual 
susceptibility  to  its  action  is  the  most  common  example  of  drug 
salivation  which  is  met  with  in  practice. 

Dribbling  of  saliva  may  occur,  although  the  amount  is  not  in- 
creased, because  of  inability  to  retain  it,  in  idiocy,  facial  paralysis, 
diphtheritic  paralysis,  and  chronic  bulbar  palsy. 

III.  The  Gums. — Colour. — The  pallor  of  the  gums  is  noticeable 
in  all  forms  of  anaemia.  A  greenish-blue  line  at  the  edges  of  the 
gums  is  significant  of  poisoning  by  copper.  A  blue  or  gray-blue  line, 
with  a  grayish  deposit  upon  the  teeth,  is  indicative  of  lead  poisoning, 
but  may  be  absent  if  the  teeth  are  well  kept.  A  blue  or  red  line  is 
seen  in  mercurial  stomatitis,  while  a  purple  coloration  occurs  in 
scurvy.  A  red  line  along  the  gingival  margins  in  young  adults  was 
formerly  supposed  to  indicate  the  imminence  of  tuberculosis,  and 
may  be  present  in  diabetes  and  the  cancerous  cachexia,  or  as  a  symp- 
tom of  a  chronic  affection  of  the  teeth  and  their  sockets  (pyorrhoea 
alveolaris).  Lack  of  cleanliness  is  not  an  uncommon  cause  of  mar- 
ginal redness. 

Red^  Spongy,  or  Ulcerated  Gums. — Carious  or  ill-kept  teeth,  with 
abundant  tartar,  may  produce  red  and  spongy  gums.  Gangrenous 
stomatitis  usually  involves  the  gums  to  a  very  marked  degree,  and 
the  less  severe  forms  of  oral  inflammation  will  cause  a  general  red- 
ness in  which  the  gums  will  share.  Spongy,  red,  and  bleeding,  per- 
haps ulcerated,  gums  occurring  in  artificially  fed  infants  may  be  due 
to  scurvy.  A  similar  condition  in  an  older  person  may  be  the  result 
of  an  idiosyncrasy  for  mercury  or  an  abuse  of  the  drug. 

Swollen  or  spongy  gums  are  also  met  with  in  some  cases  of  digest- 
ive disorders,  leucaemia,  phthisis  pulmonalis,  diabetes,  purpura,  and 
phosphorus  poisoning.  Ulceration  along  the  line  of  the  gums,  rarely 
extending  to  the  cheeks  or  tongue,  is  particularly  characteristic  of 
ulcerative  stomatitis.  Finally,  localized  or  general  redness  and  swell- 
ing may  attend  the  eruption  of  the  teeth. 


DENTITION 


223 


IV.  The  Teeth. — Dentition. — The  temporary  or  deciduous  teeth 
appear  with  greater  regularity  as  to  order  than  as  to  time.  The 
average  order  and  times  of  eruption  are  as  follows  (Holt)  : 

(1)  Two  lower  central  incisors 6  to    9  months. 

(2)  Four  upper  incisors 8  to  12       " 

(3)  Two  lower  lateral  incisors  and  4  an- 

terior molars ....   12  to  15       " 

(4)  Four  canines 18  to  24      " 

(5)  Four  posterior  molars 24  to  30      " 

At  1  year  a  child  should  have 6  teeth. 

At  li  years  a  child  should  have 12     " 

At  2  years  a  child  should  have 16     " 

At  2^  years  a  child  should  have 20     " 

The  permanent  set  arrive  as  follows  : 

First  molars 6  years. 

Incisors 7  to    8  years. 

Bicuspids 9  to  10      " 

Canines 12  to  14      " 

Second  molars 12  to  15      " 

Third  molars 17  to  25      " 

Early  Dentitio7i. — Eruption  of  the  teeth  in  advance  of  the  usual 
dates  is  not  of  special  significance.  It  has  been  noted  in  children 
who  are  the  subjects  of  hereditary  syphilis,  and  also  as  part  and  par- 
cel of  the  precocity  exhibited  by  infants  with  a  transmitted  predispo- 
sition to  tuberculosis. 

Delayed  Dentition. — The  most  common  cause  of  delay  in  teething 
is  rachitis,  together  with  other  conditions  or  diseases  involving  mal- 
nutrition, particularly  if  occurring  in  the  first  5  or  6  months  of  the 
infant's  life,  so  that  the  delay,  if  observed,  is  more  significant  of  the 
past  than  the  present  status.  A  late  appearance  of  the  teeth  may  be 
indicative  of  cretinism.  A  case  of  mine  had  but  4  teeth  at  2  years 
•of  age. 

Difficult  Dentition. — There  has  been,  and  is,  much  difference  of 
opinion  in  regard  to  the  influence  of  teething  in  causing  disease. 
The  physician  is  too  apt  to  coincide  with  the  views  of  the  mother  or 
nurse  in  this  respect.  The  safe  rule  is  to  exhaust  every  other  possi- 
bility before  concluding  that  the  symptoms  which  may  be  present 
are  caused  solely  by  dental  irritation.  The  departures  from  the  nor- 
mal in  otherwise  robust  children  which  may  safely  be  considered  as 
direct  results  of  the  irritation  due  to  erupting  teeth  are  :  loss  of  appe- 
tite, disturbed  sleep,  fretfulness,  slight  fever  (100°  to   101°),  and 


224 


THE  EVIDENCES  OF  DISEASE 


either  constipation  or  a  slight  diarrhoea.  In  feeble  or  poorly  nour- 
ished infants  the  attacks  may  be  more  severe,  amounting  to  an  acute 
indigestion  with  high  fever,  the  temperature  remaining  elevated  for 
2  or  3  days.  All  other  possible  causes — e.  g.,  improper  food,  expo- 
sure, fatigue,  tonsilitis — must  be  carefully  excluded,  and  on  inspec- 
tion the  gums  over  the  advancing  teeth  should  be  red,  swollen,  and 
tender,  ordinarily  with  some  salivation. 

Shape  and  Structure  of  the  Teeth. — Notched. — If  the  permanent 
upper  central  incisors  are  somewhat  rounded  and  peglike,  tapering 

from  gum  to  edge,  with  a  single 
shallow  and  discoloured  notch 
in  the  edge,  it  is  good  but  not 
infallible  evidence  of  inherited 
syphilis.  These  teeth  are  apt 
to  be  small,  placed  somewhat 
irregularly,  and  stand  apart  from 
one  another  (Fig.  37).  If  kera- 
titis and  middle-ear  disease  co- 
exist, a  positive  diagnosis  of 
syphilis  may  be  made. 

Dentated    or    Furrotoed. — If 

_j„^  ^   »^  .  va#^      >*•  ^^®  edges  of  the  teeth  are  den- 

'■HE  .''ii^iaBBBll^P  ■    tated,  malnutrition  or  struma  is 

^^^^'  ■•  /!f/MLM^y^-^.  likely  to  be  the  cause.     Grooves 

or  furrows  running  transversely 
across  the  teeth  are  indicative 
of  an  acute  illness  during  in- 
fancy or  childhood  sufficiently 
severe  to  interfere  with  their 
nutrition.  Pitted  teeth,  the 
molars  exhibiting  the  greatest  changes,  are  caused  by  the  various 
forms  of  stomatitis. 

Loosened  and  Decayed  Teeth.— Loosening  of  the  teeth  in  their 
sockets  is  associated  with  spongy,  ulcerated,  or  bleeding  gums  (</.  v.). 
Movability  of  the  teeth  is  therefore  usually  due  either  to  mercurial 
stomatitis,  pyorrhoea  alveolaris,  scurvy,  purpura  haemorrhagica,  phos- 
phorus poisoning,  or  gangrenous  stomatitis. 

Early,  extensive  or  rapid  dental  caries  is  most  commonly  due  to 
rachitis,  but  occurs  also  in  pregnancy,  diabetes,  and  chronic  phos- 
phorus poisoning.  The  influence  of  carious  teeth  in  causing  bad 
breath  and  dyspepsia  from  imperfect  mastication,  and  adenitis  by 
furnishing  a  source  of  irritation  or  infection,  should  not  be  over- 
looked. 


Fig.  37.— SyphiliLlc  ■■icruw-driver  teeth;" 
boy  nine  years  old  (Holt). 


TEETH— TONGUE  225 

Sordes. — A  collection  of  foul  material  upon  the  teeth  (sordes), 
sometimes  stained  with  blood  oozing  from  the  gums,  is  seen  in  con- 
ditions of  prostration,  particularly  febrile  diseases  in  which  the 
typhoid  status  is  marked. 

Grinding  of  the  Teeth.— Gritting  or  grinding  of  the  teeth  in  chil- 
dren during  sleep  is  popularly  supposed  to  indicate  "  worms,"  but 
is  usually  due  to  some  gastro-intestinal  disorder.  It  also  occurs  in 
neurotic  children  who  sleep  uneasily,  and  has  been  noted  in  certain 
maladies  of  the  nervous  system,  as  meningitis,  intracranial  tumours, 
hydrocephalus,  anterior  poliomyelitis,  epilepsy,  and  chorea. 

Defective  Mobility  of  the  Jaw. — Inability  to  open  or  close  the 
mouth  may  be  due  to  spasm  or  paralysis  of  the  muscles  of  mastica- 
tion. The  masseter,  temporal,  and  other  muscles  concerned  in  the 
act  of  chewing  are  innervated  by  motor  fibres  from  the  fifth  nerve 
(trigeminus),  and  spasm  smd paralysis  of  these  muscles  indicate  some 
interference,  organic  or  functional,  with  the  action  of  this  nerve. 

Spasm. — Trismus  or  lockjaw,  a  tonic  spasm  of  the  masseter  and 
temporal  muscles  whereby  the  jaws  are  held  firmly  together,  may 
occur  as  a  symptom  of  trismus  neonatorum,  tetanus,  strychnine 
poisoning,  hysteria,  epilepsy,  or  disease  of  the  brain,  and  is  some- 
times a  reflex  from  dentition,  gastro-intestinal  ailments,  and  intes- 
tinal parasites. 

Paralysis. — In  this  case  the  masseter  and  temporal  do  not  con- 
tract, and  there  is  inability  to  masticate  on  the  affected  side.  Paral- 
ysis of  these  muscles  may  indicate  hemorrhage  into  the  pons,  basal 
lesions  (meningitis,  tumour,  caries)  or  neuritis. 

Pain  and  sivelling  from  disease  of  the  maxillae,  mumps,  quinsy, 
and  trichiniasis  may  prevent  the  opening  of  the  mouth  and  interfere 
with  mastication. 

V.  The  Tongue. — An  inspection  of  the  tongue  is  a  part  of  the 
clinical  examination  which  is  seldom  neglected  by  the  physician.  In 
general,  the  tongue  should  be  investigated  with  reference  to  its  col- 
our, size,  coating,  dryness,  lesions  and  mobility.  Occasionally  the 
condition  of  the  sense  of  taste  requires  examination. 

Colour  and  Pigmentation  of  the  Tongue. — The  colour  of  the  tongue 
(including  coloured  areas  or  patches),  as  distinguished  from  the  colour 
of  its  coating,  is  of  some  diagnostic  value.  It  is  pallid  in  anaemia 
and  bluish  in  cyanosis.  A  bright-red  tongue  may  be  due  to  the 
exanthemata,  particularly  in  the  early  stage  of  scarlet  fever ;  or  to 
inflammation  of  the  tongue  itself  (glossitis),  differing  from  the  darker, 
raw-beef  tongue  of  the  adynamic  states.  Petechiae,  ecchymoses,  and 
infarcts  may  be  found  on  the  tongue,  and  have  the  same  significance 
as  if  found  elsewhere.     Dark  purple  or  blackish  deposits  of  pigment 


226 


THE  EVIDENCES  OF  DISEASE 


may  indicate  an  old  glossitis,  or  constitute  the  discolorations  of 
Addison's  disease.  A  black  tongue,  as  if  stained  with  iron,  if  not 
traced  to  the  taking  of  foreign  substances,  is  an  example  of  the  dis- 
ease termed  nigrities.  The  tongue  is  yellowish  in  jaundice,  and  the 
yellowness  is  particularly  marked  on  the  under  surface  of  its  tip.  A 
series  of  clearly  outlined  yellowish-white  spots  along  the  edges  of  the 
tongue  constitutes  xanthelasma. 

More  or  less  uniform  discolorations  of  the  tongue  and  its  coating 
may  be  caused  by  the  ingestion  of  various  substances,  corrosive  or 
non-corrosive.  Among  the  corrosive  substances,  ammonia,  corrosive 
sublimate,  sulphuric,  carbolic,  and  oxalic  acids  whiten  the  tongue ; 
hydrochloric,  nitric,  and  chromic  acids  produce  a  yellow  colour ;  acid 
nitrate  of  mercury,  caustic  potash,  and  caustic  soda  redden  it.  Evi- 
dence of  destructive  action  is  usually  present.  With  reference  to 
non-corrosive  drugs  or  foods,  the  tongue  is  stained  black  by  bismuth, 
charcoal,  and  iron ;  red  or  purple  by  red  fruits  or  wine ;  yellow  or 
brown  by  rhubarb,  tincture  of  opium,  tobacco,  licorice,  or  chocolate. 
Size  of  the  Tongue. — 1.  Enlargement. — Great  enlargement  of  the 

tongue  is  easily  determined. 
A  slight  increase  in  size  can  be 
assumed  to  be  present  if  the 
edges  of  the  tongue  are  in- 
dented by  the  teeth,  the  in- 
dentations existing  only  if  the 
tongue  is  swollen  beyond  its 
normal  limits. 

A  great  enlargement  of  the 
tongue  is  met  with  in  acro- 
megaly and  myxoedema.  If 
associated  with  inflammatory 
symptoms  it  is  an  acute  glos- 
sitis, due  usually  to  irritant 
poison  or  sepsis.  The  inflam- 
mation and  swelling  may  be 
unilateral  (hemiglossitis),  and 
in  this  case  a  neurotic  origin 
has  been  alleged.  Variola,  foot 
and  mouth  disease  (aphthous 
fever),  salivary  calculus,  in- 
flamed ranula,  and  actinomy- 
cotic, erysipelatous,  or  other 
inflammation  of  the  tongue  and  floor  of  the  mouth  (angina  Ludovici) 
are  additional  causes  of  a  greatly  enlarged  or  swollen  tongue.     Tu- 


Fio.  38.— Unilateral  atrophy  of  the  tongue. 


THE  TONGUE 


227 


Hypoglossal 


Glosso-pharyngeal 


Trigeminus 


mours  of  the  tongue  are  also  responsible  for  an  irregular  and  some- 
times great  increase  in  its  size.  A  slow-growing,  painless  nodule  in 
the  tongue  may  be  a  gummatous  deposit.  A  moderate  increase  in 
the  size  of  the  tongue,  as  indicated  by  the  imprint  of  the  teeth  upon 
its  edges,  is  seen  as  a 

symptom    in    anaemia,  motor  sensory 

chronic  gastric  catarrh, 
stomatitis,  scurvy,  and 
typhus  fever.  If  cya- 
nosis from  venous  ob- 
struction is  present, 
the  tongue  will  be 
swollen  and  somewhat 
edematous. 

2.  Shrinking  or  At- 
rophy of  Tongue. — The 
tongue  is  small  after  a 
profuse  hemorrhage, 
and  may  become  no- 
ticeably lessened  in 
size  in  the  later  stages 
of  typhoid  fever. 

In  atrophy  of  the 
tongue,  the  organ  has 
a  shrunken  appear- 
ance, and  its  mucous  membrane  is  thrown  into  folds.  It  is  due 
to  some  affection  of  the  hypoglossal  or  motor  nerve  of  the  tongue 
involving  its  nucleus  or  its  peripheral  portion.  It  is  always  con- 
joined with  paralysis,  and  the  paralysis  and  atrophy  affect  one 
or  both  lateral  halves  of  the  tongue  according  as  the  lesion  is  uni- 
lateral or  bilateral.  Unilateral  atrophy  of  the  tongue  (Fig.  38)  is 
sometimes  associated  with  facial  hemiatrophy.  If  the  cortical  con- 
nections of  the  nucleus  are  involved  there  will  be  paralysis  but  no 
atrophy,  or  if  the  latter  be  present  it  is  slight.  A  contracted  condi- 
tion of  the  tongue,  due  to  the  absorption,  under  treatment,  of  a  lin- 
gual gumma,  may  be  mistaken  for  paralytic  atrophy  unless  the  possi- 
bility of  such  an  error  is  remembered. 

Spasm,  Tremor,  and  Paralysis  of  the  Tongue.— The  motor  supply 
of  the  muscles  of  the  tongue  is  for  the  most  part  derived  from  the 
hypoglossal  nerve  (Fig.  39).  The  same  nerve  also  supplies  the 
muscles  which  fix  and  depress  the  hyoid  bone  in  chewing  and  swallow- 
ing. Two  muscles  are  not  supplied  by  the  hypoglossal — namely,  the 
lingualis  inferior,  which  is  innervated  by  the  chorda  tympani  branch 


Fig.  39.- 


Diagram  showing  the  motor  and  sensoTy  supply 
of  the  tongue. 


228  THE  EVIDENCES   OF   DISEASE 

of  the  seventh  (facial)  nerve,  and  the  palato-glossus  by  motor  fibres 
from  the  fifth  nerve. 

Spasm  of  the  Tongue. — Spasm  of  the  tongue  is  a  rare  symptom. 
It  may  be  tonic,  in  which  case  the  tongue  is  contracted  and  rigid ; 
or  clonic,  the  tongue  jerking  and  twitching  irregularly,  or  being  pro- 
truded and  retracted  very  rapidly,  40  or  50  times  a  minute  (Osier). 
The  movements  usually  involve  both  halves  of  the  tongue,  but  may 
be  unilateral.  Clonic  spasm  of  the  tongue  is  usually  a  part  or  symp- 
tom of  chorea,  hysteria,  and  the  epileptic  convulsion,  or  is  associated 
with  mimic  tic.  Stuttering  is  a  spasmodic  affection  of  the  lingual 
muscles.  A  curious  disorder,  of  which  a  few  instances  have  been 
reported  in  those  who  use  the  voice  incessantly  in  public,  is  a  spasm 
of  the  tongue  on  attempting  to  speak,  a  condition  analogous  to 
writer's  cramp.  Lingual  clonic  spasm  is  an  occasional  symptom  in 
disseminated  sclerosis,  general  paralysis,  and  melancholia.  In  rare 
cases  irregular  spasmodic  movements  of  the  tongue  are  due  to 
hypoglossal  irritation  without  discoverable  cause.  Eefiex  irrita- 
tion of  the  fifth  nerve  has  been  held  responsible  for  lingual  spasm, 
and,  in  some  instances,  disease  of  the  central  nervous  system  pro- 
duces it. 

Tonic  spasm  of  the  tongue  is  indicative  of  hysteria  or  reflex  irri- 
tation through  the  fifth  nerve,  occurring  in  nervously  weak  and  de- 
bilitated persons.  It  may  coexist  with  tonic  spasm  of  other  voluntary 
muscles  in  Thomsen's  disease  (myotonia  congenita). 

Tremor  of  the  Tongue. — A  coarse  tremor  or  trembling  of  the 
tongue  is  most  frequently  symptomatic  of  chronic  alcoholism,  and  is 
seen  as  well  in  delirium  tremens.  It  is  usually  present  in  the  typhoid 
state  when  the  tongue  is  protruded,  and  occurs  also  in  bromism.  It 
may  exist  as  a  part  of  paralysis  agitans.  A  fibrillary  tremor  or  fine 
twitching  of  the  muscular  bundles  of  the  tongue  may  be  seen  in  dis- 
seminated sclerosis,  general  paralysis,  and  in  bulbar  paralysis  when 
the  lingual  muscles  begin  to  atrophy.  Finally,  the  tongue  trembles 
in  neurotic  persons,  particularly  if  excited  or  agitated. 

Paralysis  of  the  Tongue. — If  one  side  of  the  root  of  the  tongue 
as  it  lies  in  the  mouth  is  higher  than  the  other,  and  if  when  protruded 
it  deviates  toward  the  same  side,  unilateral  lingual  paralysis  exists. 
There  is  apt  to  be  some  interference  with  the  speech,  and  a  slight 
difficulty  in  chewing  and  swallowing.  If  the  tongue  lies  motionless 
in  the  floor  of  the  mouth,  the  patient  being  unable  to  protrude  it, 
and  the  functions  of  speech,  mastication  and  deglutition  are  greatly 
impaired,  there  is  total  lingual  paralysis.  In  both  cases  there  may  or 
may  not  be  atrophy  and  fibrillary  twitching.  If  atrophy  does  not 
take  place  it  indicates  a  cortical  or  supranuclear  lesion ;  but  if  one 


THE  TONGUE  229 

or  both  sides  of  the  tongue  are  shrivelled,  the  lesion  is  nuclear  or 
infranuclear. 

Bilateral  paralysis  without  atrophy,  a  rare  finding,  is  due  to 
pseudo-bulbar  paralysis,  a  condition  associated  with  symmetrical 
lesions  (softening)  of  both  cortical  centres  of  the  tongue.  Bilateral 
paralysis  with  atrophy  is  usually  a  symptom  of  true  bulbar  paralysis, 
and  occasionally  of  progressive  muscular  atrophy.  Unilateral  paraly- 
sis without  atrophy  is,  in  the  majority  of  cases,  a  part  of  a  hemiplegia. 
If  the  fibres  of  the  nerve  are  involved  in  their  course  through  the 
medulla  after  leaving  their  nucleus,  the  lingual  paralysis  will  be  on 
the  side  opposite  to  the  hemiplegia,  and  the  tongue,  when  protruded, 
deviates  toward  the  sound  side. 

Lingual  paralysis,  with  atrophy  either  of  one  or  both  sides  of  the 
tongue  according  to  the  situation  or  extent  of  the  lesion,  may  also 
exist  as  a  symptom  of  general  paralysis,  chronic  lead  poisoning,  loco- 
motor ataxia  (rarely),  embolism  or  thrombosis  of  the  vascular  supply 
of  the  nuclei,  basal  meningitis,  tumour  of  the  base,  syphilitic  or 
other  disease  of  the  bone  containing  the  anterior  condyloid  fora- 
men or  of  the  first  cervical  vertebra,  tumours  of  the  upper  portion  of 
the  cord,  and  wounds  of  the  neck.  A  hospital  tramp  in  my  service 
simulated  total  glossoplegia  very  accurately  for  the  sake  of  a  night's 
lodging. 

Scars,  Fissures,  and  Ulcers  of  the  Tongue. — Scars  upon  the  tongue 
may  be  the  result  of  healed  ulcers,  epilepsy,  bulbar  palsy,  accidental 
biting  of  the  tongue  during  restless  sleep,  careless  chewing,  or  a  fall 
while  the  tongue  is  between  the  teeth.  Before  deciding  as  to  the 
cause  a  careful  inquiry  for  a  history  of  syphilis  should  be  made,  as 
they  may  be  the  result  of  healed  specific  lesions. 

Fissures  of  the  tongue  are  not  infrequently  of  normal  occurrence, 
especially  in  elderly  people.  At  other  times  they  are  significant  of 
the  habitual  use  of  irritating  food  or  drink  which  has  caused  a 
chronic  glossitis.  The  median  longitudinal  fissure  is  generally  the 
deepest.  Very  deep  inflamed  fissures  may  be  due  to  dissecting  glos- 
sitis, which  in  some  instances  is  syphilitic.  Fissures  or  losses  of 
substance  at  the  edges  of  the  tongue  are  usually  of  syphilitic  origin, 
but  may  be  due  alone  to  the  irritation  of  a  rough  or  broken  tooth. 
Fissures  are  also  met  with  as  the  result  of  erysipelatous  inflamma- 
tion, chronic  hepatic  disease,  chronic  dysentery,  and  diabetes 
mellitus. 

Ulcers  of  the  tongue  are  usually  due  to  aphthous  stomatitis,  less 
frequently  to  the  ulcerative  form.  They  are  acute  and  painful. 
Very  shallow,  red,  and  glazed  ulcerated  surfaces  occur  in  chronic 
superficial  glossitis.     Multiple  ulcers,  gray,  indolent,  stellate,  with 


230  THE  EVIDENCES  OF  DISEASE 

enlarged  cervical  glands,  may  be  tuberculous,  and  are  almost  always 
secondary  to  tuberculous  disease  elsewhere.  Somewhat  similar  mul- 
tiple ulcers  may  be  syphilitic,  but  then  the  glands  are  rarely  enlarged. 
Multiple  small  ulcers,  preceded  by  vesicles,  may  be  found  in  small- 
pox, varicella,  measles,  and  erysipelas,  as  well  as  in  pemphigus,  her- 
pes, and  eczema  of  the  tongue. 

A  single  ulcer  with  a  hard  base  and  enlarged  cervical  glands  may 
be  either  the  initial  lesion  of  syphilis  or  an  epithelioma.  In  the 
former  case  the  age  of  the  patient  is  usually  under  forty,  the  lesion 
is  on  the  tip  of  the  tongue,  it  is  not  very  painful  and  improves  under 
treatment.  A  mucous  patch  may  become  ulcerated,  and  a  gumma 
may  break  down,  forming  a  deep  sore.  A  single  ulcer,  if  opposite 
a  rough  or  jagged  tooth,  may  be  simply  the  result  of  continued 
traumatism,  but  the  presence  of  an  irritating  tooth  does  not  ex- 
clude syphilis.  An  ulcer  on  the  frenum  linguae  may  occur  dur- 
ing the  course  of  pertussis  from  the  thrusting  of  the  under  surface 
of  the  tongue  against  the  lower  incisors  during  the  paroxysms  of 
cough. 

Miscellaneous  Symptoms  and  Affections  of  the  Tongue. — Eczema  of 
the  tongue  gives  rise  to  a  condition  variously  known  as  geographical 
tongue,  annulus  migrans,  or  wandering  rash.  Eing-shaped  patches, 
red  and  denuded  of  epithelium,  are  seen  on  the  tongue,  and  under 
observation  are  found  to  spread  at  the  edge  while  healing  at  the 
centre,  coalescing  and  forming  irregular  areas  with  curved  outlines. 

The  smoker^s  patch  is  a  red,  yellowish  or  pearly  and  slightly  ele- 
vated plaque,  smooth  and  not  ulcerated,  usually  situated  upon  the 
dorsum  of  the  tongue  near  its  tip. 

Leucoplakia  buccalis  {ichthyosis,  leucoma,  leucokeratosis,  buccal 
psoriasis)  consists  of  slightly  elevated,  thickened  patches  of  irregular 
shape,  not  ulcerated,  white,  smooth,  and  hard  upon  palpation.  They 
may  furnish  the  starting  point  of  an  epithelioma. 

General  Diagnostic  Appearances  of  the  Tongue. — These  relate  to 
the  character  of  the  fur  or  coating  which  may  be  present,  or  its  dis- 
appearance ;  to  the  colour  of  the  tongue,  and  particularly  to  its  degree 
of  moisture.  The  coating  consists  of  accumulated  epithelium,  micro- 
organisms, and  food  detritus.  Dryness  of  the  tongue,  when  not 
caused  by  mouth  breathing  or  coma,  is  of  very  considerable  impor- 
tance as  an  indication  of  general  adynamia  and  prostration.  The 
following  states  of  the  tongue  are  of  value  in  diagnosis  and 
prognosis  : 

(1)  A  thin,  white,  even  furring  of  the  tongue  is  normal  in  many 
healthy  individuals,  particularly  those  who  are  in  the  habit  of  smok- 
ing, and  in  mouth  breathers.    It  may  be  indicative  of  nasopharyngeal 


THE  TONGUE  231 

catarrh  or  mild  gastric  disorders.     Such  a  coating  is  always  found 
in  moderately  febrile  states. 

(2)  A  flabby,  swollen,  indented  tongue,  covered  with  a  uniform 
yellow,  pasty  fur,  is  indicative  of  catarrhal  gastritis  or  gastro-duo- 
denitis,  usually  of  some  standing.  Heavy  smokers  and  drinkers  show 
a  similar  fur  on  rising  in  the  morning,  and  it  is  also  produced  by  the 
continuation  of  a  moderate  fever. 

(3)  A  narrow  tongue,  with  a  deep  median  fissure,  on  each  side  of 
which  is  a  thick,  rough  fur,  the  tip  and  edges  of  the  tongue  being 
red  and  denuded,  is  characteristic  of  the  typhoid  status,  whether 
arising  from  typhoid  fever  or  not,  although  it  occurs  particularly 
in  the  latter  disease. 

(4)  If  the  tongue  just  described  becomes  dry,  brown,  and  fissured, 
is  tremulously  and  slowly  protruded  and  the  patient  must  be  told  to 
retract  it,  the  typhoid  status  is  well  marked  and  ominous  of  evil.  So 
also  is  it  if  the  coating  desquamates  and — 

(5)  The  tongue  becomes  dry,  red,  and  glazed,  the  so-called 
"  beefy "  tongue.  A  change  from  either  of  these  conditions  to 
cleanliness  and  moisture  is  a  favourable  omen. 

(6)  A  broad,  flabby,  gray  tongue,  with  reddened,  irregular  spots, 
resembling  in  shape  the  lesions  upon  a  worm-eaten  leaf,  and  occurring 
in  a  child,  is  indicative  of  a  peculiar  form  of  gastro-intestinal  catarrh 
(mucous  disease  of  children). 

(7)  If  the  tongue  is  covered  with  a  white  fur  through  which  pro- 
ject greatly  swollen  and  bright-red  fungiform  papillae,  it  is  the  so- 
called  "  strawberry  tongue,"  seen  most  frequently  in  the  early  stage 
of  scarlet  fever,  but  not  pathognomonic  of  this  disease,  as  it  may  be 
present  in  other  acute  specific  infections.  Some  writers  bestow  this 
term  upon  a  tongue  which  has  lost  its  coating  and  shows  a  uniformly 
red  surface  with  projecting  papillae  (raspberry  tongue),  but  the  fore- 
going description  conforms  more  nearly  to  the  fancied  likeness. 

(8)  A  white,  creamy  fur  is  often  seen  upon  the  tongue  of  patients 
who  are  upon  an  exclusive  milk  diet.  Chalk  rubbed  upon  the  tongue 
is  said  to  have  been  employed  by  malingerers  for  the  purpose  of  simu- 
lating gastric  disease. 

(9)  Unilateral  furring  of  the  tongue  may  result  from  neuralgia  of 
the  second  and  third  divisions  of  the  trigeminus  and  from  fracture 
involving  the  foramen  rotundum,  through  which  the  second  division 
passes.  It  is  also  noted  with  unilateral  lingual  paralysis  (e.g.,  in 
hemiplegia),  which  interferes  with  the  frictional  cleansing  of  the 
organ. 

(10)  Small  and  limited  furrings  of  the  tongue  may  indicate  local 
irritation  from  a  rough  tooth  or  an  inflammation,  as  of  one  tonsil. 


232 


THE  EVIDENCES  OF  DISEASE 


(11)  A  grayish  coating  of  the  tongue  in  adults  or  a  white  coating 
in  children  may  be  due  respectively  to  an  unusually  extensive  growth 
of  leptothrix  or  thrush. 

Taste. — The  4  primary  taste  sensations  are  bitter,  sweet,  acid,  and 
salt.  There  is  some  disagreement  among  physiologists  as  to  the 
nerves  concerned  in  the  conduction  of  gustatory  sensations,  due  to 
the  fact  that  there  are  considerable  variations  in  the  course  of  the 
taste  fibres.  It  may  be  said  that  usually  these  fibres  run  both  in  the 
glosso-pharyngeal  and  trigeminus,  the  former  supplying  the  posterior 
third  of  the  tongue,  the  latter  the  anterior  two  thirds  (Fig.  39).  Never- 
theless, complete  loss  of  taste  has  resulted  from  trigeminal  disease 
alone,  more  rarely  from  lesions  affecting  only  the  glosso-pharyngeal 
nerve,  so  it  must  be  admitted  that  the  gustatory  fibres  may  at  times 
be  present  solely  in  one  or  the  other.  Some  of  the  taste  fibres  may 
pass  by  way  of  the  chorda  tympani,  as  a  partial  loss  of  taste  may  be 
present  in  facial  paralysis. 

The  sense  of  taste  is  tested  by  directing  that  the  tongue  be  protruded  and 
kept  so  while  drops  of  various  solutions  are  placed  upon  the  anterior  and 
posterior  surfaces  of  the  dorsum  upon  each  side  of  the  median  line.  For 
bitter,  a  solution  of  quinine  is  employed;  for  sweet,  sugar;  for  salt,  sodium 
chloride;  for  acid,  vinegar.  Ordinarily  a  solution  of  sugar  is  sufficient  to 
detect  any  impairment  of  taste.  The  metallic  taste  caused  by  the  passage  of  a 
weak  galvanic  current  through  the  tongue  may  be  utilized  as  a  convenient  test. 

The  disorders  of  the  gustatory  sense  are  ageusia  (loss  or  impair- 
ment of  the  sense  of  taste)  and  parageusia  (perversion  of  the  sense 
of  taste). 

Ageusia. — If  the  taste  sense  is  impaired  or  absent  it  may  be  due 
to  local  unhealthy  conditions  of  the  mucous  membrane  of  the  tongue 
involving  the  taste  buds  or  end  organs  of  the  gustatory  fibres,  as  in  a 
furred  or  coated  tongue,  or  a  tongue  which  has  been  exposed  to  the 
action  of  irritating  condiments.  If  the  tongue  is  dry  the  taste  is 
much  lessened  or  abolished.  As  the  sense  of  smell  plays  a  consider- 
able part  in  the  production  of  the  sensations  ordinarily  referred  to 
the  sense  of  taste,  a  loss  of  the  latter  may  be  complained  of  in  the 
various  diseases  of  the  nose  (coryza,  polypus,  etc.)  which  cause 
anosmia  {q.  v.).  In  all  these  cases  the  ageusia  is  bilateral  and 
general. 

Aside  from  local  conditions  of  the  mouth  and  nose,  a  loss  of  the 
taste  sense,  especially  if  unilateral  and  localized,  is  indicative  of  dis- 
ease of  the  glosso-pharyngeal  nerve  (posterior  third  of  the  tongue) ; 
or,  as  is  more  commonly  the  case,  of  trigeminal  disease  (anterior  two 
thirds  of  the  tongue).     Slight  unilateral  impairment  of  the  sense  of 


SENSE  OP  TASTE— PHARYNX  233 

taste  (hemiageusia)  is  usually  due  to  facial  paralysis.  Large  doses  of 
the  bromides  blunt  the  sense  of  taste. 

The  lesions  affecting  the  taste  may  be  basal  meningitis,  tumours, 
and  injuries.  Ageusia  may  be  one  of  the  manifold  symptoms  of 
hysteria,  which,  with  facial  paralysis,  is  the  commonest  cause  of  a 
partial  loss  of  the  taste  sense.  In  every  case  associated  symptoms 
must  determine  the  diagnosis. 

Parageusia. — Purely  subjective  perversions  of  the  sense  of  taste 
are  usually  indicative  of  hysteria,  but  may  be  hallucinations  of  the 
insane  or  constitute  the  aura  of  epilepsy. 

Various  "  bad  tastes  "  are  frequently  a  source  of  complaint.  In 
gastro-duodenal  catarrh  (biliousness)  a  coppery  taste  is  often  men- 
tioned, and  in  jaundice  the  mouth  is  bitter.  When  the  tongue  is 
furred  or  coated  from  any  cause  the  taste  is  diversely  described  as 
bad,  foul,  sweetish,  or  sour.  The  administration  of  certain  drugs, 
such  as  potassium  bromide  and  iodide  or  tartar  emetic,  may  give  rise 
to  abnormal  taste  sensations. 


SECTION   XIX 

THE  PAMTE,  TONSILS,  AKD   PHARYNX 

TECHNIC  OF  EXAMINATION 

To  examine  the  pharynx,  a  tongue  depressor  is  usually  required. 
For  house  visits,  especially  in  cases  of  contagious  diseases,  a  spoon 
with  a  broad,  smooth  handle  is  preferable  because  of  the  danger  of 
conveying  infection  by  the  use  of  a  portable  depressor.  Light  from 
a  window,  lamp,  candle,  bicycle  lamp,  or  match  may  be  utilized.  For 
ofl&ce  work,  the  head  mirror  and  Argand  or  Welsbach  burner,  or  elec- 
tric light,  with  a  suitable  condenser,  will  be  used,  so  also  a  right- 
angled  tongue  depressor,  the  width  of  which  should  be  at  least 
one  inch. 

To  use  the  tongue  depressor,  desire  the  patient  to  open  his  mouth, 
but  not  to  protrude  the  tongue  over  the  lower  teeth.  Ask  him  to 
sound  ah  (a  as  in  father),  thus  lowering  the  posterior  half  of  the 
tongue.  Then  carry  the  blade  of  the  depressor  in  until  it  passes  well 
(but  not  too  far)  over  the  highest  part  of  the  dorsum  of  the  tongue. 
By  pressing  down  and  at  the  same  time  pulling  somewhat  forward 
with  the  instrument,  the  tonsils  and  pharynx  may  be  fully  exposed. 

Note  first  the  general  colour  of  the  fauces  and  throat  as  a  whole. 
Observe  the  shape  of  the  hard  palate  and  the  existence  of  a  perfora- 


234  THE  EVIDENCES  OF  DISEASE 

tion  of  the  soft  palate,  swelling  of  the  uvula,  vesicles  or  ulcers,  and 
perhaps  test  for  paralysis  or  ansesthesia  of  the  palate. 

Note  enlargement  of  the  tonsils  (acute  or  chronic),  the  presence 
of  exudate,  evidences  of  suppuration,  ulcers  (tuberculous,  syphilitic, 
cancerous),  and  use  a  probe  to  determine  the  consistence  and  adher- 
ence of  exudate  or  follicular  plugs  if  present. 

With  reference  to  the  pharynx,  note  enlarged  follicles,  veins,  pul- 
sation, exudate,  ulcers,  bulging  of  the  posterior  wall  (retropharyn- 
geal abscess),  and,  if  required,  anaesthesia  of  the  mucosa  and  spasm 
or  paralysis  of  the  pharyngeal  muscles. 

An  abnormal  general  redness  of  or  discrete  eruptions  upon  the 
palate,  fauces,  and  pharynx  may  be  due  to  simple  inflammations  of 
the  mucous  membrane,  measles,  scarlatina,  rotheln,  roseola,  epidemic 
influenza,  erysipelas,  chronic  gastritis,  irritant  poisons,  iodism,  and 
belladonna  poisoning.  The  vesicles  of  varicella,  variola,  and  herpes 
may  also  be  seen.  So  also  with  petechias,  infarcts,  and  extravasa- 
tions of  blood  or  bleeding  surfaces. 

An  abnormal  general  pallor  of  the  same  surfaces  is  noted  in  the 
anaemias,  and  the  yellow  colour  of  jaundice  may  also  be  seen  here. 

I.  The  Palate. — («)  A  high,  narrow,  and  arched  hard  palate 
constitutes  one  of  the  stigmata  of  degeneration. 

(b)  Perforation  of  the  soft  palate  or  its  adhesion,  either  partial 
or  complete,  to  the  posterior  pharyngeal  wall,  is  usually  the  result  of 
syphilitic  ulceration.  Ulcers  of  the  palate  in  the  adult  are  almost 
always  tertiary  syphilitic  manifestations. 

(c)  Bilateral  paralysis  of  the  soft  palate  is  to  be  suspected  if 
there  is  regurgitation  of  fluids  through  the  nose  on  attempting  to 
swallow,  and  if  there  is  failure  to  pronounce  correctly  certain  sounds 
which  require  the  approximation  of  the  soft  palate  to  the  posterior 
pharyngeal  wall — e.  g.,  the  patient  says  "  beng  "  for  "  beg."  If  the 
paralysis  is  unilateral  these  symptoms  are  wanting.  Inspection  of 
the  soft  palate  during  the  utterance  of  the  long  "  ah  "  sound  will 
show  under  normal  circumstances  that  both  sides  of  the  palate  arch 
upward.  If  the  whole  palate  remains  motionless  during  phonation 
there  is  bilateral  paralysis ;  if  but  one  side  moves,  it  is  unilateral. 
The  soft  palate  is  in  all  probability  innervated  by  the  accessory 
portion  of  the  eleventh  nerve  (spinal  accessory)  by  way  of  the  pha- 
ryngeal plexus  of  the  pneumogastric,  although  it  is  proper  to  state 
that  some  authorities  consider  the  pneumogastric  itself  to  be  the 
motor  nerve  of  the  palatal  muscles. 

Paralysis  of  the  soft  palate  is  most  commonly  due  to  diphtheritic 
neuritis,  but  is  also  caused  by  bulbar  paralysis,  tumours,  basal  men- 
ingitis, and  vertebral  caries. 


TONSILS— PHARYNX  235 

(d)  Antssthesia  of  the  hard  and  soft  palates  indicates  disease  in- 
volving the  second  division  of  the  fifth  nerve,  from  which  the  sen- 
sory supply  of  the  palatal  region  is  derived. 

(e)  Vesicles  arranged  in  annular  shape  upon  the  soft  palate,  or 
perhaps  upon  the  pharyngeal  wall,  and  attended  with  a  dispropor- 
tionate amount  of  pain,  constitute  an  example  of  that  rare  disease, 
herpes  of  the  throat. 

(/)  Swelling  of  the  uvula  is  common  in  all  inflammatory  condi- 
tions of  the  pharynx  and  tonsils.  It  may  become  edematous  in 
nephritis,  severe  anaemias,  and  conditions  of  debility.  A  bloody 
extravasation  into  the  uvula  may  occur  in  peliosis  rheumatica  or  in 
diseases  which  cause  hemorrhagic  infarcts  elsewhere. 

II.  The  Tonsils.— (a)  Acute  sicelling  of  the  tonsils,  fever  and 
marked  constitutional  symptoms  being  present,  with  a  punctate, 
perhaps  confluent,  white  or  grayish  exudate  occupying  the  tonsillar 
crypts  or  surfaces,  may  be  due  to  follicular  tonsilitis,  suppurative 
tonsilitis,  tonsillar  diphtheria,  scarlet  fever,  or  measles. 

(b)  If  the  exudate,  as  in  (a),  becomes  confluent  and  spreads  to 
the  pillars  of  the  fauces,  the  soft  palate,  and  pharynx,  it  is,  in  the 
vast  majority  of  cases,  diphtheria. 

(c)  If  the  exudate,  as  in  (a),  remains  stationary  or  disappears, 
and  the  soft  palate  on  one  side  becomes  reddened,  tumid,  and  greatly 
swollen,  pushing  the  tonsil  to  or  beyond  the  median  line,  it  is  a  sup- 
purative tonsilitis  (quinsy). 

(d)  Permanent  enlargement  of  the  tonsil  is  due  to  chronic  in- 
flammation, and  is  frequently  associated  with  postnasal  lymphoid 
growths.  The  symptoms  and  signs  of  mouth  breathing  are  usually 
to  be  found. 

(e)  If  there  are  deep  ulcers  upon  both  tonsils,  circular  in  shape 
and  with  a  gray  surface,  the  remaining  portion  of  the  tonsil  present- 
ing a  normal  appearance,  it  is  almost  certain  that  they  are  of  syphi- 
litic origin. 

(/)  Irregular,  grayish,  painful  ulcers  upon  the  tonsils,  occurring 
in  the  later  stages  of  pulmonary  phthisis  and  associated  with  similar 
ulcers  upon  the  pharynx  and  larynx,  may  be  considered  tuberculous, 
although  their  appearance  upon  the  tonsils  is  a  rare  event. 

{g)  Deep,  spreading  ulceration  upon  an  enlarged  tonsil,  from 
which  an  offensive,  sanious  discharge  issues,  is,  if  it  occurs  in  an 
elderly  person,  in  all  probability  cancerous. 

(//)  Whitish  plugs  in  the  lacunae  of  chronically  enlarged  tonsils  may 
be  composed  principally  of  leptothrix  threads  or  are  small  concretions. 

III.  The  Pharynx. — (a)  Congestion  of  the  pharyngeal  mucous 
membrane  is  seen  in  acute  and  chronic  inflammations  of  the  pharynx. 


236  THE  EVIDENCES  OF  DISEASE 

and  passive  or  venous  hjrperaemia  may  be  significant  of  cardiac  valvu- 
lar disease,  aneurism,  or  mediastinal  tumour. 

(J)  Marked  pulsation  of  the  internal  carotid  may  be  caused  by 
aortic  regurgitation,  profound  anaemia,  or  possibly  by  aneurism  of 
the  vessel. 

(c)  A  dry,  reddened  condition  of  the  pharynx,  with  slight  consti- 
tutional symptoms,  is  an  acute  catarrhal  pharyngitis.  There  may 
be  an  indistinct  punctate  exudate  analogous  to  that  which  is  present 
in  follicular  tonsilitis. 

(d)  A  patient  complaining  of  sore  throat  and  intense  dysphagia,, 
with  slight  or  absent  objective  signs,  has  in  all  probability  a  rheu- 
matic pharyngitis. 

(e)  A  relaxed  dry  or  moist  mucous  membrane  showing  dilated 
veins  and  numerous  projecting,  rounded  follicles  on  the  posterior 
wall  of  the  pharynx,  is  an  example  of  chronic  pharyngitis. 

(/)  A  swollen  and  injected  mucous  membrane,  with  severe  con- 
stitutional symptoms  and  ending  in  suppuration,  is  a  phlegmonous 
pharyngitis,  fortunately  of  rare  occurrence. 

(g)  A  membranous  exudate  upon  the  pharynx  is  in  a  large  ma- 
jority of  cases  diphtheria,  and  should  be  regarded  as  such  unless 
the  diagnosis  is  disproved  by  a  bacteriological  examination.  Mem- 
branous inflammations  not  due  to  the  Klebs-Loeffler  organism — the 
diphtheroid  affections — are  for  the  most  part  the  result  of  infection 
by  the  Streptococcus  pyogenes. 

{h)  Ulcerations,  rounded  in  shape,  yellow,  sloughy,  and  surrounded 
by  a  reddened  zone,  if  occurring  in  an  adult,  are  frequently  due  ta 
syphilis.  In  the  absence  of  other  definite  symptoms  the  therapeutic 
test  will  decide  the  question.  Small  superficial  ulcers  are  usually 
follicular,  and  occur  in  connection  with  chronic  pharyngitis.  Irregu- 
lar ulcers,  with  undefined  boundaries  and  yellowish-gray  fioors,  if 
found  in  a  patient  far  gone  with  phthisis,  are  undoubtedly  tubercu- 
lous. Small  round  or  oval  ulcers  of  the  pharynx  may  be  found 
toward  the  close  of  typhoid  fever.  Ulcers  also  occur  in  diphtheria, 
lupus,  and  cancer. 

(^■)  Bulging  forward  of  the  posterior  pharyngeal  wall,  with  the 
rapid  onset  of  dysphagia  and  dyspncea,  particularly  in  children,  is 
due  to  an  acute  retropharyngeal  abscess.  If  chronic  and  without 
urgent  symptoms  it  is  probably  an  abscess  caused  by  cervical  caries 
affecting  the  bodies  of  the  vertebrae. 

(j)  Motor  and  Sensory  Disorders  of  the  Pharynx. — (1)  Ances- 
thesia  of  the  pharynx  is  indicative  of  some  interference  with  the 
sensory  functions  of  the  glosso-pharyngeal  and  pneumogastric 
nerves,  and  is  found  in  diphtheritic  neuritis,  hysteria,  and  bulbar 


PHARYNX— DYSPHAGIA  237 

paralysis.     Globus  hystericus  is  a  functional  disorder  of  the  ninth 
nerve. 

(2)  Spasm  of  the  pharyngeal  muscles  on  attempting  to  swallow  is 
a  functional  affection  of  the  motor  portions  of  the  same  nerves.  It 
may  be  present  in  neurotic  and  hysterical  individuals,  in  hydrophobia 
true  or  false,  in  tetanus  and  strychnine  poisoning.  It  is  probably  an 
element  in  globus  hystericus. 

(3)  Paralysis  oi  the  pharynx,  if  bilateral,  causes  difficulty  in  swal- 
lowing, the  food  is  not  passed  into  the  esophagus,  and  portions  may 
enter  the  larynx.  If  the  paralysis  is  unilateral,  there  is  little  if  any 
difficulty  in  deglutition.  Pharyngeal  paralysis  indicates  an  involve- 
ment of  the  nuclei  of  the  ninth  and  tenth  cranial  nerves  or  of  the 
nerves  in  their  course,  as  in  bulbar  paralysis,  Landry's  paralysis,  and 
neuritis ;  or  basal  lesions,  as  meningitis,  tumour,  or  aneurism. 


SECTION  XX 
DYSPHAGIA 

Dysphagia,  difficulty  or  pain  in  the  act  of  swallowing,  attends  a 
variety  of  conditions,  the  more  important  of  which  are  as  follows : 

Mouth  and  Fauces. — Glossitis,  cancer  or  other  tumour  of  the 
tongue,  and  the  various  forms  of  stomatitis  may  cause  painful  or 
difficult  swallowing.  So  also  with  tonsilitis,  follicular  or  suppura- 
tive, tonsillar  concretions,  and  the  various  forms  of  pharyngitis,  in- 
cluding rheumatism  of  the  pharynx  and  retropharyngeal  abscess. 
Diphtheria,  and  the  eruptions  of  scarlpt  fever  (erythema),  measles 
(macules),  varicella,  variola,  and  herpes  (vesicles)  may  be  responsible 
for  dysphagia.  Difficult  swallowing  may  be  due  to  spasm  or  paralysis 
of  the  palate  and  pharynx,  the  causes  of  which  have  just  been  con- 
sidered. Trichiniasis  may  cause  difficulty  in  chewing  and  swallow- 
ing because  of  the  stiffness  and  soreness  of  the  muscles  due  to  the 
presence  of  the  parasite. 

Larynx. — Ordinary  laryngitis  causes  some  uneasiness  in  swallow- 
ing. Dysphagia  may  be  due  to  cancer  of  the  larynx,  and  the  atro- 
cious pain  attending  tuberculous  ulceration  is  well  known. 

Esophagus. — The  diseases  of  the  esophagus  which  lead  to  diffi- 
culty or  pain  in  deglutition  are :  spasm  (oesophagismus),  inflamma- 
tion (oesophagitis),  in  which  case  pain  is  felt  in  the  episternal  notch 
and  behind  the  upper  sternum,  cancer,  stricture,  and  impacted  for- 
eign body. 


238  THE  EVIDENCES  OP  DISEASE 

Pressure  from  Outside. — Dysphagia,  in  the  absence  of  demon- 
strable lesions  in  the  mouth,  pharynx,  larynx,  and  esophagus,  may 
be  caused  by  the  pressure  of  an  enlarged  thyroid  gland,  thoracic 
aneurism,  enlarged  bronchial  glands,  lymphadenoma,  mediastinal 
tumour,  and  large  pericardial  or  pleural  effusions. 


SECTION  XXI 

EXAMINATIOX   OF   THE   LAKYNX   AND   LINGUAL 

TONSIL 

There  is  required  a  strong  light  (Argand  gas  burner,  student 
lamp,  Welsbach  burner,  electric  light)  with  a  suitable  condenser 
(Mackenzie's)  and  various  sizes  of  laryngoscopic  mirrors.  The  shank 
of  the  laryngoscopic  mirror  should  be  stronger  and  much  less  flexible 
than  some  of  those  which  are  now  in  the  market.  The  mirror  for 
ordinary  use  should  be  about  1  inch  or  a  little  less  in  diameter.  A 
forehead  mirror,  3  to  3|  inches  in  diameter,  with  a  central  perfora- 
tion, worn  preferably  over  the  left  eye,  is  employed  to  direct  the  light. 
The  patient  sits  erect,  the  examiner  facing  him.  The  light  is  placed 
to  the  patient's  right  on  a  level  with  his  mouth.  The  laryngeal  mir- 
ror is  warmed,  its  heat  tested  on  the  examiner's  hand,  and  the  light 
directed  upon  the  patient's  mouth.  He  is  then  desired  to  throw  his 
head  slightly  backward  and,  seizing  the  tongue  between  his  thumb 
and  forefinger,  a  handkerchief  having  been  interposed  to  prevent 
slipping,  to  roll  it  out,  forward  and  downward  over  the  edge  of  the 
lower  teeth.  At  the  same  time  ask  him  to  sound  all  {a  in  father), 
which  lowers  the  root  of  the  tongue  and  raises  the  soft  palate.  The 
throat  mirror,  held  delicately  like  a  pen,  reflecting  surface  down,  is 
then  passed  over  the  dorsum  of  the  tongue  without  touching  any- 
thing until  its  back  rests  against  the  uvula  and  soft  palate.  The 
mirror  is  then  to  be  carried  upward  and  backward,  pushing  the  soft 
palate  and  uvula  before  it,  until  it  rests  almost  against  the  posterior 
pharyngeal  wall.  By  slightly  raising  or  lowering  the  handle  of  the 
mirror  the  epiglottis,  larynx,  and  surrounding  parts  may  be  brought 
into  view  (Fig.  40). 

The  base  of  the  tongue  should  be  examined,  by  bringing  the  mir- 
ror somewhat  forward,  for  the  presence  of  hypertrophy  of  the  lingual 
tonsil,  a  mass  of  rounded  projections  bulging  backward  into  the 
space  between  the  tongue  and  epiglottis  (glosso-epiglottic  fossa) ;  for 
red  and  painful  swelling,  with  or  without  punctate  or  membranous 


EXAMINATION  OP  LARYNX  239 

exudate,  somewhat  similar  to  that  which  is  seen  in  lacunar  tonsili- 
tis ;  and  for  ulceration. 

The  epiglottis  varies  considerably  in  shape  and  position,  and  in 
some  cases  may  interfere  seriously  or  totally  with  a  good  view  of  the 
larynx.  It  should  be  inspected,  its  an- 
terior surface  in  particular,  for  cysts  or 
edematous  swelling.  Passing  backward 
from  either  side  of  the  base  of  the  epi- 
glottis to  the  arytenoid  cartilages  are 
the  ary-epiglottic  folds.    Outside  of  these        _  '/  .^\ 

folds  lie  the  pyriform  sinuses. 

In  the  larynx  the  white  gleam  of  the 
true  vocal  cords  is  usually  the  first  thing 
to  catch  the  eye.  The  funnel  shape  of 
the  larynx  and  the  depth  of  the  vocal  

cords  (1    inch)  below   the   margin   of  the      Fig.  40.— Usual  view  of  the  normal 

arv-epiglottic  folds  are  not  appreciated       larynx  and  front  wall  of  tiie 
from  a  study  of  the  usual  cuts,  because       'Z'^^T  ';'^'  >i"  vtr  ^'\7 

•^  '  Krieg's  Atlas,  with  slight  modifi- 

Of  the  lack   of  perspective  of  the  latter.  cations  by  Farlow ;  original  in 

The  true  cords  are  pearl-white  in  colour,  colour), 
reaching  ^om  the  apex  of  the  thyroid  car- 
tilage anteriorly  to  the  arytenoid  cartilages  posteriorly.  Their  anterior 
ends  are  often  hidden  from  view  by  the  epiglottis,  but  if  the  patient 
is  requested  to  sound  a  high-pitched,  almost  falsetto,  eh,  the  epiglot- 
tis is  lifted  forward  and  the  vocal  cords  come  together,  lying  parallel 
and  almost  in  contact.  During  respiration  the  vocal  cords  diverge 
posteriorly,  leaving  between  them  a  triangular  opening,  base  to  the 
rear.  On  each  side  of  the  true  cords  the  dark  openings  of  the  lateral 
ventricles  may  or  may  not  be  seen,  and  a  little  above  and  to  the  out- 
side of  these  are  the  reddish  ventricular  bands  (the  false  vocal  cords). 
At  the  posterior  extremities  of  the  vocal  cords  are  two  knoblike  ele- 
vations or  prominences,  the  arytenoid  cartilages.  When  the  vocal 
cords  are  widely  separated  during  forced  inspiration  the  trachea  may 
be  seen  as  far  down  as  its  bifurcation,  including  the  openings  of  the 
primary  bronchi. 

Autoscopy  by  the  method  of  Kirstein  dispenses  with  the  use  of  a 
laryngeal  mirror  and  involves  the  employment  of  a  special  instru- 
ment by  which  the  base  of  the  tongue  is  depressed  to  an  extent 
which  allows  the  posterior  half  of  the  vocal  cords  and  trachea  to  be 
directly  inspected.  Illumination  is  secured  either  by  an  electric  light 
attached  to  the  special  tongue  depressor,  or  from  the  ordinary  head 
mirror.  This  method  appears  at  present  to  be  of  limited  applica- 
bility. 


240  THE  EVIDENCES  OF  DISEASE 

In  studying  the  larynx  and  its  parts,  one  observes  the  presence  of 
swelling  or  ulceration.  Tumours  on,  above,  or  below  the  vocal  cords 
may  be  noted.  In  tuberculosis  there  may  be  swelling  of  the  epiglot- 
tis and  ary-epiglottic  folds  and,  if  laryngeal  phthisis  exists,  multiple 
ulcers  may  be  seen,  especially  on  the  fold  between  the  arytenoid  car- 
tilages (interarytenoid  fold).  Syphilitic  or  cancerous  ulcers  are  usu- 
ally single.  A  gray-pink  or  reddish  colour  of  the  vocal  cords  is  indic- 
ative of  laryngitis,  and  pinkish  nodules  may  be  present  on  the  edges 
of  the  cords.  General  pallor  of  the  mucous  membrane  of  the  larynx 
may  attend  certain  cases  of  laryngeal  tuberculosis ;  general  redness 
is  present  in  most  inflammatory  or  syphilitic  laryngeal  diseases. 

Laryngeal  Paralysis. — Finally,  the  mobility  of  the  vocal  cords 
should  be  determined  by  causing  the  patient  to  phonate  {ah  or  eh)  and 
to  breathe  somewhat  rapidly,  observing  the  manner  in  which  the  vocal 
cords  approach  and  depart  to  and  from  each  other  and  the  middle 
line  (Fig.  41',  to  which  subsequent  references  apply).  The  move- 
ment of  each  cord  should  be  estimated  separately.  Under  normal 
circumstances  the  cords  meet  in  the  middle  line  during  phonation 
(A)  and  separate  widely  while  breathing  (B),  especially  during  inspi- 
ration. All  the  muscles  of  the  larynx  are  supplied  by  the  recurrent 
laryngeal  except  the  crico-thyroid,  which  receives  its  motor  innerva- 
tion from  the  superior  laryngeal  branch  of  the  pneumogastric. 

(1)  If  there  is  total  bilateral  paralysis  of  the  recurrent  nerves,  the 
cords  remain  in  the  "  cadaveric  position,"  i.  e.,  midway  between  the 
median  line  and  extreme  abduction  (C).  They  do  not  move  inward 
during  phonation,  nor  outward  during  inspiration. 

(2)  If  the  paralysis  is  unilateral  (usually  on  the  left  side),  the 
paralyzed  cord  remains  in  the  cadaveric  position  (D),  while  its  fellow 
moves  in  and  out  during  phonation  and  respiration,  even  crossing 
the  middle  line  during  phonation  (adduction). 

The  foregoing  description  refers  to  total  paralysis  of  all  the  mus- 
cles supplied  by  one  (or  both)  recurrent  laryngeal  nerves.  Although 
all  of  these  muscles  are  innervated  by  the  same  nerve,  yet  either  the 
abductors  or  the  adductors  may  be  alone  affected,  paralysis  of  the 
abductors  occurring  first  and  most  frequently. 

(3)  In  abductor  paralysis  (affecting  the  posterior  crico-arytenoid 
muscles)  one  or  both  sides  may  be  involved.  If  unilateral,  the  para- 
lyzed cord  stands  in  the  median  line  and  does  not  move  outward 
during  inspiration  (E) ;  if  bilateral,  the  cords  lie  together  as  during 
normal  phonation,  but  fail  to  move  outward  during  inspiration  (F). 

(4)  In  adductor  paralysis  (affecting  the  lateral  crico-arytenoid 
muscles),  if  bilateral,  the  cords  lie  apart,  as  they  do  during  normal 
inspiration  (B),  but  fail  to  come  together  (or  make  a  sudden  and 


A.  Normal  larynx  during  phonation. 


E.  Right-side  (abductor)  paralysis  uf  poste- 
rior crico-arytenoid  muscles. 


B.  Normal  larynx  during  deep  inspiration  ;         F.  Bilateral  paralysis  of  the  posterior  crico- 
also  position  in  adductor  paralysis  (lateral  arytenoid  muscles, 

crico-arytenoid  muscles). 


C.  Bilateral  paralysis  of  the  recurrent  nerves. 


G.  Paralysis  of  both  internal  thyroarytenoid 
muscles. 


D.  Paralysis  of  the  left  recurrent  nerve.  H.  Paralysis  of  the  interarytenoid  muscle. 

Fig.  41.— Showing  paralyses  of  the  vocal  cords  (after  Wesener). 

241 


242  THE  EVIDENCES   OF  DISEASE 

unsuccessful  attempt  to  do  so)  when  phonation  is  attempted.  If  the 
paralysis  is  unilateral  (rare),  one  cord  fails  to  approach  its  fellow  in 
the  median  line  during  phonation. 

(5)  If  the  internal  thyro-arytenoid  muscles  (adductors)  alone  are 
paralyzed,  the  cords  endeavour  to  approach  the  median  line  during 
phonation,  but  the  movement  is  only  partly  accomplished,  thus  leav- 
ing an  elliptical  opening  between  them  (G). 

(6)  If  the  anterior  f  or  f  of  the  cords  come  together  during  phona- 
tion, leaving  a  triangular  cleft  or  space  posteriorly  (H),  there  is  paral- 
ysis of  the  transverse  adductor,  the  interarytenoid  muscle. 

Causes  and  Diagnostic  Value  of  Laryngeal  Paralysis. — Paralysis 
of  the  muscles  of  the  larynx  is  rarely  if  ever  due  to  cortical  disease, 
but  is  caused  by  lesions  affecting  the  nuclei  or  origin  of  the  vagus  in 
the  medulla  or  the  nerve  itself  at  some  part  of  its  course.  Thus  it 
may  be  implicated  at  its  deep  origin  by  the  lesions  of  bulbar  paral- 
ysis, syringomyelia,  locomotor  ataxia,  or  multiple  sclerosis ;  or  an 
injury,  tumour,  or  disease  of  the  base  of  the  brain  may  involve  the 
nerve  near  its  superficial  origin.  The  causes  of  paralysis  most  fre- 
quently encountered  are  those  which  affect  the  pneumogastric  or  its 
laryngeal  branches  in  the  neck  or  the  thorax — viz.,  in  the  necJc,  ert 
larged  cervical  glands,  enlarged  thyroid  gland,  tumours  of  the  neck 
or  pharynx,  and  caries  of  the  cervical  vertebrae ;  in  the  thoraXy 
aneurism  of  the  aorta,  abscess,  tumour,  or  enlarged  glands  in'  the 
mediastinum,  esophageal  cancer,  and,  rarely,  compression  resulting 
from  inflammation  of  the  pericardium  or  pleura  and  pulmonary 
tuberculosis.  The  nerve  and  its  branches  may  become  inflamed 
(neuritis)  or  the  laryngeal  muscles  themselves  undergo  pathological 
changes  terminating  in  paralysis  as  an  effect  of  the  toxines  of  a  num- 
ber of  the  acute  specific  infections,  notably  diphtheria ;  or  chronic 
poisoning,  especially  from  lead  and  alcohol. 

Total  bilateral  paralysis  is  most  commonly  indicative  of  aneurism 
of  the  thoracic  aorta,  cancer  of  the  esophagus,  or  great  thyroid 
enlargement. 

Abductor  paralysis  is  usually  due  to  organic  disease,  is  commonly 
unilateral,  and  is  the  most  frequent  variety  of  laryngeal  palsy. 

Adductor  paralysis,  if  bilateral,  is  as  a  rule  of  functional  origin 
(especially  hysteria) ;  if  unilateral,  it  is  due  to  hysteria  or  lead 
poisoning. 

Paralysis  of  the  interarytenoid  muscle  (adductor)  may  be  the  result 
of  catarrhal  laryngitis,  but  is  most  apt  to  be  a  symptom  of  hysteria. 

Paralysis  of  the  internal  thyro-arytenoid  muscles  (adductors)  is  a 
not  uncommon  result  of  overuse  of  the  voice  and  laryngeal  inflam- 
mation. 


LARYNX— VOICE  AND  SPEECH 


243 


The  following  table,  from  Gowers'  work,  is  frequently  quoted  in 
this  connection  (see  also  Voice  and  Speech,  in  the  following  section) : 


Symptoms 

'No  voice;  no 
cough ;  stridor  only 
on  deep  inspiration. 

Voice  low  pitched 
and  hoarse;  no 
cough ;  stridor  absent 
or  slight  on  deep 
breathing. 

Voice  little 
changed ;  cough  nor- 
mal ;  inspiration  diflB- 
cult  and  long,  with 
loud  stridor. 

Symptoms  incon- 
clusive ;  little  affec- 
tion of  voice  or 
cough. 

Xo  voice ;  perfect 
cough ;  no  stridor  or 
dyspnoea. 


Signs 

Both  cords  mod- 
erately abducted  and 
motionless. 

One  cord  moder- 
ately abducted  and 
motionless,  the  other 
moving  freely,  and 
even  beyond  the  mid- 
dle line,  in  phonation. 

Both  cords  near 
together,  and  during 
inspiration  not  sep- 
arated, but  even 
drawn  nearer  to- 
gether. 

One  cord  near  the 
middle  line  not  mov- 
ing during  inspira- 
tion, the  other  nor- 
mal. 

Cords  normal  in 
position  and  moving 
normally  in  respira- 
tion, but  not  brought 
together  on  an  at- 
tempt at  phonation. 


Lesion 
Total       bilateral 
palsy. 

Total     unilateral 
palsy. 


Total    abductor 
palsy. 


Unilateral  abduc- 
tor palsy. 


Adductor  palsy. 


SECTION  xxn 

VOICE  AND   SPEECH 

There  are  certain  alterations  in  the  voice  sounds,  in  the  manner 
of  speech,  and  in  the  ability  to  produce  or  understand  written  or 
spoken  words  or  thoughts  which  are  of  much  importance  in  diagno- 
sis.    Tlie  significant  symptoms  relating  to  the  voice  and  speech  are  : 

I.  Aphonia  and  Hoarseness. — Loss  of  voice  or  whispering 
voice  (aphonia),  and  coarse  or  harsh  quality  of  the  voice  (hoarseness 


244  THE  EVIDENCES  OF  DISEASE 

or  dysphonia),  are  both  due  to  some  interference  with  the  function 
of  the  vocal  cords.  The  imperfect  or  abolished  action  of  the  cords 
may  be  due  to  local  and  inflammatory  disease  of  the  larynx,  or  dis- 
ease of  or  pressure  upon  the  recurrent  laryngeal  nerve.  Aphonia 
may  come  suddenly  or  be  preceded  by  hoarseness,  or  the  latter  alone 
may  be  present.  The  cough  and  respiration  may  be  modified  in 
sound  by  the  existence  of  hoarseness  or  aphonia. 

Laryngeal  Causes  of  Aphonia. — In  the  majority  of  cases  aphonia 
and  hoarseness  are  due  to  some  form  of  laryngitis,  acute  or  chronic, 
simple  or  specific,  as  in  the  ordinary  catarrhal  variety  and  that  due 
to  measles,  variola,  diphtheria,  syphilis,  or  tuberculosis.  CEdema  of 
the  glottis  and  retropharyngeal  abscess  are  fortunately  rare  causes. 
Excessive  use  of  the  voice,  by  inducing  congestion  of  the  cords,  is  a 
common  cause  of  hoarseness  or  aphonia.  Tumour  of  the  larynx, 
impacted  foreign  bodies,  and  cicatricial  stenosis  of  the  larynx  may 
be  found  responsible.  The  laryngeal  muscles  may  be  involved,  and 
thereby  stiffened,  in  trichiniasis. 

Aphonia  from  Involvement  of  the  Laryngeal  Nerves. — The  larynx 
receives  its  nervous  supply  from  the  superior  laryngeal  branch  of  the 
pneumogastric  and  the  inferior  or  recurrent  branch  of  the  same 
nerve.  These  nerves  may  be  involved  in  consequence  of  lesions 
affecting  their  nuclei,  or  in  their  course  by  inflammation  (neuritis) 
or  by  pressure.  Interference  with  their  functions  gives  rise  to  anaes- 
thesia of  the  larynx  or  paralysis  of  the  laryngeal  muscles,  manifested 
by  aphonia,  hoarseness,  and,  if  the  abductors  are  affected,  dyspnoea. 
An  examination  of  the  action  of  the  vocal  cords  during  respiration 
and  phonation  (page  240)  is  required  to  determine  which  muscles 
are  affected. 

If  there  is  a  deep,  hoarse  voice  and  a  brassy  cough,  with  a  tend- 
ency for  particles  of  food  to  enter  the  larynx,  there  is  probably 
interference  with  the  superior  laryngeal  nerve,  giving  rise  to  anaes- 
thesia of  the  upper  portion  of  the  larynx  and  paralysis  of  the  crico- 
thyroid muscles.  This  interference  may  be  due  to  bulbar  paralysis, 
diphtheritic  neuritis,  or  to  the  pressure  of  a  goitre  or  carotid  aneu- 
rism. 

If  there  is  aphonia  without  cough  or  dyspnoea,  it  may  be  due  to 
paralysis  of  all  the  laryngeal  muscles  caused  by  bulbar  paralysis, 
tumours  of  the  medulla,  diphtheria,  or  pressure  upon  both  recurrent 
nerves ;  or  to  complete  paralysis  of  the  adductors,  which  is  usually 
of  hysterical  origin,  but  may  occur  from  overuse  of  the  voice,  or 
laryngitis. 

Hoarseness,  with  easy  fatigue  upon  slight  use  of  the  voice,  is 
indicative  of  unilateral  abductor  paralysis,  of  which  the  most  com- 


VOICE  AND  SPEECH  245 

mon  cause  is  an  aneurism  of  the  thoracic  aorta,  less  frequently  a 
mediastinal  tumour  pressing  upon  one  recurrent  nerve.  If  right- 
sided,  it  may  be  due  to  a  much  thickened  pleura.  Bronchocele,  can- 
cer of  the  upper  part  of  the  esophagus,  and  innominate  or  sub- 
clavian aneurism  are  other  possible  causes. 

A  weak,  rough,  low-pitched  voice  may  be  noted  as  a  result  of  total 
unilateral  paralysis  due  to  involvement  of  one  recurrent  nerve  by  the 
same  causes  as  in  the  preceding  variety. 

It  should  be  remembered  that  normal  voice  and  phonation  may 
coexist  with  a  dangerous  form  of  laryngeal  paralysis — bilateral  palsy 
of  the  abductors — but  in  this  case  there  is  inspiratory  dyspnoea  with 
loud  stridor.  It  may  be  due  to  laryngitis,  rarely  to  hysteria,  and  is 
a  symptom  of  locomotor  ataxia,  bulbar  palsy  and  pressure  from  an- 
eurism or  tumour. 

A  curious  rattling,  rough  voice  (the  so-called  ventricular  voice) 
is  due  to  the  occasional  vicarious  vibration  of  the  false  vocal  cords 
or  ventricular  bands,  in  cases  where  the  true  cords  are  paralyzed  or 
destroyed  by  ulceration.  Other  peculiar  abnormalities  of  the  voice 
consist  in  a  double  or  triple  splitting  of  the  sounds.  In  the  first 
variety  the  two  sounds,  although  simultaneous,  differ  in  pitch  (diplo- 
phonia,  diphthongia) ;  it  is  due  to  a  small  tumour  on  the  edge  of  one 
vocal  cord,  or  to  unilateral  paralysis  of  the  cords.  The  triple  voice 
is  a  very  uncommon  finding,  and  is  caused  by  a  pedunculated  tumour, 
which  has  its  attachment  below  the  vocal  cords.  During  the  early 
portion  of  phonatory  expiration  (which  is  clear)  the  growth  rises, 
during  the  middle  part  (which  is  hoarse)  it  lies  between  the  cords, 
and  during  the  latter  part  (which  is  again  clear)  the  tumour  has  been 
protruded  to  a  point  above  the  glottis. 

II.  Nasal  Voice. — The  peculiar  quality  of  voice  which  goes  by 
this  name  is  sometimes  a  matter  of  habit.  It  is  of  service  to  recog- 
nise two  varieties  of  the  nasal  voice.  The  first,  the  open  nasal,  is 
caused  by  non-closure  of  the  naso-pharyngeal  opening  by  the  soft 
palate  (e.  g.,  diphtheritic  paralysis),  and  may  be  imitated  by  speaking 
without  opening  the  mouth  ;  the  second,  the  closed  or  stopped  nasal,  is 
due  to  nasal  stenosis,  resembling  the  tone  imparted  to  the  voice  by 
speaking  while  the  nose  is  pinched  between  the  thumb  and  forefinger. 

The  open  nasal  tone  is  indicative  of  paralysis  of  the  soft  palate, 
destruction  of  the  soft  palate  by  ulceration,  usually  syphilitic,  or  a 
congenital  cleft  of  the  palate.  The  closed  nasal  voice,  when  present, 
is  often  suggestive  of  coryza,  hay  asthma,  hypertrophic  rhinitis,  nasal 
polypus,  or  postnasal  adenoids.  It  is  present  also  with  enlarged  fau- 
cial  tonsils,  suppurative  tonsilitis,  acute  pharyngitis,  and  retropha- 
ryngeal abscess.  A  slight  nasal  intonation  may  be  noted  in  the  early 
18 


246  THE  EVIDENCES  OF  DISEASE 

stage  of  scarlet  fever,  pharyngeal  diphtheria,  variola,  and  typhus 
feyer. 

lil.  Alterations  in  the  Manner  of  Speech. — (1)  Dumbness 
or  mutism — inability  or  unwillingness  to  speak — may  be  present  in 
hysteria,  idiocy,  melancholia,  and  dementia.  Feigned  inability  to 
speak  is  sometimes  resorted  to  by  malingerers,  and  a  real  inability, 
due  to  cerebral  fatigue,  may  succeed  a  severe  and  exhausting  illness, 
particularly  typhoid  fever.  Great  swelling  of  the  tongue  may  abso- 
lutely prevent  articulation.  Mutism  exists  in  those  who  are  congeni- 
tally  deaf,  or  in  children  who  become  totally  deaf  before  the  power  of 
speech  is  permanently  acquired.  Furthermore,  the  power  of  speech 
is  almost  entirely  lost  in  some  forms  of  aphasia. 

(2)  Anarthria,  indistinct  or  imperfect  speech,  the  impairment  vary- 
ing in  extent,  may  be  an  evidence  of  paralysis  of  the  tongue,  soft 
palate,  and  facial  muscles,  paralysis  of  the  latter  affecting  particularly 
the  labials  j9,  Z»,/,  m,  v,  w,  and  the  vowels  o  and  u.  Another  variety 
of  anarthria,  a  difficulty  in  pronouncing  the  dentilinguals  fZ,  t,  th,  Sy 
z,  n,  I,  and  r,  with  an  indistinct  mumbling  speech,  is  suggestive  of 
bulbar  or  pseudo-bulbar  paralysis,  and  may  be  noted  more  rarely  in 
amyotrophic  lateral  sclerosis.  If  the  lips  are  involved,  the  labials 
also  are  affected  and  speech  becomes  almost  impossible.  The  speech 
may  be  very  indistinct  as  well  as  weak  and  whispering  in  the  typhoid 
status  and  conditions  of  exhaustion.  Glossitis,  parotitis,  and  the 
absence  of  teeth  may  be  responsible  for  a  mumbling  manner  of 
talking. 

(3)  A  slow,  interrupted  manner  of  speech,  the  words  being  slurred 
over,  somewhat  as  if  the  patient  were  intoxicated,  with  tremulousness 
of  the  tongue  and  lips,  is  observed  in  general  paresis. 

(4)  A  piping,  querulous  voice,  with  manifest  hesitation  in  begin- 
ning a  sentence,  the  words  then  being  rapidly  spoken,  is  quite  char- 
acteristic of  paralysis  agitans. 

(5)  Scanning  speech,  in  which  the  words  are  spoken  slowly,  each 
syllable  accented  as  if  reading  verse,  is  an  important  symptom  of  dis- 
seminated (insular)  sclerosis,  but  is  also  found  in  Friedreich's  (heredi- 
tary) ataxia. 

(6)  Hesitant  or  embarrassed  speech,  amounting  in  severe  cases  to 
a  confused  and  incoherent  verbal  tangle,  may  be  due  to  chorea. 

(7)  Interrupted  speech,  two  or  three  words  at  a  time  being  gasp- 
ingly uttered,  is  observed  in  those  who  are  suffering  from  marked 
dyspnoea  as  well  as  during  the  incidence  of  a  chill  or  rigour.  It  is 
to  some  extent  an  index  of  the  severity  of  these  symptoms. 

IV.  Aphasia. — The  term  aphasia  embraces  a  variety  of  defects 
in  the  use  or  the  comprehension  of  language,  either  spoken  or  writ- 


APHASIA  247 

ten.  In  order  to  understand  and  interpret  this  symptom  and  its 
several  forms  one  must  first  have  a  conception  of  the  normal  manner 
and  mechanism  of  the  faculty  of  language.  The  subject  is  in  reality 
extremely  complex,  and  exceptional  cases  are  accumulating  year  by 
year.  So  far  as  possible  the  statements  made  here  are  those  the 
truth  of  which  is  either  admitted  or  considered  as  probable  by  good 
authority. 

Normal  Speech  Mechanism. — The  normal  exercise  of  the 
faculty  of  language  depends  upon  the  existence  and  integrity  of  cer- 
tain cerebral  centres :  (1)  Psychical  centres  of  intelligent  perception, 
(2)  sensory  receptive  centres,  (3)  emissive  or  motor  centres,  (4)  the 
association  tracts.  Finally,  there  are  the  basal  ganglia  for  the  special 
senses  and  the  nuclei  in  the  medulla  and  spinal  cord  actuating  the 
muscles  employed  in  articulate  speech,  which  constitute  respectively 
the  sensory  and  vaoiov  peripheral  apparatus. 

(1)  The  Psychical  Centres. — An  intelligent  perception  of  an  ob- 
ject, whatever  the  latter  may  be,  depends  upon  the  evidence  of  its 
character  derived  from  the  senses  of  sight,  sound,  taste,  smell,  touch, 
and  muscular  sense.  The  memories — i.  e.,  the  retention  and  recall 
of  these  various  impressions — constitute  the  mental  image  of  the 
object.  The  mental  images  thus  formed  are  stored  up  in  either  the 
right  or  left  hemisphere,  although  the  exact  localization  of  these 
centres  in  the  hemisphere  has  not  yet  been  determined. 

If,  ip  addition  to  the  evidence  thus  obtained,  the  name  of  the 
object  has  been  heard  and  spoken,  read  and  written,  further  memo- 
ries of  the  sound  of  its  name,  the  muscular  actions  in  speaking  its 
name,  the  appearance  of  the  name  as  written  or  printed,  and  the 
muscular  actions  in  writing  it,  constituting  the  toord  image,  are  added 
to  the  mental  image,  and  a  complete  and  intelligent  conception  of  the 
object  is  secured. 

As  thought  precedes  and  may  be  independent  of  language,  the 
mental  image  of  an  object  as  it  presents  itself  to  the  various  senses 
is  to  be  distinguished  from  the  word  image  which  results  from 
education.  Words  are  merely  the  symbols  by  which  we  receive  or 
communicate  ideas.  In  receiving  ideas  through  the  medium  of  lan- 
guage one  hears  the  spoken  word,  sees  the  written  or  printed  word,  and 
in  some  cases  sees  expressive  gestures  (e.  g.,  lip  reading  and  sign  lan- 
guage of  the  deaf).  In  communicating  ideas  by  means  of  language, 
one  speaks  the  word,  writes  the  word  or  makes  significant  gestures. 
The  faculty  of  language  has  therefore  a  receptive  or  sensory  side,  and 
an  emissive  or  motor  side,  for  both  of  which  special  cortical  centres 
have  been  found  to  exist  in  the  left  hemisphere  in  right-handed,  the 
right  hemisphere  in  left-handed,  individuals.     A  considerable  num- 


248  THE  EVIDENCES  OP  DISEASE 

ber  of  speech  centres  may  ultimately  be  demonstrated.  At  the  pres- 
ent time  the  existence  of  three  such  centres  is  proved,  while  a  fourth 
is  accepted  by  some  and  denied  by  others. 

(2)  Sensory  or  Receptive  Speech  Centres. — Two  sensory  cortical 
speech  centres  have  been  accurately  localized,  of  which  one  is  for  the 
perception  and  memory  of  the  sotmd  of  spoken  words.  It  is  situ- 
ated in  the  posterior  part  of  the  first  and  corresponding  upper 
portion  of  the  second  temporal  convolutions  ( C\  Fig.  42) ;  while 
the  other,  for  the  memory  of  the  visual  appearance  of  written 
or  printed  words,  lies  in  the  angular  and  inferior  parietal  convo- 
lutions {D). 

(3)  Motor  or  Emissive  Speech  Centres. — In  conveying  our  thoughts 
to  others  we  speak  or  write.  Just  as  in  learning  the  sounds  or 
appearance  of  words  constant  repetition  stores  the  sensory  speech 
centres  with  auditory  or  visual  memories,  so  there  are  centres  which 
by  steady  practice  become  familiar  with  the  complicated  series  of 
muscular  actions  involved  in  uttering  or  writing  words.  The  centre 
for  memories  of  articulate  or  motor  speech  is  in  the  posterior  portion 
of  the  third  frontal  convolution  (Broca's,  B).  The  existence  of 
a  special  centre  for  the  memories  of  writing  movements  is  not 
definitely  proved,  but  is  considered  probable  by  good  authority. 
It  is  assigned  to  the  posterior  portion  of  the  second  frontal  convo- 
lution {A). 

(4)  Association  Tracts. — The  various  motor  and  sensory  speech 
centres  are  believed  to  be  connected  by  association  tracts  or  fibres 
with  each  other  and  with  the  hypothetical  psychical  and  ideation 
centres.  These  in  turn  are  put  in  communication  with  the  special- 
sense  basal  ganglia  and  the  motor  nuclei  in  the  medulla  and  spinal 
cord  by  means  of  the  projection  fibres.  The  fibres  which  unite 
the  speech  centres  are  also  called  transcortical.,  those  passing  to  and 
from  the  lower  ganglia  and  nuclei,  subcortical  fibres.  It  is  conjec- 
tured with  some  show  of  probability  that  the  island  of  Eeil  (insula) 
may  contain  a  centre  of  ideation  to  which  converge  fibres  from  the 
several  speech  centres.  Fig.  45  shows  the  various  association  tracts 
between  the  speech  centres. 

In  the  use  of  language  the  motor,  auditory,  and  visual  memories 
are  interdependent.  The  word  image  as  a  whole  is  made  up  of  the 
memory  of  its  sound  as  heard,  its  appearance  as  written,  and  the 
effort  made  in  uttering  or  writing  it,  and  it  is  by  means  of  the 
association  fibres  that  these  various  elements  are  harmonized  and 
correlated  in  hearing,  reading,  and  speaking. 

A  break  in  the  nervous  mechanism  described  produces  various 
disturbances  in  the  language  faculty,  the  nature  and  severity  of  such 


^^ 


'"TTSoT^- 


Fio.  42. — Showing  the  localization  of  the  principal  motor  and  sensory  functions  of  the 
brain  upon  the  outer  surface  of  the  left  hemisphere.  Red  lettering  =  motor;  black 
lettering  =  sensory.  Compare  with  Figs.  43  and  44.  Brain  itself  redrawn  after  a 
photograph  from  Dana. 


Fig.  43. — Showing  the  principal  convolutions  and  fissures  of  the  outer  hemisphere  of  the 
brain.    Compare  with  Figs.  42  and  44.    Red  lettering  =  convolutions;  black  letter- 
inff  =  fissures.    Same  brain  as  in  Fig.  42  above. 
^  24ft 


250 


THE  EVIDENCES  OF  DISEASE 


disturbances  depending  upon  the  locality  and  extent  of  the  causal 
lesion.  In  order  to  produce  symptoms  referable  to  but  one  of  the 
centres  a  small  and  strictly  delimited  lesion  must  exist.  More  ex- 
tensive and  diffuse  lesions  of  the  same  centre  will  affect  the  com- 
bined actions  of  the  other  centres  with  a  corresponding  increase  in 
the  variety  of  speech  disorders. 

The  Symptomatology  of  the  Language  Faculty.  —  (1) 
Apraxia. — If  an  individual  has  to  a  greater  or  less  extent  lost  the 
power  of  recognising  or  understanding  the  nature  and  uses  of  objects 


Fig.  44. — Showinfr  the  functions,  convolutions,  and  fissures  of  the  median  aspect  of  the 
right  hemisphere.  Compare  with  Figs.  42  and  43.  Ked  lettering  =  functions  and 
convolutions;  black  lettering  =  fissures.     Brain  redrawn  from  Dana. 

or,  possibly,  the  identity  of  persons,  the  condition  is  termed  apraxia. 
The  varieties  of  apraxia  correspond  in  number  and  character  to  the 
varieties  of  sensation.  An  object,  a  pencil,  for  example,  may  be  seen 
and  even  handled,  but  evidently  without  any  conception  of  its  use — 
mind  blindness  (visual  amnesia).  A  sound — e.  g.,  the  ringing  of  a 
telephone  bell — may  be  heard,  but  it  awakens  no  thought  of  answer- 
ing it — mind  deafness  (auditory  amnesia).  The  odour  of  gas  in  a 
room  does  not  suggest  a  leaky  burner — mind  anosmia.  A  taste  is 
not  recognised  as  belonging  to  a  certain  edible — miiid  ageusia.  The 
usually  characteristic  feel  of  a  fabric  gives  no  clew  to  its  composition 
— v^ind  atactiUa. 

Apraxia  is  closely  allied  to,  and  is  usually  although  not  invaria- 
bly found  in  connection  with,  the  various  forms  of  aphasia — i.  e.,  an 
inability  to  produce  or  understand  spoken  or  written  speech.     In- 


APHASIA 


251 


deed,  one  form  of  aphasia,  word  blindness  or  alexia,  may  be  consid- 
ered to  be  a  limited  mind  blindness.  So  also  word  deafness  may  be 
classed  under  mind  deafness. 


Motor  speech  centre 
(Broca's; 


Island  of  Reil 

Auditory  speech  centre 


Visual  speech  centre 

(for  written  and 
printed    words) 

Lesion  at  this  point  causes 
word  blindness  and  also 
right  lateral  homonymous 
hemianopsia,  because  of 
interference  with  optic 
radiations 


Centre  for  vision  in  general 


ASSOCIATION    TRACTS 


Optic  radiations 


Fig.  45. — Showing  the  a.ssociation  tracts  of  the  left  hemisphere  of  the  brain. 

(2)  Aphasia  and  its  Varieties. — The  principal  varieties  of  aphasia 


are 


Motor  aphasia. 


Sensory  aphasia.  ...  j  »     ,.' 
Conduction  aphasia. 


(  Aphemia. 
/  Agraphia. 
Visual, 
ditory. 


As  aphasia  implies  a  loss  of  power  to  produce  or  to  understand 
spoken  or  written  speech,  it  is  evident  that  we  may  have  a  motor 
aphasia,  inability  to  express  thought ;  or  sensory  aphasia,  inability  to 


252  THE  EVIDENCES  OF  DISEASE 

perceive  and  interpret  thought  which  has  been  clothed  in  language 
or  other  means  of  expression.  It  is  necessary  to  discriminate  aphasia 
from  anarthria.  The  latter  (page  246)  is  due  to  a  partial  or  com- 
plete paralysis  of  the  muscles  of  articulation  arising  from  disease  of 
the  peripheral  nerves  (or  their  nuclei)  which  innervate  these  muscles, 
their  cortical  centres  being  intact.  On  the  other  hand,  in  aphasia 
the  centres  in  the  cortex  are  involved,  while  the  peripheral  muscular 
and  nervous  articulating  mechanism  is  unimpaired. 

{a)  Motor  or  Ataxic  Aphasia. — This  embraces  as  its  most  im- 
portant division  aphemia.,  the  loss  of  power  to  utter  words,  although 
the  patient  knows  what  he  desires  to  say,  because  he  can  not  revive 
the  motor  memories  for  articulating  them ;  and  agrapJiia,  inability 
to  write  words  for  lack  of  power  to  recall  the  motor  memories  of  the 
muscular  actions  involved  in  writing.  Subsidiary  motor  defects  of 
expression  are :  Motor  amimia,  loss  of  ability  to  convey  ideas  by  ges- 
tures ;  motor  amusia,  loss  of  power  of  musical  expression — e.  g.,  sing- 
ing ;  musical  agraphia,  loss  of  the  ability  to  write  music. 

{b)  Sensory  Aphasia. — The  principal  varieties  of  sensory  aphasia 
are  the  auditory  and  visual.  Auditory  aphasia  or  word  deafness  is,  as 
its  name  indicates,  an  inability  to  recognise  words  when  spoken. 
The  patient  hears,  but  does  not  understand,  as  if  listening  to  a  for- 
eign language.  Visual  aphasia  or  alexia  is  a  condition  in  which  the 
patient  sees,  but  does  not  recognise  or  understand  written  or  printed 
words.  Subsidiary  sensory  defects  are  :  sensory  amimia,  loss  of  the 
ability  to  understand  gestures ;  and  sensory  amusia,  loss  of  the  ability 
to  recognise  musical  sounds  when  heard. 

Two  other  symptoms  of  some  importance  are  :  paraphasia,  in 
which  the  subject  employs  the  wrong  words,  repeats  words,  or  talks 
with  an  unintelligible  confusion  of  language  ;  and  paragraphia,  a 
similar  mixture  or  confounding  of  words  on  attempting  to  express 
himself  in  writing. 

(3)  Examination  for  Apraxia  and  Aphasia. — With  reference  to 
the  examination  of  patients  for  the  purpose  of  determining  the  pres- 
ence of  these  symptoms  some  very  elaborate  schedules  have  been 
devised  (Eskridge,  Starr),  better  fitted  for  the  specialist  in  neurology 
than  for  the  practitioner  of  inner  medicine.  For  the  latter,  Dana's 
12  questions  probably  embrace  all  that  is  required  in  the  great  ma- 
jority of  cases,  and  they  are  here  given,  with  some  additions  and  ex- 
planatory comment. 

To  Determine  the  Presence  of  Word  Deafness  (Auditory  Aphasia) 

1.  Can  he  hear  sounds  ?  This  determines  the  presence  or  absence 
of  ordinary  deafness. 


APHASIA  253 

2.  Can  he  hear  spoken  words  ?    If  so,  then 

3.  Can  he  understand  the  words  spoken  ?  This  may  be  ascer- 
tained by  asking  him  to  put  out  his  tongue,  to  open  and  close  his  hand 
or  take  up  some  article.  If  he  does  not  comply  with  these  requests, 
and  evidently  can  not  attach  any  meaning  to  them,  he  has  word 
deafness,  the  principal  symptom  of  auditory  aphasia. 

To  Determine  the  Presence  of  Word  Bundness  {Alexia,  Visual  Aphasia) 

4.  Can  he  see  objects  ?  This  determines  the  presence  or  absence 
of  ordinary  vision. 

5.  Can  he  see  words  written  or  printed  and  read  them  silently  ? 

6.  Can  he  understand  written  or  printed  words — i.  e.,  can  he  read 
intelligently  ?  This  may  be  ascertained  by  writing  out  a  question — 
e.  g.,  "  How  long  have  you  been  ill  ? "  or  a  direction,  "  Close  your 
eyes."  If  he  fails  to  respond,  there  is  alexia  or  word  blindness,  the 
principal  symptom  of  visual  aphasia. 

To  Determine  the  Presence  of  Motor  Aphasia  (Aphemia) 

7.  Can  he  speak  voluntarily  ? 

8.  Can  he  repeat  words  ? 

9.  Can  he  read  aloud  ?  If  he  is  unable  to  do  these  things  he  has 
motor  aphasia  or  aphemia. 

To  Determine  the  Presence  of  Agraphia 

10.  Can  he  write  voluntarily  ? 

11.  Can  he  write  to  dictation  ? 

12.  Can  he  copy?  If  he  is  unable  to  do  these  things  there  is 
agraphia,  a  symptom  which  may  be  found  in  all  forms  of  aphasia. 
If  he  can  not  write  voluntarily  because  of  inability  to  remember 
words  or  their  appearance,  but  can  write  to  dictation,  it  is  sensory 
agraphia.  If  he  can  not  write  either  voluntarily  or  to  dictation  it  is 
a  motor  agraphia. 

To  these  may  be  added  the  following  : 

To  Determine  the  Presence  of  Paraphasia  and  Paragraphia 

13.  When  speaking,  does  he  commit  errors  in  the  use  of  words  ? 
That  is,  does  he  use  one  word  for  another,  so  that  the  result  is  more 
or  less  unintelligible,  amounting  in  some  cases  to  an  empty  babble  ? 
If  so,  there  is  paraphasia.  ^ 

14.  When  writing,  does'  he  commit  errors  in  the  use  of  words  ?  If 
the  written  speech  is  similar  in  character  to  the  spoken  speech  as 
described  under  13,  preceding,  there  is  paragraphia. 

Paraphasia  and  paragraphia  are   the   symptoms   of  conduction 


254  THE  EVIDENCES  OF  DISEASE 

aphasia  (lesion  of  the  association  tracts),  but  this  form  of  aphasia  is 
usually  combined  with  the  auditory  or  visual  form. 

To  Determine  the  Presence  of  ]VJixd  Blindness 

15.  Does  he  recognise  ordinary  objects  seen  and  their  uses  ?  Put 
before  the  patient  pen,  ink  and  paper,  a  hand  mirror,  a  match  (any 
two  or  three  other  familiar  objects  will  answer),  and  request  him  to 
write  or  ignite  the  match.  If  he  can  not  pick  out  the  proper  article 
he  is  the  subject  of  mind  blindness,  provided  that  he  is  not  unable 
to  understand  the  request  because  of  the  presence  of  word  deafness. 

To  Determine  the  Presence  of  Mind  Deafness 

16.  Does  he  recognise  ordinary  sounds — i.  e.,  does  the  ring  of  a 
bell,  the  noise  of  an  opening  door,  the  raking  of  a  fire,  and  similar 
sounds,  awaken  a  recognition  of  their  import  ?  If  not,  the  patient 
has  mind  deafness. 

It  must  be  remembered  that  there  are  variations  in  the  com- 
pleteness of  all  speech  defects  which  have  been  described.  There 
may  be  only  a  partial  loss  of  any  one  of  the  normal  powers  of 
expression,  depending  mainly  upon  the  extent  of  the  productive 
lesion. 

Aphasic  Symptoms  with  Eeferek^ce  to  Localization  of 
Lesions. — Having  determined  and  noted  the  departures  from  the 
normal  use  of  the  language  faculty — i.  e.,  the  apraxic  and  aphasic 
symptoms  present — ^by  means  of  the  examination  as  detailed,  it 
remains  to  draw  an  inference  as  to  the  seat  of  the  causative  lesion. 
Following  are  the  symptom  groups  of  the  aphasias  which  possess  a 
localizing  value : 

(1)  Motor  Aphasia. — If  the  patient  can  read  silently,  write  volun- 
tarily, write  to  dictation,  copy,  and  hear  and  understand  spoken 
words,  but  can  not  speak  voluntarily,  repeat  words,  or  read  aloud 
(motor  aphasia,  aphemia),  there  is  a  small  lesion  of  Broca's  convolu- 
tion, third  frontal  {B,  Fig.  42). 

If  the  patient  can  hear  and  understand  spoken  words,  read  and 
understand  written  or  printed  words,  and  copy,  but  can  not  speak 
voluntarily,  repeat  words,  read  aloud,  write  voluntarily  or  to  dicta- 
tion (motor  aphasia,  aphemia,  plus  agraphia),  there  is  a  marked 
lesion  of  the  third  frontal  convolution.  This  is  the  most  frequent 
form  of  aphasia.  In  the  severest  cases  there  is  a  lessened  power  of 
understanding  written  or  spoken  speech. 

(2)  Visual  Aphasia. — If  the  patient  can  speak  voluntarily,  and 
understand  spoken  words,  but  can  not  understand  written  or  printed 
words,  write  voluntarily,  write  to  dictation,  or  copy  (visual  aphasia 


APHASIA  256 

plus  agraphia),  there  is  a  lesion  involving  the  cortex  of  the  angular 
gyrus  and  supramarginal  lobule  (i>,  Fig.  43). 

If  the  patient  can  not  understand  written  or  printed  words  or 
copy,  but  can  write,  the  lesion  involves  the  subcortical  substance  of 
the  angular  gyrus.  Visual  aphasia  is  often  associated  with  hemi- 
anopia,  and  some  hemiataxia  and  hemianassthesia, 

(3)  Auditory  Aphasia. — If  the  patient  can  speak  voluntarily, 
read  intelligently,  and  write  voluntarily,  but  can  not  understand 
spoken  words,  repeat  words,  or  write  to  dictation  (auditory  aphasia), 
there  is  a  small  subcortical  lesion  of  the  first  and  second  temporal 
convolutions  (C). 

If  the  patient  can  speak  voluntarily,  but  can  not  understand 
spoken  words,  read  intelligently,  read  aloud,  repeat  words,  write  to 
dictation,  or  copy  (auditory  aphasia  jpZ?/s  visual  aphasic  and  agraphia 
symptoms),  there  is  an  extensive  lesion  of  the  first  and  second  tem- 
poral convolutions. 

(4)  Conduction  Aphasia. — If  the  patient  uses  the  wrong  words 
or  talks  jargon  {paraphasia),  and  makes  similar  mistakes  in  writing 
(paragraphia),  but  can  speak  voluntarily,  understand  spoken  words, 
read,  and  write,  it  is  indicative  of  an  interruption  of  the  association 
tracts  between  the  various  centres,  and  the  lesion  is  ordinarily  in  the 
island  of  Eeil  or  the  convolutions  about  the  fissure  of  Sylvius.  It 
should  be  remembered  that  unmixed  conduction  aphasia  is  not  at 
all  frequent.     It  generally  coexists  with  auditory  or  visual  aphasia. 

(5)  Mind  Blindness. — If  the  patient  can  not  understand  the  uses 
and  nature  of  seen  objects,  there  is  mind  blindness,  which  is  indica- 
tive of  a  considerable  lesion  (cortical  or  subcortical)  involving  the 
angular  gyrus  and  supramarginal  lobule,  essentially  the  same  lesion 
as  that  of  visual  aphasia  (word  blindness). 

The  Diseases  which  cause  Aphasia. — In  the  majority  of 
cases  aphasia  is  one  of  the  symptoms  of  organic  focal  cerebral  dis- 
ease, occurring  in  the  left  hemisphere  in  the  right-handed  and  ince 
versa.  It  may  be  found  in  cerebral  hemorrhage,  thrombosis,  embo- 
lism, abscess,  tumour,  or  gumma  and  depressed  fracture  of  the  skull. 
The  diagnosis  between  these  various  lesions  must  be  made  from  the 
associated  symptoms. 

More  rarely  it  has  been  noted  in  hysteria  and  neurasthenia,  and 
has  followed  an  epileptic  convulsion.  It  is  an  occasional  symptom 
in  migraine,  and  may  be  present  during  convalescence  from  exhaust- 
ing fevers,  particularly  typhoid.  Sudden  fright  has  been  considered 
as  causative  in  certain  cases. 


256  THE  EVIDENCES  OF  DISEASE 

SECTION   XXIII 
COUGH 

In  the  majority  of  cases  cough  is  a  symptom  of  disease  of  the 
larynx,  trachea,  bronchial  tubes,  lungs,  or  pleura.  Less  frequently  it 
is  due  to  disease  of  the  nasopharynx,  and  still  more  infrequently  it 
is  a  result  of  hysteria  and  disease  or  irritation  in  organs  not  forming 
a  part  of  the  respiratory  apparatus.  If  not  caused  by  disease  of  the 
respiratory  apparatus,  it  is  frequently  spoken  of  as  "  reflex  "  cough, 
which  is  a  misnomer,  cough  being  always  a  reflex  action,  "  Trans- 
ferred "  would  be  a  better  term,  and  "  extra-respiratory  "  corresponds 
more  nearly  to  the  facts. 

Cough  may  be  considered  with  reference  to  the  indications  from 
its  character,  and  also  with  reference  to  its  possible  causes. 

I.  Diagnostic  Indications  from  the  Character  of  Cough. — 
(a)  Dry  Cough. — Cough  without  expectoration  or  with  the  occasional 
expulsion  of  a  small  pellet  of  mucus  is  caused  by  the  first  stage  of 
acute  bronchitis,  pulmonary  phthisis,  bronchial  asthma,  pertussis, 
epidemic  influenza,  and  acute  pneumonia ;  pleurisy ;  diseases  of  the 
nasopharynx  and  larynx ;  inhalation  of  irritating  fumes  or  dust; 
elongated  uvula  or  enlarged  lingual  tonsil ;  foreign  bodies ;  and  "  re- 
flex "  or  extra-respiratory  conditions.  A  single,  slight,  dry  cough, 
frequently  repeated,  is  the  "  hacking  "  cough  premonitory  of  pul- 
monary phthisis. 

(Z>)  Loose  Cough. — Cough  with  expectoration  occurs  in  the  later 
stages  of  acute  bronchitis,  pertussis,  pneumonia,  pulmonary  phthisis, 
bronchial  asthma,  bronchiectasis,  and  pulmonary  gangrene. 

(c)  Paroxysmal  Cough. — Cough  coming  in  fits  or  paroxysms  is 
most  characteristically  seen  in  pertussis.  It  also  occurs  in  conditions 
attended  with  increased  secretion,  continuing  until  the  bronchial 
tubes  are  cleared,  as  in  the  second  stage  of  acute  bronchitis  and  the 
softening  stage  of  pulmonary  phthisis.  A  paroxysmal  cough  with 
a  considerable  interval  between  the  seizures  may  be  due  to  abscess 
of  the  lung,  bronchiectasis,  and  phthisical  or  gangrenous  cavities. 
Under  such  circumstances  large  quantities  are  expectorated  in  a  short 
time,  the  cough  ceasing  when  the  cavity  is  emptied  and  recurring 
when  it  refills.  A  somewhat  significant  fact  in  these  cases  is  that  the 
coughing  fit  is  precipitated  by  change  of  position.  The  inference  is 
that  a  cavity  exists,  the  contents  of  which  are  permitted  by  the 
changed  posture  to  flow  into  the  bronchial  tubes  and  thus  initiate 
the  paroxysm.  Enlargement  of  the  bronchial  glands,  mediastinal 
tumour,  and  other  extra-respiratory  lesions  will  produce  a  paroxysmal 


COUGH  25Y 

but  dry  cough.     A  coughing  fit  terminating  in  vomiting  is  of  some 
importance  as  a  symptom  in  pertussis  and  pulmonary  phthisis. 

(d)  Lary)igeal  Cough. — A  dry  cough,  variously  described  as 
"croupy,"  hoarse,  ringing,  brassy,  or  metallic  in  character,  is  that 
caused  by  laryngeal  irritation,  either  direct  or  transferred.  A  certain 
amount  of  clinical  experience  is  necessary  to  enable  one  to  appreciate 
the  fine  shades  of  difference  between  the  designated  qualities ;  but  the 
distinctions  are  real,  although  elusive  in  description. 

The  conditions  which  may  be  indicated  by  a  laryngeal  cough  are 
spasm  of  the  larynx,  laryngitis,  tuberculous  or  syphilitic  ulceration 
of  the  larynx,  inhalation  of  dust  particles  in  certain  occupations,  im- 
pacted foreign  body  in  larynx,  food  particles  entering  the  larynx  in 
pharyngeal  paralysis,  elongated  uvula,  or  enlarged  tonsils.  The 
monotonous,  croaking,  nervous  cough  of  hysteria  and  the  barking 
cough  of  puberty  are  laryngeal  in  character.  A  brassy,  metallic 
cough  arises  from  irritation  of  the  recurrent  laryngeal  branch  of  the 
pneumogastric  by  the  pressure  of  thoracic  aneurism,  cancer  of  the 
esophagus,  enlarged  bronchial  glands,  and  mediastinal  tumour. 

(e)  Suppressed  Cough. — A  voluntary  effort  to  suppress  a  cough  is 
usually  a  sign  that  the  act  of  coughing  is  particularly  painful  or 
exhausting,  as  in  pleural  inflammations  (especially  diaphragmatic 
pleurisy),  pneumonia,  pleurodynia,  acute  peritonitis,  and  abdominal 
rheumatism.  A  child  with  developed  pertussis  will  vainly  endeavour 
to  restrain  the  paroxysm  because  of  the  discomfort  experienced. 
Patients  with  acute  coryza  and  bronchitis  often  complain  that  cough- 
ing is  painful,  either  because  of  substernal  soreness  in  the  early  stages, 
or  intensification  of  pain  in  the  inflamed  accessory  nasal  sinuses  dur- 
ing the  latter  part  of  the  disease. 

(/)  Inability  to  Cough. — If  the  diaphragm  is  paralyzed,  either 
from  disease  of  the  nervous  system  or  because  of  overstretching  by 
ascites  or  abdominal  growths,  cough  becomes  difficult  or  impossible. 
Sinking  in  of  the  epigastrium  during  inspiration  is,  in  the  absence 
of  laryngeal  obstruction,  indicative  of  diaphragmatic  paralysis. 

An  oncoming  inability  to  cough,  if  it  occurs  in  the  later  stages  of 
pulmonary  disease  attended  with  profuse  secretion,  is  of  bad  omen, 
especially  if  the  retained  material  can  be  heard  rattling  in  the  tubes. 
It  is  indicative  of  extreme  prostration,  and  is  found  with  pulmonary 
phthisis,  lobar  and  broncho-pneumonia,  chronic  bronchitis,  and  pul- 
monary oedema. 

(g)  Winter  Cough. — A  cough  which  disappears  in  the  summer  and 
returns  with  the  advent  of  cold  weather  is  usually  due  to  chronic 
bronchitis,  but  may  be  significant  of  a  very  chronic  form  of  pulmo- 
nary phthisis. 


258  THE  EVIDENCES  OP  DISEASE 

II.  Summary  of  the  Causes  of  Cough. — From  the  diagnos- 
tic point  of  view  the  causes  of  cough  may  be  divided  into  two  classes  : 
(a)  Direct  or  respiratory  causes,  embracing  the  diseases  of  the  larynx, 
bronchi,  lungs,  and  pleura,  to  which  the  majority  of  coughs  will  be 
found  due;  and  (b)  indirect,  reflex,  transferred  or  non-respiratory 
causes,  including  all  others.  In  general,  although  with  some  excep- 
tions, non-respiratory  coughs  are  persistent,  spasmodic,  dry,  afebrile, 
without  pulmonary  physical  signs  and  without  impairment  of  the 
general  health. 

(a)  Direct  Causes. — It  is  unnecessary  to  recapitulate  here  the 
diseases  (including  new  growths)  of  the  larynx,  bronchi,  lungs,  and 
pleura,  all  of  which  must  be  excluded  by  means  of  the  history  and  a 
careful  physical  and  laryngoscopic  examination  before  searching  else- 
where for  a  possible  cause. 

(b)  Indirect  and  Unusual  Causes. — 1.  JVasal  Cavities. — The  va- 
rious forms  of  rhinitis  (hypertrophic,  atrophic,  and  vasomotor),  spurs 
and  deviations  of  the  septum,  nasal  polypi,  and  the  irritation  of  dry 
crusts  may  be  responsible  for  cough.  In  such  cases  sensitive  areas 
are  found  by  the  probe,  irritation  of  which  produces  cough,  and  the 
application  of  cocaine  to  the  same  areas  will  relieve  it. 

2.  Pharynx. — Postnasal  adenoid  or  lymphoid  growths  and  the 
collection  of  thick  mucus  in  the  same  locality,  acute  or  chronic 
pharyngitis  (follicular,  atrophic,  or  hypertrophic),  leptothrix,  papil- 
lomata,  elongated  uvula,  and  paralysis  of  the  palate  or  pharynx  may 
give  rise  to  cough.  In  children  a  cough  coming  on  at  night  during 
recumbency  may  be  due  to  the  trickling  of  a  free  mucous  secretion 
into  the  larynx  from  the  postnasal  space,  or  to  enlarged  tonsils  or 
long  uvula  touching  the  pharyngeal  walls. 

3.  Tongue. — Enlargement  of  the  lingual  tonsil,  which  lies  in  the 
space  between  the  root  of  the  tongue  and  the  epiglottis  (the  glosso- 
epiglottic  fossa),  is  the  cause  of  a  number  of  reported  cases  of  obsti- 
nate cough,  the  cough  disappearing  when  the  swelling  was  reduced. 

4.  Ear. — By  the  auriculo-temporal  branch  of  the  fifth  nerve  an 
irritation  may  be  conveyed  which  will  cause  cough,  as  in  that  which 
results  from  probing  or  syringing  of  the  ear,  or  from  the  presence  of 
impacted  wax  or  foreign  bodies. 

5.  Miscellaneous  Causes. — Cough  may  signify  pressure  effects 
from  enlarged  bronchial  glands,  mediastinal  tumour  or  abscess, 
thoracic  aneurism,  or  caries  of  the  dorsal  vertebrae.  It  is  a  not  infre- 
quent symptom  of  cardiac  disease,  such  as  dilatation,  hypertrophy, 
and  valvular  lesions.  "  Stomach  cough  "  is  found  at  times  in  the 
subjects  of  chronic  gastric  catarrh,  due  most  probably  to  the  low 
grade  of  accompanying  pharyngitis. 


COUGH— SPUTUM  259 

"  Liver  cough  "  may  occur  as  a  symptom  of  enlarged  liver  in  con- 
sequence of  pressure  against  the  diaphragm,  or  in  connection  with 
hepatic  abscess,  hydatids,  gallstones,  perihepatitis,  and  subphrenic 
abscess,  presumably  from  irritation  or  involvement  of  the  diaphrag- 
matic pleura.  In  a  case  of  multiple  hepatic  abscesses  observed  by 
me,  and  which  came  to  autopsy,  each  chill  heralding  the  formation 
of  an  abscess  was  accompanied  by  a  violent^paroxysm  of  cough.  An 
enlarged  or  inflamed  spleen  may  for  similar  reasons  give  rise  to  cough. 

Habitual  cough  may  be  incident  to  occupations  which  involve 
the  inhalation  of  dust  or  irritating  fumes,  and  is  not  infrequent  in 
excessive  tobacco  smokers.  The  loud  "  barking  "  cough  of  puberty 
occurs  mainly  in  boys  of  neurotic  family  affiliations  (Clark).  Denti- 
tion in  infants  and  an  inflamed  tooth  in  older  persons  will,  it  is  said, 
produce  sufficient  transferred  irritation  to  cause  a  cough.  It  has 
been  stated  that  the  cough  of  hysteria  sounds  as  if  it  was  intended 
to  attract  attention.  Aspiration  of  a  pleural  exudate  will  often  cause 
a  somewhat  violent  fit  of  coughing.  Finally,  cough  has  been  at- 
tributed, perhaps  upon  inadequate  evidence,  to  irritation  from  dis- 
ease of  the  uterus,  ovaries,  mammary  glands,  or  testicles. 


SECTION   XXIV 

SPUTUM   (INCLUDING  HEMOPTYSIS)   AND  ITS   GEOSS 

CHAEACTERS 

The  naked-eye  examination  of  the  sputum  is  made  with  refer- 
ence to  its  quantity,  consistence  and  apparent  composition,  colour, 
and  odour.  The  microscopic  examination,  which  with  reference  to 
parasitic  diseases  is  more  important  than  the  macroscopic,  is  dealt 
with  elsewhere  (Index — Sputum,  microscopic  examination  of). 

Scanty  or  Absent  Sputum. — A  small  amount  of  sputum  is  expec- 
torated in  the  first  stage  of  acute  bronchitis  and  asthma,  and  in 
laryngitis  and  pleurisy.  In  children  under  the  age  of  seven  years 
the  sputum  is  usually  swallowed  and  does  not  appear. 

Abundant  Sputum. — Almost  the  only  important  diagnostic  evi- 
dence from  the  quantity  of  sputum  relates  to  the  cases  in  which  a 
large  amount,  particularly  if  it  be  purulent,  is  expectorated  in  a 
brief  time.  In  such  cases  a  suspicion  may  be  entertained  of  the  ex- 
istence of  phthisical,  gangrenous,  or  actinomycotic  cavities,  or  a 
bronchiectasis ;  or  the  rupture  into  a  bronchus  of  an  empyema,  ab- 
scess of  the  lung,  liver,  or  kidney,  or  a  subphrenic  abscess. 


260  THE  EVIDENCES  OP  DISEASE 

Watery  or  serous  sputum,  which  may  be  blood-stained,  occurs  in 
pulmonary  oedema  and  the  catarrhal  form  of  influenza.  A  thin  and 
watery  expectoration,  partly  regurgitated  and  partly  hawked  uj), 
sometimes  in  considerable  quantity,  is  an  occasional  symptom  in  the 
gastric  disorders  of  neurotic  elderly  people. 

Viscid  Sputum. — A  thick,  viscid,  gelatinous  sputum,  adhering  to 
the  container  even  if  the  latter  is  inverted,  is  somewhat  characteristic 
of  lobar  pneumonia,  but  may  occur  also  in  phthisis,  pertussis,  and 
broncho-pneumonia. 

Mucous  Sputum. — A  diffluent,  clear  sputum,  resembling  egg  al- 
bumen and  composed  mainly  of  mucus,  is  observed  in  the  early  stages 
of  pneumonia,  bronchitis,  and  phthisis  pulmonalis,  at  the  termina- 
tion of  an  asthmatic  attack,  in  developed  pertussis,  and  pharyngitis, 
laryngitis,  measles,  influenza,  and  emphysema. 

Muco-purulent  Sputum. — A  mixture  of  opaque  yellowish  streaks 
of  pus  with  mucus  constitutes  this  variety  of  sputum.  It  is  noted 
toward  the  end  of  measles  and  pertussis,  in  resolving  pneumonia, 
phthisis,  and  subacute  or  chronic  bronchitis. 

Purulent  Sputum. — Sputum  composed  purely  of  pus  is  of  infre- 
quent occurrence,  and  when  found  is  indicative  of  the  rupture  into 
a  bronchus  of  an  abscess  of  the  lung,  liver,  or  kidney,  or  a  subphrenic 
abscess,  or  purulent  pleurisy.  An  opaque  yellow  sputum,  consisting 
very  largely  of  pus,  is  found  with  bronchiectasis,  phthisical  cavities, 
broncho-pneumonia,  and  in  chronic  or  the  later  stages  of  acute 
bronchitis. 

Frothy  Sputum. — Sputum  containing  numerous  small  air  bubbles 
may  be  noted  in  bronchitis,  broncho-pneumonia,  and  emphysema, 
but  its  most  important  association  is  with  pulmonary  oedema,  in 
which  case  it  resembles  water  made  frothy  with  soap. 

Nummular  Sputa. — If  upon  being  deposited  in  water  certain  por- 
tions of  the  sputum  sink  to  the  bottom,  because  airless,  and  assume 
a  button-shaped  or  coinlike  form,  it  is  said  to  indicate  chronic  bron- 
chitis, or  bronchiectatic  or  phthisical  cavities. 

Rusty  Sputum. — A  viscid,  rusty  sputum  is  generally  indicative  of 
a  lobar  pneumonia,  but  it  may  also  be  found  in  acute  tuberculo-pneu- 
monic  phthisis,  and  in  some  forms  of  pyaemia. 

Prune-juice  Sputum. — Expectoration  of  material  resembling 
prune  juice,  the  colour  being  due  to  altered  blood,  is  witnessed  late 
in  the  adynamic  and  septic  forms  of  lobar  pneumonia,  and  in  gan- 
grene or  cancer  of  the  lung. 

Currant-jelly  Sputum. — Sputum  of  this  character  is  found  in  can- 
cer of  the  lung,  and  has  been  reported  as  one  of  the  manifestations 
of  hysteria. 


GROSS  CHAEACTERS  OF  SPUTUM  261 

Black  Sputum. — Sputum  of  a  black  or  black-speckled  appearance 
is  found  in  persons  Avho  have  inhaled  smoke  or  coal  dust  for  long 
periods,  and  is  sometimes  present  in  gangrene  of  the  lung. 

Yellotu  or  Green  Sputum. — This  may  be  caused  by  an  abscess  of 
the  liver  which  has  ruptured  into  a  bronchus  (bile  pigment),  or  in 
some  cases  of  pneumonia  (altered  haemoglobin). 

Anchovy  Sauce. — A  dark,  brownish  sputum  is  indicative  of  a  rup- 
tured amoebic  abscess  of  the  liver,  and  the  parasites  may  be  found 
by  a  microscopic  examination. 

Fetid  Sputum. — An  offensive,  bad-smelling  expectoration  usually 
means  bronchiectases,  gangrene  of  the  lung,  phthisical  cavities  con- 
taining decomposed  material,  pulmonary  actinomycosis,  or  an  empy- 
ema or  subphrenic  abscess  discharging  into  a  bronchus. 

Sputtim  containing  shreds  or  casts  may  be  noted  in  plastic  bron- 
chitis, diphtheria  (especially  of  the  larynx),  and  rarely  in  pneumonia. 
Casts,  unless  large  and  branching,  are  more  apt  to  be  found  during 
the  microscopic  examination.  Suspicious  masses  should  be  floated 
in  water  and  unravelled  with  needles. 

Blood-streaked  Sputum. — Sputum  more  or  less  streaked  with  blood 
may  be  due  to  the  arts  of  the  malingerer  (wounding  gums  or  cheeks), 
to  violent  vomiting  or  coughing,  spongy  gums,  eroded  tonsils,  and 
slow  leakage  from  an  aortic  aneurism  through  a  small  opening  in  a 
bronchus.  It  may  be  present  as  a  sequel  of  haemoptysis  and  in  can- 
cer or  abscess  of  the  lung,  acute  broncho-pneumonia,  emphysema,  and 
plastic  bronchitis.  If  the  blood  is  dark  it  may  be  due  to  pulmonary 
infarcts.  Most  commonly  it  is  found,  lasting  for  days  or  weeks  at  a 
time,  in  the  middle  stage  of  pulmonary  phthisis. 

Hsemoptysis. — In  order  to  constitute  haemoptysis  an  appreci- 
able amount  of  pure  or  nearly  pure  blood  must  be  spat  out,  not 
merely  sputum  streaked  or  stained  with  blood.  The  amount  may  be 
small  and  continue  for  several  days  or,  as  with  the  rupture  of  an 
aneurism,  sufficiently  large  to  cause  death  in  a  short  time. 

Large  and  rapidly  fatal  haemoptysis,  fortunately  a  rare  occurrence, 
is  almost  invariably  due  either  to  a  ruptured  aneurism  or  to  the  ero- 
sion of  a  vessel  of  considerable  size  in  a  large  phthisical  cavity. 
Lesser  hemorrhages  are  caused  for  the  most  part,  in  the  order  of 
frequency,  by  pulmonary  tuberculosis,  disease  of  the  heart,  and  dis- 
ease of  the  blood  vessels. 

There  may  be  premonitory  symptoms,  such  as  dyspnoea,  cough, 
and  substernal  soreness  or  oppression,  but  in  many  cases  it  occurs 
without  warning.  A  tickling  sensation  is  felt  in  the  larynx,  and, 
with  a  slight  cough,  warm,  salty  blood  fills  the  mouth.  After  the 
hemorrhage  has  ceased,  sputum,  blood-stained  or  containing  small 
19 


262  THE  EVIDENCES  OP   DISEASE 

dark  clots,  may  be  expectorated  for  several  days.  If  the  amount  of 
blood  is  small,  the  immediate  symptoms  are  simply  those  due  to  the 
mental  shock  and  perturbation  which  usually  attend  the  attack ;  if 
large,  the  evidences  of  acute  internal  hemorrhage  {q.  v.)  are  present. 

It  is  necessary  to  exclude  the  nose,  pharynx,  larynx,  and  buccal 
cavity  as  the  sources  of  the  blood  by  a  careful  examination  for  vari- 
cosities, erosions,  and  ulcerations,  as  well  as  spongy,  bleeding  gums. 
Haemoptysis  has  been  caused  by  bleeding  varicose  veins  of  the 
lingual  tonsil  (Kinxicutt). 

The  gastric  origin  of  the  hemorrhage  may  be  eliminated  by  noting 
that  the  blood  is  coughed  up,  is  bright  red,  frothy,  and  alkaline.  On 
auscultation  of  the  chest  bubbling  rales  may  be  detected,  and  the 
sputa  are  tinged  with  blood,  while  subsequently  tarry  stools  are  excep- 
tional. The  patient  is  usually  able  to  state  whether  the  blood  is 
coughed  up  or  vomited. 

The  causes  of  hcBmoptysis  are  as  follows : 

(1)  Pulmo7iary  Disease. — In  the  majority  of  cases  haemoptysis  is 
due  to  pulmonary  tuberculosis.  It  may  be  the  first  obvious  symp- 
tom, in  which  case  it  comes  from  a  congested  area  of  the  bronchial 
mucous  membrane,  and  the  amount  lost  may  be  very  considerable, 
but  practically  never  lethal.  In  cases  which  subsequently  develop 
unmistakable  signs  of  the  disease  there  can  be  no  doubt  that  tuber- 
cles were  present  at  the  time  of  the  hemorrhage.  If  the  haemoptysis 
comes  on  at  an  advanced  period,  especially  if  cavities  exist,  it  may  be 
due  to  the  erosion  of  a  vessel  of  considerable  size,  and  prove  fatal. 
Small  recurring  pulmonary  bleedings  may  be  present  for  considerable 
periods  in  cases  of  quiescent  or  arrested  tuberculosis.  Small  haemop- 
tyses  may  occur  in  the  initial  stage  of  lobar  pneumonia  :  and  either 
small  or  large  in  bronchiectasis  and  abscess,  gangrene,  or  cancer  of 
the  lung.  It  not  infrequently  attends  the  expulsion  of  the  casts  in 
plastic  (fibrinous)  bronchitis,  or  may  be  a  preliminary  symptom  of 
the  attack.     It  has  also  occurred  with  emphysema. 

(2)  Cardiac  Disease. — A  not  uncommon  cause  of  haemoptysis,  usu- 
ally small  and  recurring,  is  pulmonary  venous  obstruction  arising 
from  valvular  disease  of  the  heart.  As  a  rule  it  occurs  late  in  the 
course  of  the  disease,  except  with  mitral  stenosis,  in  which  it  may  be 
an  early  symptom.  It  is  due  to  the  rupture  of  small  veins  or  leakage 
from  an  engorged  mucous  membrane.  It  may  be  due  to  cardiac 
hypertrophy,  especially  that  associated  with  chronic  nephritis  and 
arteriosclerosis  involving  the  branches  of  the  pulmonary  artery. 
Small  haemoptyses  may  also  be  caused  by  pulmonary  infarction  occur- 
ring with  valvular  disease  and  arising  from  embolism  or  thrombosis. 
If  the  infarcted  area  is  large  and  in  the  usual  site,  consolidation  and 


HEMOPTYSIS— THE  NECK  263 

bronchial  breathing  may  be  found  in  one  of  the  lower  lobes.     If  the 
embolism  is  septic,  abscess  or  gangrene  may  follow. 

(3)  Vascular  Disease. — A  large  and  almost  immediately  fatal 
haemoptysis  may  be  due  to  the  rupture  of  a  thoracic  or  innominate 
aneurism.  On  the  other  hand,  slight,  continued  spitting  of  blood 
may  be  the  result  of  a  small  opening  from  an  aneurism,  or  the  oozing 
of  blood  through  the  fibrinous  layers  of  the  aneurismal  sac  into  a 
bronchus.  Haemoptysis  also  occurs  in  gouty  persons  over  fifty  years 
of  age  as  a  result  of  endarteritis  affecting  the  branches  of  the  pul- 
monary artery  (Clark). 

(4)  Diseases  and  Conditions  of  the  Blood. — The  diseases  of  the 
blood  which  are  liable  to  cause  hemorrhages  elsewhere  may  also  be 
responsible  for  bleeding  from  the  lungs — i.  e.,  haemophilia,  purpura, 
scurvy,  leucaemia,  and  the  severe  anaemias,  although  this  is  rarely  the 
case  with  the  last.  Cholsemia  (jaundice)  has  been  known  to  produce 
it.  The  blood  dyscrasiae  of  the  severe  infections  may  give  rise  to 
broncho-pulmonary  bleeding,  as  in  typhus  fever,  typhoid  fever,  the 
hemorrhagic  type  of  variola,  and  the  exanthemata  in  general. 

(5)  Miscellaneous  Causes. — There  are  cases  of  haemoptysis  occur- 
ring in  young  persons  without  obvious  cause  and  not  followed  by 
pulmonary  or  other  disease.  The  third  leg  of  diagnosis,  i.  e.,  time, 
must  necessarily  decide  the  question  as  to  its  innocuous  nature  in  a 
given  case.  In  hysteria  there  may  be  spitting  of  a  bloody  fluid  of  a 
pale-red  colour,  not  pure  blood,  which  comes  in  all  probability  from 
the  mouth  or  pharynx,  and  its  occurrence  may  lead  to  an  incorrect 
diagnosis  of  phthisis  pulmonalis.  On  microscopical  examination 
cylindrical  or  ciliated  epithelial  cells  are  absent.  There  are  unques- 
tionable cases,  although  of  rare  occurrence,  in  which  the  menstrual 
flow  is  replaced  by  periodical  haemoptyses — vicarious  menstruation. 
Mediastinal  tumours  by  pressure  or  extension  may  have  blood-spit- 
ting as  a  symptom.  In  China  and  Japan  there  is  an  endemic  hae- 
moptysis due  to  the  presence  of  the  distomum  in  the  bronchial  tubes. 


SECTION   XXV 
THE  NECK 


1.  Shape. — A  short,  thick  neck  is  traditionally  associated  with  the 
apoplectic  habit.  A  long,  scrawny  neck,  with  a  projecting  larynx, 
frequently  coexists  with  the  phthisinoid  chest,  and  is  not  rarely 
significant  of  the  tuberculous  diathesis. 


264  THE  EVIDENCES  OF  DISEASE 

2.  Rigid  Neck. — Rigidity  of  the  neck,  slight  or  marked,  may  be 
due  to  disease  of  the  cervical  vertebrae,  as  in  caries  or  rheumatoid 
arthritis  affecting  the  cervical  vertebrae,  and  to  rheumatism  of  the 
cervical  muscles.  Inflammatory  disease  of  the  throat  accompanied 
by  painful  and  swollen  cervical  glands  may  interfere  with  the  free 
movement  of  the  neck.  Boils  or  carbuncles  (perhaps  diabetic)  are 
other  causes  of  inability  or  disinclination  to  move  the  neck.  (See 
also  Head,  abnormal  fixity  of.) 

3.  Prominence  of  Sterno-mastoids. — If  both  sterno-mastoids  stand 
out  in  unusually  bold  relief,  search  should  be  made  for  some  cause  of 
frequent  or  long-continued  dyspnoea,  such  as  bronchial  asthma, 
emphysema,  chronic  bronchitis,  or  cardiac  disease.  If  one  muscle  is 
prominent,  it  may  be  due  to  tonic  wryneck,  congenital  thickening  or 
tumour  of  the  muscle,  a  cyst,  or  a  tuberculous  abscess. 

4.  Clavicle. — Localized  enlargements  upon  the  clavicle,  resembling 
the  callus  resulting  from  fracture,  if  occurring  in  adults  in  the  absence 
of  trauma,  are  probably  syphilitic  nodes. 

Swelling  or  tumefaction  above  the  clavicles  is  most  commonly  due 
to  emphysema,  the  enlarged  apex  of  the  lung  rising  abnormally  high, 
or  to  myxcedema.  An  inflammatory,  semi-edematous,  brawny  swell- 
ing in  this  locality  may  be  indicative  of  that  rare  accident,  perfora- 
tion of  the  esophagus  from  malignant  disease  or  ulceration. 

5.  Thyroid  Gland. — Enlargement. — A  tumour  in  close  relation  with 
the  trachea,  and  moving  with  it  during  the  act  of  swallowing,  is  an 
enlarged  thyroid  gland.  The  enlargement  is  usually  greater  on  one 
side.  The  presence  or  absence  of  induration,  fluctuation,  pulsation, 
or  systolic  thrill  (and  murmur)  must  be  determined. 

If  fluctuation  is  found,  it  is  in  all  probability  a  fibrocyst  (simple 
goitre),  or  very  rarely  an  abscess  of  the  gland.  If  pulsation,  thrill, 
and  murmur  exist  and  the  enlargement  is  unequal  and  varying,  the 
associated  symptoms  usually  will  be  found  to  declare  it  a  case  of  ex- 
ophthalmic goitre  {q.v.).  If  the  pulsating  enlargement  is  on  the 
right  side,  the  possibility  of  its  being  either  an  innominate  aneurism 
or  a  dynamic  (neurotic)  pulsation  should  be  remembered.  A  solid, 
hard  enlargement  is  usually  a  simple  goitre,  but  may  be  due  to  ade- 
noma, cancer,  tuberculosis,  or  gumma  of  the  gland. 

The  thyroid  sometimes  enlarges  during  menstruation,  returning 
to  the  normal  size  during  the  interval.  Tumours  or  aneurism  in  the 
root  of  the  neck  and  behind  the  sternum  may  cause  thyroid  swelling, 
pressure  hindering  the  return  circulation  from  the  gland. 

Atrophied  Thyroid. — An  unusual  depression  in  the  location  of 
the  thyroid  gland,  owing  to  its  atrophy,  is  found  in  myxcedema  and 
cretinism  (congenital  or  sporadic). 


THE  NECK  265 

6.  Trachea  and  Larynx. — Inspiratory  desceiit  of  the  larynx  is  seen 
in  all  conditions  which  give  rise  to  laryngeal  stenosis  and  in  exten- 
sive pulmonary  collapse  or  consolidation,  bronchial  asthma,  and 
laboured  breathing  in  general.  Occurring  in  patients  who  are  criti- 
cally ill  it  is  usually  of  bad  omen. 

Displacement  of  the  trachea  to  one  side  or  the  other  may  be  due  to 
thoracic  aneurism,  mediastinal  tumours,  or  chronic  fibroid  phthisis. 
In  the  latter  case  it  is  drawn  to  the  affected  side  by  the  shrinking 
lung.     Aneurism  of  the  innominate  pushes  it  to  the  left. 

Tracheal  tugging,  a  valuable  sign  in  suspected  thoracic  aneurism, 
is  rarely  visible  upon  inspection.  It  depends  upon  the  fact  that  the 
arch  of  the  aorta  curves  back  over  the  left  bronchus,  and  if  an  aneu- 
rismal  dilatation  of  the  arch  is  present  each  systolic  distention  of  the 
vessel  presses  down  upon  the  bronchus,  thereby  pulling  the  trachea 
downward.  To  determine  its  presence,  stand  behind  the  patient. 
Let  him  close  his  mouth  and  raise  his  chin.  The  tips  of  the  fore- 
fingers are  then  placed  firmly  upon  either  side  of  the  cricoid,  press- 
ing upward,  when,  if  a  downward  tug  is  present,  it  will  be  detected. 

7.  Enlarged  Lymphatic  Glands  of  Neck. — If  the  lymph,  as  it 
passes  through  the  lymph  glands,  contains  toxic  or  infective  material, 
either  from  simple  inflammation,  specific  bacterial  infection,  or  malig- 
nant disease  of  the  parts  from  which  it  comes,  the  glands  enlarge. 
The  glands  of  the  neck,  because  of  the  manifold  varieties  of  disease 
which  may  occur  in  their  tributary  regions,  are  frequently  found  to 
be  enlarged,  especially  in  children.  In  the  large  majority  of  cases 
the  enlargement  is  an  acute  simple  inflammation  terminating  in 
resolution,  sometimes  in  suppuration.  Next  most  frequent  is  tuber- 
culous or  syphilitic  enlargement.  Finally,  the  increase  in  size  may  be 
due  to  the  hyperplasia  (lymphoma)  of  leucaemia  and  Hodgkin's  dis- 
ease, or  to  a  neoplasm  (especially  cancer)  secondary  to  a  focus  else- 
where. 

For  diagnostic  purposes  it  is  necessary  to  note  the  location  of  the 
enlarged  glands,  whether  the  enlargement  is  acute  or  of  long  stand- 
ing, their  consistence  (hard  or  fluctuating),  and  if  they  are  well  de- 
fined or  matted  together.  According  to  the  location  of  the  enlarged 
nodes  various  regions  should  be  examined  for  the  presence  of  a  causa- 
tive disease  (see  Fig.  46). 

(a)  The  vpper  deep  cervical  glands,  behind  the  ramus  and  at  the 
angle  of  the  jaw,  become  acutely  swollen  and  painful  to  a  varying 
degree  in  diphtheria,  follicular  tonsilitis,  scarlet  fever,  measles, 
rotheln,  varicella,  roseola  and  variola,  as  well  as  in  erysipelas,  glan- 
ders, pertussis,  suppurative  tonsilitis,  and  retropharyngeal  abscess. 

Chronic  enlargement  of  the   deep  cervical  glands,  if  they  are 


266 


THE  EVIDENCES  OF  DISEASE 


matted  together  and  tend  to  suppurate,  may  be  tuberculous ;  if 
small  and  non-suppurating,  syphilitic ;  if  large,  separate,  non-sup- 
purating, and  forming  a  part  of  similar  extensive  changes  elsewhere, 
Hodgkin's  disease  ;  rarely  leuc^mic  ;  perhaps  a  secondary  malignant 
growth,  particularly  a  sequence  of  gastric  cancer  and  sometimes  the 
only  palpable  evidence  of  the  existence  of  the  latter.  Septic  ear  dis- 
ease and  carious  teeth  may  also  cause  some  enlargements  here. 


PAROTID 

UPPER  PHARYNX 
SKIN  or  FACE 
NASAL  rOSSAC. 
(POST.PCRT.) 
ANT.  PORT,  or 
SCALP. 


SUBMAXILLARY 
SKINOt  FACE  AND    ' 

NECK. 
EXT.  EAR 
LOITER  UP 
BUCCAL  CAVITY. 
GUMS.LOI^CRJAW. 
ANT.PORTTONGUC. 


SUPRA-HYOID. 

ANT.  PORT.TQNGUE.] 
LOWER  LIP  J 


©D 


POST  AURIC  &  Ota  P 

POSTPORT.Or  SCALP. 


UPPER  DEEP  CERVIC. 

[BUCCAL    CAVITY. 
POST  PORT  TONGUE. 
TONSILS  AND  PALATE. 
LOWER  PHARYNX. 
LARYNX. 
ORBIT. 

ROOF  OFMOUTH. 
NASAL  CAVITIES. 

5UPERPIC.  CERV. 
(skin  OF  FACE  AND 

NECK 
I  SCALP 

[external  ear. 


Fig.  46. — Diagram  showing  the  various  groups  of  glands  in  tlie  head  and  neck  and  the 
regions  which  should  be  examined  to  discover  a  cause  for  enlargement  of  particular 
groups. 

(b)  The  parotid  lymph  nodes^  overlying  and  in  the  substance  of 
the  parotid  gland  in  front  of  the  ear,  are  enlarged  in  inflammatory  or 
other  disease  of  the  upper  pharynx  and  skin  of  the  face. 

(c)  The  posterior  auricular  glands,  particularly  those  lying  under 
the  upper  extremity  of  the  trapezius  (occipital),  may  become  en- 
larged as  a  result  of  syphilis  or  from  cutaneous  disease  of  the  poste- 
rior portion  of  the  scalp.     The  superficial  cervical  group  lying  above 


ARTERIES  AND  VEINS  OF  NECK  267 

the  clavicle,  between  the  sterno-mastoid  and  trapezius,  becomes  swol- 
len in  cutaneous  disease  of  the  face,  neck,  and  external  ear. 

(d)  The  submaxillary  group,  and  sometimes  the  suprahyoid,  are 
enlarged,  because  of  carious  teeth,  stomatitis,  syphilis,  mumps,  rose- 
ola, diphtheria,  and  cancer  of  the  lower  lip  or  anterior  portion  of  the 
tongue. 

8.  Condition  of  the  Arteries  in  the  Neck.— (a)  Pulsation,  abnor- 
mally visible  or  violent,  of  the  carotids  may  be  due  to  a  variety  of 
causes.  It  occurs  as  the  result  of  exertion  or  excitement.  It  may 
be  most  violent  in  anaemia  and  large  hemorrhages.  It  is  seen  in  the 
atheromatous  vessels  of  elderly  people,  in  aneurism  and  in  the  ex- 
tremely rare  cases  of  obliteration  of  the  descending  aorta.  It  may 
be  a  symptom  of  left  ventricular  hypertrophy  and  aortic  regurgita- 
tion. It  is  an  occasional  concomitant  of  fevers,  particularly  sun- 
stroke and  the  early  stage  of  variola.  It  is  not  infrequent  in  the 
cerebral  apoplexies.  Finally,  it  may  be  a  manifestation  of  exoph- 
thalmic goitre  or  be  of  neurotic  origin,  the  vessel  walls  apparently 
possessing  an  unnatural  elasticity  (dynamic  pulsation). 

In  the  majority  of  cases  excessive  carotid  pulsation  may  be  attrib- 
uted to  one  of  four  causes — atheroma,  anaemia,  aortic  regurgitation, 
or  a  general  neurosis  (neurasthenia,  hysteria)  attended  by  other  evi- 
dences of  vasomotor  instability. 

{h)  Pulsation  iti  the  episternal  notch  is  sometimes  found  as  a  nor- 
mal condition  in  old  people.  Like  excessive  throbbing  in  the  carotids 
and  abdominal  aorta,  it  is  not  infrequently  of  anaemic  or  neurotic 
origin,  in  this  case  affecting  the  innominate.  More  rarely  an  aneu- 
rism of  the  same  vessel  may  be  responsible  for  it.  Provided  it  is  well 
marked,  it  may  be  due  to  an  aneurism  of  the  transverse  arch  of  the 
aorta.  As  a  rarity  it  is  caused  by  an  abnormal  origin  of  the  right 
subclavian  to  the  left  of  the  median  line  or  an  unusually  large  thy- 
roidea  ima  artery.  The  subclavian  artery  sometimes  pulsates  with 
unusual  visibility  when  the  lung  of  the  same  side  is  retracted  or 
extensively  consolidated. 

9.  Condition  of  the  Veins  in  the  Neck. — The  jugular  veins  are 
sufficiently  large,  superficial,  and  near  the  heart,  to  afford  particular 
advantages  in  determining  the  condition  of  the  circulation  through 
the  right  heart.     The  right  jugulars  are  best  fitted  for  examination. 

It  is  desirable  to  observe  whether  the  jugular  veins  are  col- 
lapsed, distended,  or  pulsating.  If  distended,  the  external  jugular 
can  always,  and  under  ordinary  circumstances  usually,  be  seen  trav- 
ersing the  surface  of  the  sterno-mastoid.  Under  normal  conditions 
neither  the  internal  jugular  nor  its  bulb — i.  e.,  its  junction  with  the 
subclavian  vein — can   be   seen.     The   bulb  lies  directly  behind  the 


268 


THE  EVIDENCES  OF  DISEASE 


lower  end  of  the  sterno-mastoid  between  the  sternal  and  clavicular 
attachments.  If  distended,  it  becomes  apparent  as  a  small  rounded 
mass  in  this  locality  and,  if  greatly  engorged,  rises  half  an  inch 
above  the  upper  border  of  the  sterno-clavicular  articulation.     Ve- 


LAt5INUS 

THROMBOSIS  OF  = 

EMPTY  JUGULAI 

INr  PETROSAL  51NUS 

INT.  JUGULAR 


hJS, 


VALVE 
JUG.  BULB. 
INNOMINATE  VEIN. 

^''''SURVCRACAVA. 

PRESSURE  ON  THESE 
VESSELS  CAUSES  OVER- 
rULL  JUGULARS.) 

RT.AURICLE 


TRICUSPID  VALVE 

'ISUr.  CAUSES 
;STOL.  JUGULAR 
JLSATION. 


J 

Fig,  47. — Diagram  of  the  right  external  and  internal  jugulars,  showing  the  mechanism 
of  jugular  collapse,  distention,  and  pulsation. 

nous  swelling  or  pulsation  is  most  marked  when  the  patient  is  re- 
cumbent. 

(a)  A  collapsed  jugular,  the  vein  remaining  permanently  more  or 
less  empty,  even  if  pressure  is  made  upon  it  just  above  the  clavicle. 


VEINS  OF  NECK  269 

is  significant  of  thrombosis  of  the  lateral  sinus  (Fig.  47).  Sudden 
diastolic  collapse  is  seen  in  extensive  adhesive  pericarditis  (see  (c) 
below). 

{b)  Distended  or  engorged  jugulars^  without  abnormal  pulsation, 
are  seen  during  the  act  of  coughing,  or  when  the  glottis  is  closed  to 
facilitate  straining  or  lifting  efforts.  Aneurism,  especially  if  intra- 
pericardial,  and  mediastinal  tumour,  by  compressing  the  superior 
vena  cava  or  innominate  vein,  may  be  responsible  for  permanent 
overfulness.  The  various  causes  of  obstructed  pulmonary  circula- 
tion, which  may  ultimately  lead  to  tricuspid  regurgitation,  tend  to 
engorge  the  jugulars. 

(c)  Resjnratory  swelling  and  collapse  of  the  jugulars  is  under  nor- 
mal conditions  so  slight  as  not  to  be  appreciable.  But  if  engorged, 
they  collapse  noticeably  during  inspiration  because  of  the  aspirating 
power  of  the  chest  cavity,  and  swell  during  expiration  when  the 
suction  action  is  least.  This  phenomenon  is  seen  particularly  in 
asthma  and  emphysema.  It  is  inversed  in  indurative  mediastino- 
pericarditis,  because  of  the  obstruction  to  the  venous  flow  due  to 
pulling  and  bending  of  the  adherent  vena  cava  superior  by  the  act  of 
inspiration. 

(d)  Pulsating  Jugulars. — If  pulsation  of  the  jugulars  (Fig.  47) 
is  observed,  it  is  absolutely  requisite  to  determine  its  relation  to  the 
apex  beat — i.  e.,  is  it  presystolic  or  systolic — and  whether  or  not  it  is 
a  communicated  impulse  from  the  carotid  artery,  which  may  be  pres- 
ent when  the  vein  is  distended  or  the  artery  throbbing  violently.  The 
patient  should  be  requested  to  breathe  very  quietly  in  order  to  elimi- 
nate the  respiratory  oscillation,  if  present. 

Presystolic  pulsation  is  normal  and  is  seen  in  many  healthy  indi- 
viduals, especially  when  recumbent,  as  an  undulation  or  flicker  at  the 
root  of  the  neck.  It  is  caused  by  the  auricular  systole  giving  rise  to 
a  back  wave  which  stops  at  the  valve  situated  just  above  the  jugular 
bulb.  It  may  be  unusually  marked  in  anaemia  and  in  the  rare  condi- 
tion of  tricuspid  stenosis  if  the  patient  is  in  the  upright  position. 

Systolic  pulsation  is  synchronous  with  the  apex  beat  and  {^patho- 
logical. It  is  almost  invariably  due  to  regurgitation  through  an 
incompetent  tricuspid  valve.  If  the  valve  in  the  internal  jugular 
remains  competent  the  pulsation  is  seen  only  in  the  jugular  bulb,  but 
under  these  circumstances  the  vein  is  usually  sufficiently  distended  to 
render  this  valve  unable  to  close  and  the  systolic  pulsation  extends 
upward  into  the  neck. 

Sphygmographic  tracings  from  the  jugular,  both  in  health  and 
disease,  exhibit  certain  undulations  and  variations  for  which  a  per- 
fectly satisfactory  explanation  has  not  yet  been  reached.     The  dia- 


270 


THE  EVIDENCES  OP  DISEASE 


gram  (Fig.  48)  shows  all  that  is  required  for  clinical  purposes — 
viz.,  the  normal  presystolic  impulse  due  to  the  auricular  systole, 
which,  if  tricuspid  regurgitation  exists,  does  not,  as  in  health,  termi- 
nate with  the  ventricular  systole,  but  is  immediately  followed  by 
a  greater  systolic  impulse  due  to  the  latter. 


NORMAL 

PRESYSTOLIC 

PULSATION 


AUR. 
SYST. 

VENTRICULAR 
SYSTOLE 

DIASTOLE 

Fig.  48. — Diagram  showing  the  presystolic  and  systolic  jugular  pulse. 


To  determine  that  the  venous  pulsation  is  systolic  the  finger 
should  be  placed  upon  the  vein  at  the  root  of  the  neck  and  run  up- 
ward so  as  to  empty  the  vessel.  If  there  is  no  regurgitation  the  vein 
refills  slowly,  the  blood  running  into  it  from  the  small  collaterals ; 
but  if  the  tricuspid  and  jugular  valves  are  incompetent,  successive 
systolic  impulses  are  seen  rising  from  below,  and  the  vein  is  very 
shortly  again  distended  and  pulsating.  If  there  is  any  question  as 
to  the  pulsation  being  transmitted  from  the  neighbouring  carotid, 
the  finger  may  be  laid  upon  the  vein  midway  between  ear  and  clavicle, 
which,  if  the  pulsation  is  communicated,  will  cause  the  peripheral 
portion  above  to  become  more  distended  and  to  pulsate  more  strongly, 
while  the  lower  portion  collapses  and  pulsation  ceases.  But  if  the 
pulsation  is  in  the  vein  it  will  continue  as  before. 

Although,  as  stated,  a  systolic  venous  pulse  is  usually  indicative 
of  tricuspid  insufficiency  (relative  or  absolute),  it  may,  as  a  clinical 
curiosity,  be  due  to  a  patent  foramen  ovale  coexisting  with  mitral 
insufficiency,  the  regurgitant  current  passing  from  the  left  to  the 
right  auricle  and  thence  to  the  superior  cava  and  jugulars ;  or  to  the 
still  rarer  case  of  a  thoracic  aneurism  communicating  with  the  supe- 
rior cava. 


THE  EXTRExMITIES— NAILS  271 

An  additional  rare  phenomenon,  which  simulates  systolic  venous 
pulse,  is  a  sudden  diastolic  collapse  of  the  jugulars  occurring  in  cer- 
tain cases  with  extensive  pericardial  adhesions,  the  walls  of  the  heart 
contracting  with  difficulty  because  of  the  adhesions,  and  springing 
suddenly  into  diastolic  expansion,  thus  aspirating  the  venous  contents. 


SECTION  XXVI 
THE  EXTKEMITIES 

There  are  certain  signs  and  symptoms  manifesting  themselves 
largely  in  the  extremities,  which,  with  some  exceptions,  have  been 
grouped  elsewhere  (see  Index)  in  order  to  avoid  unnecessary  repeti- 
tion and  promote  better  comprehension.  These  are :  Tremor,  spasm, 
contractures,  athetoid  and  choreic  movements  of  the  extremities, 
hemiplegia,  paraplegia,  monoplegia,  wrist  and  foot  drop,  pain,  anaes- 
thesia and  its  varieties,  hypersesthesia,  paraesthesia,  condition  of  the 
joints,  and  station  and  gait. 

1.  Nails. — (a)  The  bed  of  the  finger  nail  by  its  tint  shows  excel- 
lently well  the  presence  of  general  cyanosis,  less  perfectly  the  exist- 
ence of  unaemia.  It  is  said  that  if  pressure  on  the  finger  tip  com- 
pletely exsanguinates  the  nail  bed  not  more  than  50  per  cent  of 
hjemoglobin  remains  in  the  blood. 

(b)  The  subungual  pulse,  an  alternate  paling  and  reddening  of 
the  nail  bed  corresponding  to  the  cardiac  systole  and  diastole  (capil- 
lary pulse),  is  sometimes  easily  visible,  but  often  requires  slight  pres- 
sure on  the  nail  tip  to  develop  it,  the  pale  area  produced  by  the  pres- 
sure reddening  with  each  pulse  beat.  It  is  seen  in  aortic  regurgita- 
tion, chlorosis,  anaemia,  severe  hemorrhage,  and  other  conditions  in 
which  the  peripheral  arteries  are  quickly  filled  and  as  quickly 
emptied.  The  capillary  pulse  may  also  be  seen  by  pressing  a  bit  of 
glass  on  the  inner  surface  of  the  lip,  or  in  the  red  line  caused  by 
scratching  the  skin. 

(c)  A  transverse  groove  in  the  nails,  unless  due  to  traumatism, 
usually  indicates  a  recent  acute  illness.  The  growth  of  the  nail 
from  matrix  to  end  requires  about  6  months,  and  a  rough  estimate 
as  to  the  date  of  the  illness  may  be  made  from  the  position  of  the 
groove. 

{d)  Hard,  brittle,  and  longitudinally  striated  nails  are  found  in 
gouty  individuals. 

(e)  Malformation,  fragility,  and  dryness  or  cracking  of  the  nails 


272  THE  EVIDENCES  OF  DISEASE 

may  be  due  to  injury  or  syphilis,  or  may  represent  trophic  defects 
resulting  from  nerve  injuries,  neuritis,  syringomyelia,  pulmonary 
osteo-arthropathy,  Raynaud's  disease,  and  scleroderma  affecting  the 
fingers.  Arrested  growth  of  the  nails  may  be  present  in  hemiplegia 
and  acute  infantile  paralysis.  It  may  be  demonstrated  by  spotting  a 
nail  on  each  hand  with  nitric  acid  and  comparing  the  rate  of  growth. 

(/)  A  great  hypertrophy  of  the  nails,  mainly  in  the  lateral  dimen- 
sion, without  defective  structure,  has  been  described  {megalonychosis, 
Keyes),  which  may  be  mistaken  for  acromegaly,  or  the  clubbed  fin- 
gers of  pulmonary  or  cardiac  disease,  or  pulmonary  osteo-arthrop- 
athy ;  but  they  lack  the  brittleness  and  striations  of  the  last,  the 
bone  changes  of  acromegaly  are  not  present,  and  there  is  no  long- 
standing disease  of  heart  or  lungs. 

(7i)  Ecchymoses  and  ulcers  at  the  bases  of  the  nails  may  be  pres- 
ent in  victims  of  the  chloral  habit.  An  unhealthy  ulceration  of 
long  standing  around  the  nail  {onychia)  in  a  child  may  be  due  to 
syphilis  or  the  scrofulous  diathesis. 

{i)  An  indolent  sore  near  the  nail,  whether  indurated  or  not, 
with  enlargement  of  the  lymphatic  gland  above  the  inner  condyle,  if 
occurring  in  a  physician  or  other  person  liable  to  have  been  in  con- 
tact with  syphilis,  is  probably  an  initial  lesion. 

2.  Hand  and  Fingers. — {a)  The  spade  hand,  large,  coarse, 
thick-fingered,  with  broad  nails,  is  seen  as  an  evidence  of  myx- 
cedema,  in  which  the  enlargement  affects  mainly  the  soft  parts ;  and 
of  acromegaly,  in  which  the  enlargement  affects  the  bones  (Figs.  49 
and  50). 

(5)  The  claio  hand,  also  called  ape  hand  and  mainren-griffe  (griffin 
hand),  is  a  deformity  which  occurs  in  consequence  of  paralysis  and 
atrophy  of  the  interossei  and  lumbrical  muscles.  Paralysis  of  these 
muscles  leads  to  a  dorsal  extension  of  the  proximal  phalanges  with 
flexion  of  the  others,  and  when  atrophy  takes  place  the  claw  hand 
results  (Fig.  51).  This  abnormality  suggests  the  existence  of  a 
neuritis  of  the  median  and  ulnar  nerves,  particularly  the  latter,  or 
progressive  muscular  atrophy.  Similar  deformities  may  be  due  to 
amyotrophic  lateral  sclerosis  (the  spastic  form  of  progressive  muscu- 
lar atrophy),  syringomyelia,  and,  very  rarely,  the  adult  type  of 
chronic  anterior  poliomyelitis. 

(c)  Atrophy  of  the  muscles  of  the  hand  and  forearm  occurs  not 
only  in  the  diseases  just  mentioned,  but  also  to  a  slighter  degree  in 
cerebral  paralysis,  and,  in  consequence  of  disuse,  from  rheumatic  or 
gouty  affections  of  the  hand. 

{d)  Coldness  of  the  hands  and  feet,  with  or  without  a  tendency  to 
sweating,  if  persisting  for  weeks  or  months,  is  most  commonly  due  to 


Fig.  49. — Cast  drawing  of  normal  hand  for  purposes  of  comparison. 


Fig.  50.— Spade  hand. 


Fig.  51.— Claw  hand  (Gray) 


274 


THE  EVIDENCES  OF  DISEASE 


neurasthenic  conditions,  anaemia,  chronic  digestive  disorders,  rheu- 
matic or  gouty  affections,  and  cardiac  or  pulmonary  diseases  inter- 
fering with  the  circulation.  Sudden  or  transient  coldness  of  the 
extremities  is  observed  in  many  persons,  especially  those  of  a  nervous 
temperament,  under  excitement  or  anxiety,  as  well  as  in  shock,  col- 
lapse, anginose  attacks,  hemorrhages,  and  the  premonitory  chilliness 
of  rising  fever.  It  is  necessary  to  discriminate  between  actual  lower- 
ing of  the  temperature  palpable  to  the  observer  and  a  subjective  sen- 
sation of  coldness.     The  latter  is  a  paraesthesia. 

(e)  Excessive  stveating  of  the  hands  may  be  due  to  hysteria,  pro- 
gressive muscular  atrophy,  bromidosis,  and  excessive  leucorrhoea. 

(/)  Glossy  skin,  smooth,  close  fitting  and  hairless,  is  an  evidence 
of  nutritive  disturbance  caused  by  injury  to  a  nerve,  neuritis,  or 
affections  of  the  trophic  centres. 

(g)  A  red  or  waxy  fugitive  swelling  which  does  not  pit  upon 
pressure  is  probably  an  example  of  angioneurotic  cedema. 

(h)  A  waxy  or  dusky  blue  col- 
our of  the  fingers,  followed  per- 
haps by  areas  of  dry  gangrene, 
may  be  caused  by  Raynaud's  dis- 
ease, alcoholic  neuritis,  leprosy, 
or  frostbite.  If  painless  whitlows 
form  (Fig.  52),  it  will  come  under 
the  head  of  Morvan's  disease, 
which  is  sometimes  neuritis,  in 
other  cases  the  neuritic  form  of 
syringomyelia. 

(i)  Cluhhed  fingers,  the  finger 
ends  becoming  bulbous  and  the 
nails  much  curved  longitudinally 
and  laterally,  are  seen  in  condi- 
tions which  cause  long-continued 
congestion  of  the  peripheral  veins, 
such  as  congenital  malformation 
or  acquired  valvular  disease  of  the 
heart  in  children .  Prolonged  dysp- 
noea, chronic  bronchitis,  emphy- 
sema, chronic  pulmonary  phthisis, 
old  and  extensive  pleuritic  adhe- 
sions, may  also  be  responsible  for 
this  change  in  shape.  A  similar  clubbing  is  present  in  pulmonary 
osteo-arthropathy  (Figs.  53  and  54),  but  with  this  there  are  in  addi- 
tion enlargements  of  the  ends  of  the  bones  of  both  arms  and  legs. 


Fig.  52. — Morvan's  disease. 


HAND  AND  FINGERS 


275 


{j)  Distorted  fingers^  not  merely  abnormal  positions,  but  notable 
irregular  changes  in  their  shape,  are  due  to  gout,  arthritis  deformans, 
and,  less  frequently,  to  chronic  rheumatism.     In  gout  the  deformity 


Fio.  53.— Hand  of  pulmonary  osteo-arthropathy,  due  to  chronic  bronchitis  of  thirty  years' 

standing. 


Fig.  54. — Skiagraph  of  hand  iu  Fig.  53,  aWuvc. 

is  largely  due  to  deposits  of  sodium  urate  in  and  about  the  phalangeal 
and  metacarpo-phalangeal  joints,  and  tophi  (chalky,  uratic  masses) 
are  frequently  seen.      In   arthritis  deformans  there  are  extensive 


276  THE  EVIDENCES  OP  DISEASE 

changes  in  the  articular  extremities  of  the  phalanges  (Fig.  55), 
leading  in  part  to  absorption  of  bone,  in  part  to  the  development  of 
exostoses.  Trophic  changes  and  wasting  of  muscles  may  be  present 
to  such  an  extent  as  to  give  a  close  resemblance  to  the  hand  of 
progressive  muscular  atrophy. 

In  both  gout  and  arthritis  deformans  the  fingers  may  be  deflected 
toward  the  ulnar  side  of  the  hand,  and  the  Joints  are  anchylosed  in 
varying  degrees.  The  deformities  resulting  from  one  may  closely 
resemble  those  of  the  other  so  that  a  differential  diagnosis  may  be 
difficult.  If  the  excrescences  found  are  easily  recognised  as  tophi, 
or  proved  to  be  such  by  their  superficial  seat,  or  by  ulceration  or 
incision  giving  exit  to  a  chalky  material,  the  gouty  nature  of  the 
deformity  is  settled.     Otherwise  the  discrimination  is  to  be  made 


Fig.  55. — Hands  of  arthritis  deformans.    Drawing  made  by  permission  of  Dr.  G.  R.  Hall. 

by  the  history,  and  the  presence  of  associated  symptoms  and  Joint 
changes,  or  tophi  elsewhere — e.  g.,  ear  and  great  toe. 

Heberden's  nodes,  knobby  enlargements  of  the  proximal  ends  of 
the  terminal  phalanges  (Figs.  56  and  57),  may  also  be  due  either  to 
gout  or  arthritis  deformans.  Small  vesicles,  "  crab-eye  "  cysts,  may 
form  over  the  nodes. 

In  determining  the  existence  of  enlarged  Joints  it  must  not  be 
forgotten  that  atrophy  or  wasting  of  the  soft  parts  may  cause  an 
apparent  increase  in  the  size  of  the  Joints. 

(j'c)  A  flexed  finger  may  be  due  to  the  contraction  of  a  scar  re- 
sulting from  a  burn  or  a  felon,  but  if  a  dense  ridge  is  found  pass- 
ing from  the  palm  to  the  finger,  not  of  traumatic  origin,  it  is  a  case 
of  Dupuytren's  contraction  (of  the  palmar  fascia).     The  patient  is 


HAND  AND  FINGERS  277 

usually  under  the  erroneous  impression  that  it  is  a  contracted  ten- 
don.    The  contraction  may  be  of  gouty  origin,  although  there  is 


Fio.  56. — Hand  showing  Heberden's  nodes. 


Fig.  57. — Skiagraph  of  liand  in  Fig.  56,  above. 

some  basis  for  considering  it  to  be  a  neurogenic  condition.     (See 
also  Contractures.) 
20 


278  THE  EVIDENCES  OF  DISEASE 

(l)  Scleroderma. — Here  may  be  mentioned  the  hand  of  sclero- 
derma, in  which  the  skin  becomes  thickened  and  firmly  fused  to 
the  subcutaneous  tissues.  The  skin  is  glossy,  dry,  and  smooth,  and 
because  of  its  tense,  unyielding  character  the  fingers  and  hands 
become  immovable.  The  disease  (probably  a  trophic  neurosis)  may 
affect  localized  portions  of  the  body  or,  less  commonly,  be  diffused 
over  the  entire  surface. 

(m)  Handwriting. — Total  inability  to  write  may  be  due  to  apha- 
sia {q.  v.),  mental  defects,  and  lack  of  education. 

Indistinct  or  illegible  writing  may  indicate  carelessness,  gouty 
or  rheumatic  hands,  writer's  cramp,  or  the  tremor  of  old  age,  dis- 
seminated sclerosis,  alcoholism,  general  paralysis,  or  coarse  cerebral 
lesions.  "  Mirror  writing,"  in  which  words  are  written  from  right  to 
left  and  reversed,  as  if  seen  in  a  mirror,  may  be  a  result  of  some  cere- 
bral lesions,  deficient  mental  development,  and  perhaps  hysteria. 

3.  Arm. — (a)  (Edema  of  one  arm  and  hand  may  be  the  result  of 
a  tumour  of  the  mediastinum  or  lung,  aneurism  of  the  arch  of  the 
aorta,  innominate  (right  arm)  or  axillary  artery,  thrombosis  of  the 
axillary  vein,  enlargement  of  the  axillary  glands,  or  trichiniasis. 

(Z>)  A  slow  enlargement  of  the  loiver  ends  of  both  radial  bones  in 
a  weak  or  poorly  fed  child  is  probably  due  to  rachitis,  and  confirma- 
tory evidence  may  be  found  in  other  regions. 

(c)  Circumscribed  bony  swellings  of  long  duration  on  the  sub- 
cutaneous surface  of  the  ulna  are  syphilitic  nodes.  Eecent,  round, 
and  superficial  indurated  swellings  in  the  same  locality,  with  a  mot- 
tled or  bruised  appearance  of  the  skin,  are  the  lesions  of  erythema 
nodosum,  which,  however,  occurs  more  commonly  over  the  tibia. 
Painless,  non-inflammatory,  circumscribed  indurations  about  the 
elbow  are  probably  gummata. 

{d)  Pain  and  tenderness  over  the  head  of  the  radius^  with  restric- 
tion in  the  movement  of  the  joint,  is  sometimes  observed  after  over- 
use of  the  arm. 

(e)  Stiffness  and  pain  in  the  shoulder  joint,  increased  by  damp 
weather,  and  occurring  as  a  rule  in  an  elderly  person,  is  a  rheumatic 
inflammation  of  the  ligaments ;  but,  if  accompanied  with  an  ina- 
bility to  elevate  the  arm,  it  may  be  due  to  neuritis  of  the  circumflex, 
nerve. 

(/)  Enlargement  of  the  humerus,  radius,  or  ulna  of  a  chronic 
nature,  accompanied  by  constant  deep-seated  pain  which  increases  at 
night,  may  be  due  to  syphilitic  periostitis. 

{g)  If  the  humerus  becomes  acutely  swollen  or  painful  during  the 
course  of  typhoid  fever  or  scarlatina,  it  is  an  acute  periostitis  whick 
may  eventuate  in  necrosis  and  abscess. 


FOOT  AND  LEG 


279 


4.  Foot  and  Leg. — (a)  CEdema  {q.  v.)  of  both  lower  extremities 
arising  from  general  conditions  is  described  elsewhere,  but  oedema 
of  one  leg  only  may  be  due  to  thrombosis  of  the  femoral  vein  or 
varicose  veins  of  the  leg.  Unilateral  oedema  may  accompany  rheu- 
matic or  gouty  inflammation  of  the  foot. 

(b)  Enlarged  glands  in  the  groin  occur  in  two  main  groups — one 
along  Poupart's  ligament,  the  other  over  and  around  the  saphenous 
opening.  Their  loca- 
tion and  the  areas 
drained  by  them  are 
shown  in  Fig.  58. 

Acute  swelling  (ad- 
enitis) results  from 
the  virus  of  chancroid, 
gonorrhoea,  and  syph- 
ilis. Enlargements 
due  to  the  last-named 
disease  are  usually 
small,  hard,  and  pain- 
less. There  is  a  rare 
acute  adenitis  occur- 
ring in  the  course  of 
acute  articular  rheu- 
matism, which  yields 
to  the  salicylates. 

Ch  ron  ic  swellings 
may  be  tuberculous, 
secondary  to  tubercu- 
lous disease  in  the  hip 
or  knee,  but  a  simple 
adenitis  due  to  inter- 
trigo, eczema,  or  vari- 


Poupart's  Ligament  Group 

Perinaeum 

Genitalia 

Buttocks  (.internal  aspect) 

Lumbar  region 


Saphenous  Group 

Foot 

Knee 

Leg 

Buttocks  (external  aspect) 


Fig.  58. — Diagram  of  the  gland 
groups  iu  tlie  groiu,  and  the 
regions  which  should  be  ex- 
amined lor  sources  of  infec- 
tion when  these  glands  arc 
enlarged. 


cose  ulcer  may  become  tuberculous.  The  enlarged  glands  may 
be  a  part  of  Hodgkin's  disease,  in  which  case  similar  changes  will 
be  found  elsewhere.  In  tertiary  bone  or  genital  syphilis  the  in- 
guinal glands  may  undergo  gummatous  changes,  but  this  is  ex- 
tremely infrequent.  Malignant  disease  of  the  genitalia,  especially 
epithelioma  and  carcinoma,  may  secondarily  invade  these  glands, 
and  they  are  not  infrequently  affected  in  gastric  cancer.  Very  sel- 
dom they  may  enlarge  because  of  the  presence  of  parasites,  echino- 
coccus,  cysticercus,  and  Filaria  sanguinis  hominum.  Aside  from 
glandular  disease,  swellings  in  the  groin  may  be  due  to  femoral  aneu- 
rism, retained  testicle,  and  a  small  incarcerated  hernia,  the  latter 


280  THE  EVIDENCES  OP   DISEASE 

sometimes  of  great  importance  as  a  possible  explanation  of  abdomi- 
nal pain  or  the  symptoms  of  intestinal  obstruction.  A  fluctuating 
swelling  at  the  apex  of  Scarpa's  triangle,  internal  to  the  femoral  ves- 
sels, may  be  a  psoas  abscess. 

(c)  The  femoral  artery  in  elderly  emaciated  individuals  may  be 
thickened  and  rigid.     Under  these  circumstances  it  may  pulsate  so 


Fig.  59. — Syphilitic  disease  of  the  tibia,  showing  the  sabre-like  deformity,  in  a  boy  nine 

years  old  (Holt). 

visibly  as  to  simulate  aneurism.  On  the  other  hand  pulsation  may 
be  absent  because  of  closure  of  its  lumen  by  the  arteritis  which  is 
present,  gangrene  occurring  as  a  sequel. 

{d)  Chronic  painful  enlargement  of  the  tibia,  the  pain  being 
worse  at  night,  with  a  somewhat  characteristic  deformity  (Fig.  59), 
is  a  sypMlitic  periostitis^  late  hereditary  if  occurring  in  a  child, 
tertiary  in  the  adult. 

{e)  Eedness,  heat,  and  oedema  of  thigh  or  anterior  and  inner  as- 


FOOT  AND  LEG  281 

pect  of  the  leg,  occurring  with  a  rise  of  temperature  in  the  course 
of  the  acnte  specific  fevers,  may  be  an  acute  periostitis  of  femur  or 
tibia,  with  sequent  suppuration  and  necrosis. 

(/)  Curvatures  of  the  leg  bones  are  most  commonly  due  to  ra- 
chitis, but  also  occur  in  osteitis  deformans,  mollities  ossium,  and  cre- 
tinism. Shortening  of  one  leg  may  be  the  result  of  tuberculous  dis- 
ease of  the  hip  or  an  old  infantile  paralysis. 

{g)  JVodes,  small  circumscribed  bony  growths  situated  upon  the 
tibia,  are  tertiary  syphilitic  manifestations.  Reddened  or  bruised- 
looking  patches,  having  a  nodelike  feeling  on  palpation,  are  probably 
the  manifestations  of  erythema  nodosum,  but  scurvy  and  the  various 
forms  of  purpura  should  not  be  overlooked  as  a  possible  explanation. 
Painless,  non-inflammatory  indurations  scattered  over  the  leg  may 
be  gummata,  some  of  which  may  subsequently  ulcerate.  Multiple 
annular  ulcers,  nearer  the  knee  than  the  ankle,  are  probably  tertiary 
syphilitic  lesions. 

(//)  An  abnormal  increase  in  the  size  of  the  calves  in  a  child, 
combined  with  difficulty  in  walking  and  going  upstairs,  owing  to 
weakness  of  the  apparently  hypertrophied  muscles,  is  noted  in  pseudo- 
hypertrophic muscular  paralysis. 

(i)  Atrophy  of  the  anterior  and  outer  muscles  below  the  knee  is 
a  symptom  of  the  rather  uncommon  peroneal  type  of  progressive  mus- 
cular atrophy. 

( /)  Varicose  veins  of  the  leg  may  be  significant  of  excessive  stand- 
ing, faBcal  accumulation,  abdominal  tumours,  pregnancy,  or  other 
conditions  interfering  with  the  return  circulation.  The  making  of 
an  abdominal  examination  in  cases  of  varicose  veins  of  the  leg  may 
be  the  means  of  avoiding  a  mortifying  mistake. 

{k)  A  painful  oedema  and  congestion  of  the  leg  and  foot,  with  a 
knotty  condition  of  the  veins  behind  the  internal  malleolus,  in  a 
gouty  individual,  may  be  due  to  phlebitis  of  the  deep  veins  of  the  leg. 

{I)  Perforating  ulcer  of  the  foot,  occurring  with  locomotor  ataxia, 
and  rarely  with  diabetes,  presents  itself  as  a  deep,  circular  lesion,  usu- 
ally under  the  great  toe,  and  often  leads  to  necrosis  of  the  bones. 

{m)  Redness  and  swelling  confined  to  the  surface  of  the  metatarso- 
phalangeal joint  of  the  great  toe  may  be  of  gouty  origin,  or  a  bursitis 
arising  from  shoe  pressure  upon  a  deformed  joint.  In  the  latter  case 
the  attack  is  not  sudden,  and  there  is  no  constitutional  disturbance. 

{n)  Gangrene  of  the  foot,  beginning  in  the  toes,  is  most  frequently 
a  consequence  of  diabetes  or  disease  of  the  arteries  in  elderly  persons 
(dry,  senile  gangrene).  Less  often  it  is  a  result  of  the  embolism  of 
cardiac  disease  and  thrombosis  due  to  the  specific  infections,  espe- 
cially enteric    fever  and   scarlatina.     Raynaud's   disease,   and   very 


282 


THE  EVIDENCES  OF  DISEASE 


rarely  exoplithalmic  goitre,  may  give  rise  to  gangrene  of  the  toes  or 
localized  patchy  spots  of  necrosis.  Ergotism,  trauma,  and  frostbites 
are  other  causes  which  may  be  responsible  for  this  condition. 

(o)  Burning  pain  in  the  sole  of  the  foot,  with  a  mottled,  dusky 
redness,  both  of  which  are  made  worse  by  walking  and  relieved  by 
elevating  the  limb,  constitute  erythromelalgia,  or  red  neuralgia  of  the 
feet. 

{p)  Abnormal  size,  distortion,  atrophy,  clubbing,  and  contractures 
affecting  the  feet  and  toes,  as  well  as  changes  in  the  toe  nails,  are, 
when  found,  due  in  the  main  to  the  same  causes  which  produce  simi- 
lar changes  in  the  upper  extremities — viz.,  disease  of  joints,  acromeg- 
aly, myxoedema,  pulmonary  osteo-arthropathy,  hysteria,  locomotor 
ataxia,  Friedreich's  ataxia,  anterior  poliomyelitis,  cerebral  paralysis, 
progressive  muscular  atrophy,  and  multiple  neuritis. 

{q)  Clubfoot  and  Flat  Foot. — These  deformities  are,  as  a  rule,  con- 
genital, but  may  result  from  a  previous  infantile  paralysis  (anterior 
poliomyelitis).  The  history  usually  determines  this  point,  but  it 
may  be  borne  in  mind  that  if  the  deformity  is  paralytic  the  limb 
is  usually  atrophied,  the  muscles  are  flaccid,  and  the  deformity  may 
be  temporarily  reduced  without  much  difiiculty.     The  varieties  are : 

Pes  (or  talipes)  equinus,  in  which  there  is 
a  drawing  up  of  the  heel  so  that  the  patient 
walks  upon  the  ball  of  the  toes  or  even  upon 
the  dorsum  of  the  foot  (Fig.  60) ;  or,  as  in  a 
second  variety  vrith  a  nearly  normal  position 
of  the  heel,  there  is  a  sharp  dropping  of  the 
front  portion  of  the  foot.  This  may  occur  in 
pseudo-hypertrophic  paralysis.  There  is  also 
a  slight  deformity,  caused  by  contraction  of 
the  plantar  fascia  from  arrested  growth  of  the 
latter,  as  a  remote  result  of  anterior  poliomye- 
litis. The  tarsal  arch  is  exaggerated,  the  dis- 
tance between  the  ball  of  the  foot  and  the 
heel  is  lessened,  the  proximal  phalanges  are 
extended,  and  the  terminal  phalanges  flexed. 
The  deformity,  as  a  whole,  bears  some  resem- 
blance to  the  claw  foot. 

Pes  varus  is  an  inversion  of  the  foot,  so 
that  the  patient  walks  upon  its  outer  border 
(Fig.  61). 

Pes  valgus  is  an  eversion  of  the  foot,  so 
that  the  bones  on  the  inner  side  of  the  knee  and  ankle  are  abnor- 
mally prominent,  and  the  arch  of  the  foot  is  lost.     It  is  an  exag- 


FiG.  60. — Pes  equinus. 


KERNIG'S  SIGN 


283 


gerated  flat  foot  (pes  planus).  The  latter  is  quite  frequently  respon- 
sible for  a  painful  condition  of  the  heel  or  sole  of  the  foot  for  which 
gout,  rheumatism,  or  other  causes  of  painful  feet  may  have  been 
held  responsible. 

Pes  calcaneus  (usually  with  valgus),  the  foot  being  drawn  up  to 


Fio.  61. — Pes  varus. 


Fig.  62. — Pes  calcaneus. 


the  leg  by  contraction  of  the  extensors  and  everted,  the  patient  walk- 
ing upon  the  inner  side  of  the  heel  (Fig.  62),  is  one  of  the  unusual 
deformities  resulting  from  infantile  paralysis,  and  may  exist  in  con- 
nection with  spina  bifida. 

(r)  Kernig's  Sign. — In  order  to  elicit  this  sign  (recently  studied  by 
Herrick)  the  thigh  must  be  placed  at  a  right  angle  to  the  body,  the 
patient  lying  upon  the  side  or,  better,  upon  the  back.  The  same 
object  can  be  accomplished  by  having  him  sit  upon  the  edge  of  the 
bed,  thighs  horizontal,  legs  hanging  vertically  downward.  An 
attempt  is  then  made  to  extend  the  leg,  thus  bringing  it  in  a  line 
with  the  thigh.  If  meningitis  is  present,  it  will  be  diflBcult  or  impos- 
sible to  extend  the  leg  because  of  the  presence  of  a  marked  flexor 
contracture  (of  the  hamstring  muscles),  and  the  procedure  is  often 
painful.  In  delirious  patients  gentle  but  persistent  traction  must  be 
used  before  the  muscles  yield ;  but,  if  a  true  Kernig's  contraction 
exists,  the  muscles  do  not  give  way  even  to  a  long-continued  steady 
effort,  and  if  the  patient  is  in  the  dorsal  position  the  pelvis  may 
generally  be  lifted  from  the  bed  without  causing  the  leg  to  extend. 

It  is  necessary  to  exclude  sciatica  in  particular,  and  old  contrac- 
tures, as  well  as  disease  of  the  knee  or  hip  joint  and  myositis.  This 
sign  is  present  in  from  80  to  90  per  cent  of  cases  of  meningitis,  or 
cerebro-spinal  fever.  It  is  a  differential  symptom  of  much  value,  as 
it  is  only  exceptionally  present  in  other  diseases. 


284  I'HE   EVIDENCES  OF   DISEASE 

SECTION   XXVII 
THE  BACK 

The  back  should  be  examined  for  curvatures  of  the  spinal  column, 
prominence  of  spinous  processes  or  scapulae,  swellings,  and  stiffness. 
(For  pain  and  tenderness  in  the  back,  see  Index.) 

(a)  Kyphosis. — A  posterior  curvature  of  the  spine  with  the 
convexity  directed  backward  (kyphosis)  is  seen  in  many  elderly  per- 
sons, especially  in  the  dorsal  region,  and  it  forms  a  part  of  the 
changes  which  constitute  an  emphysematous  chest.  A  kyphotic 
condition  of  the  spine  may  be  present  in  a  rachitic  child  or  in  old 
or  young  persons  who  are  weakened  by  acute  or  long-continued  ill- 
ness. These  posterior  curvatures  are  to  be  distinguished  from  the 
more  or  less  sharply  angled  kyphosis  of  Pott's  disease  of  the  spine 
and  mollities  ossium  localized  in  the  cervical,  dorsal,  or  lumbar 
region.  In  some  patients,  children  in  particular,  there  is  a  some- 
what unusual  but  normal  prominence  of  the  7th  cervical  {vertebra 
prominens)  or  8th  and  9th  dorsal  spinous  processes. 

{h)  Scoliosis. — A  lateral,  in  reality  a  rotary-lateral,  curvature 
of  the  spine  (scoliosis),  with  prominence  of  one  scapula,  is  wit- 
nessed most  frequently  in  girls  from  8  to  15  years  of  age.  It  may 
indicate  unequal  length  of  the  lower  extremities  ;  the  habit  of  stand- 
ing habitually  on  one  leg  or  carrying  weights  on  one  arm ;  muscular 
weakness  from  fever  or  anaemia ;  and  general  debility,  congenital  or 
acquired.  Its  most  common  cause  is  rachitis.  It  may  also  result 
from  the  tilting  of  the  pelvis  in  old  sciatica,  paralysis  due  to  anterior 
poliomyelitis  and  cerebral  paralysis,  and  mollities  ossium.  It  is  not 
infrequently  encountered  as  a  result  of  the  contraction  of  one  lung 
after  a  pleurisy  or  an  empyema. 

(c)  Lordosis. — An  unnatural  curvature  of  the  spine,  with  the 
convexity  looking  forward  (lordosis),  when  found,  is  usually  in  the 
lumbar  region,  and  is  indeed  an  exaggeration  of  the  normal  curve  in 
this  locality.  It  may  be  due  to  the  dragging  weight  of  pregnancy, 
ascites,  and  all  large  abdominal  tumours.  It  is  apt  to  occur  in  the 
course  of  pseudo-muscular  hypertrophy. 

{cl)  Prominent  Scapulae. — If  both  scapulae  are  abnormally 
projecting,  it  is  probable  that  the  patient  has  an  alar  or  pterygoid 
chest.  If  one  scapula  projects,  it  indicates  the  existence  of  lateral 
curvature  and  its  existing  causative  conditions ;  or  paralysis  of  the 
serratus  magnus  on  that  side  (Fig.  63).     If  the  left  scapula  projects. 


THE  BACK 


285 


it  is  possibly  due  to  an  aneurism  of  the  arch  of  the  aorta  which  has 
bulged  out  the  left  interscapular  region. 

(e)  Lumbar  Bulging.— A  swelling  in  the   posterior  lumbar 
region  on  one  or  the  other  side  of  the  spinal  column,  either  solid, 
fluctuating,  or  edematous, 
may  be  due  to  malignant 
disease  of  the  kidney,  pyo- 
nephrosis or  hydronephro- 
sis,  hydatids  of    the   kid- 
ney, perinephritic 
abscess,  or  an  ab- 
scess     connected 
with  caries  of  the 
spine.    In  the  lat- 
ter case    there   is 
usually  a  coexist- 
ing   angular    ky- 
phosis. 

(/)  Stiff  Back.— Stiff- 
ness and  lack  of  mobility 
in  flexion,  extension,  and 
lateral  bending  of  the  spine, 
with  or  without  pain  in  so 
doing,  may  be  caused  by 
muscular  rheumatism(lum- 
bago)  or  strain  of  the  back 
muscles,  arthritis  deformans,  or  a  tonic  spasm  of  the  muscles,  as  in 
opisthotonus. 

Chronic  stiffness  or  anchylosis  of  the  vertebral  column  without 
involvement  of  other  joints,  except,  perhaps,  those  of  the  hip  and 
shoulder,  may  be  due  to  injury.  Pott's  disease,  chronic  or  gonorrhoea! 
rheumatism,  paralysis  agitans,  arthritis  deformans,  or  certain  laborious 
occupations.  Two  other  varieties  of  chronic  spondylitis  have  been 
described,  which  are  believed  by  some  authors  to  be  special  types  of 
disease,  and  dependent  on  other  causes  than  those  just  mentioned. 

The  first  is  the  so-called  spondylitis  rhizomelia  (StrCmpell-Marie). 
The  disease,  which  attacks  men  only,  at  or  beyond  middle  age,  begins 
usually  in  the  hip  joints,  which  become  anchylosed,  the  process  sub- 
sequently extending  to  the  spine  and  the  shoulder  joints,  very  rarely 
to  the  knee  joints.  The  spine  becomes  rigid,  and  there  is  kyphosis, 
usually  not  very  marked.  The  dorsal  and  gluteal  muscles  are  atro- 
phied, and  exostoses  are  found  upon  the  vertebrae  and  sacral  bones. 
There  is  but  little  pain  attending  the  process. 


Fig.  63. — Paralysis  of  the  serratus  magnus 
(Leszyusky). 


286  THE  EVIDENCES  OF   DISEASE 

In  the  second  type  (Bechterew-Marie)  the  trouble  begins  in  the 
spine,  which  becomes  anchylosed  and  kyphotic,  the  shoulders  stoop, 
the  head  is  lowered  and  carried  forward,  and  there  is  much  intercos- 
tal pain.  The  hip  and  shoulder  joints  are  slightly  if  at  all  affected. 
The  disease  is  often  hereditary. 

Dana,  who  has  made  a  careful  study  of  the  subject,  believes  that 
these  two  conditions  are  not  special  maladies,  but  that  the  first  is  a 
form  of  arthritis  deformans,  and  the  second  either  arthritis  defor- 
mans or  syphilitic  meningitis. 

(g)  Swellings. — A  rounded  congenital  tumour  in  the  middle 
line,  especially  if  translucent  and  reducible,  and  associated  with  club- 
foot or  hydrocephalus,  is  a  spina  bifida.  Fluctuating  swellings,  cer- 
vical, dorsal,  lumbar,  or  sacral,  may  be  abscesses  in  connection  with 
disease  of  the  vertebrae  or  sacro-iliac  joint.  A  fatty  tumour  (lipoma), 
unless  lobulated,  may  simulate  an  abscess,  and  require  aspiration  for 
a  differential  diagnosis.  An  unusual  case  seen  in  consultation  was 
that  of  a  suppurating  dermoid  cyst  anterior  to  the  sacrum.  The  pus 
worked  its  way  outward  through  the  greater  sacro-sciatic  foramen, 
causing  a  typical  sciatica,  for  which  it  was  mistaken  until  a  fluctuat- 
ing swelling  appeared  in  the  buttock.  Two  radical  operations  re- 
sulted in  recovery.  A  red,  brawny  swelling,  usually  in  the  cervical 
region,  discharging  pus  by  one  or  more  openings,  is  a  carbuncle,  and 
when  found  requires  an  examination  of  the  urine  for  sugar. 


SECTION   XXYIII 

THEORY    AXD    PEACTICE    OF    PALPATION,  AUSCULTA- 
TION, AXD   PERCUSSION 

I.    PALPATION 

Palpation,  the  use  of  the  tactile  sense  of  the  hand  and  fingers,  is 
an  indispensable  means  of  obtaining  information.  The  remarkable 
extent  to  which  the  "  educated  touch  "  may  be  developed  is  exemp- 
lified in  many  physicians. 

In  the  practice  of  palpation  care  should  be  taken  to  keep  the  nails 
short.  The  hands  should  always  be  warmed  before  touching  the  pa- 
tient. Neglect  of  these  points  may  seriously  impair  the  usefulness 
of  the  practitioner.  All  rough  or  abrupt  pressure  should  be  avoided. 
The  hand  at  first  should  be  laid  flat  upon  the  part ;  later  the  fingers 
and  their  tips  may  be  employed  to  determine  and  localize  more 
accurately  any  discoverable  abnormality.  If  palpating  deep-seated 
organs,  or  if  there  is  a  large  amount  of  overlying  fat  or  fiuid,  the 


PALPATION— PERCUSSION  287 

palpating  hand  may  be  usefully  re-enforced  by  pressing  upon  it  with 
the  other,  thus  sparing  the  palpating  hand  much  muscular  exertion, 
and  leaving  unimpaired  its  power  of  tactile  appreciation. 

When  palpating,  the  points  to  be  determined  with  reference  to 
the  part  or  organ  are  : 

Shape. — Rounded,  ovoid,  irregular,  nodular. 

iSize. — Hazelnut,  almond,  English  walnut,  lemon,  orange,  foetal 
iiead,  etc. 

Consistence. — Hard,  soft,  edematous,  brawny. 

Movable. — Freely,  slightly,  with  or  not  with  respiration. 

Tenderness. — Slight,  marked,  deep-seated,  superficial. 

Fluctuation. — The  undulation  of  an  inclosed  fluid  produced  by 
the  pressure  of  the  finger,  and  appreciated  by  another  finger  placed 
on  the  opposite  side  of  the  inclosing  cavity. 

Fremitus. — Vibrations  originating  in  the  larynx  during  phonation, 
and  transmitted  through  the  trachea,  bronchi,  and  lung  substance  to 
the  surface  of  the  chest. 

Pulsations. — Character  and  locality  noted. 

Thrill. — Vibrations  originating  in  the  heart  or  blood  vessels,  and 
transmitted  to  the  surface. 

II.    PERCUSSION 

(1)  Theory  of  Percussion. — If  any  portion  of  the  body  is 
sharply  struck  by  the  finger,  the  part  tapped  either  resounds  to  the 
impact  or  gives  out  a  dead,  non-resonant  sound,  like  that  resulting 
from  percussion  of  a  mass  of  moist  clay.  Resonance  upon  percussion 
shows  that  the  part  percussed  is  so  constructed  that  it  is  able  to  vibrate 
with  some  regularity,  whereas  a  non-resonant  (dull)  sound  is  due  to 
an  almost  entire  lack  of  such  power.  The  term  "  clear  "  is  employed 
as  a  synonym  for  "  resonant."  Resonance,  therefore,  has  some  of  the 
characters  of  a  musical  tone,  the  latter  consisting  of  a  series  of  uni- 
form and  regular  vibrations,  while  the  dull  sound,  not  arising  from 
regular  vibrations,  is  technically  a  noise.  The  structures  of  the  body 
which  resound  when  perciissed  are  the  bones  and  the  air-containing 
organs.  Bone  tissue  is  sufficiently  elastic  to  vibrate  when  struck. 
The  air  in  the  hollow  or  air-containing  viscera  vibrates  rhythmically 
when  percussed,  and  the  vibrations  are  increased  or  diminished  by 
the  degree  of  tension  of  the  containing  walls. 

Bone  (or  osteal)  resonance  has  a  character  of  its  own^-e.  g.,  per- 
cussion of  the  sternum  or  cranium.  As  there  are  wide  differences  in 
the  size,  complexity,  and  tension  of  the  air  cavities  in  the  organs 
containing  air  (stomach,  intestines,  lungs),  the  character  of  the  per- 
cussion sound  or  note  is  often  quite  distinctive.    The  stomach  cavity 


288  THE  EVIDENCES  OF   DISEASE 

is  large  and  simple,  and  emits  a  drumlike  (tympanitic)  sound,  while 
the  lung,  with  its  complicated  arrangement  of  multitudinous  air  cells 
and  tubes,  affords  a  percussion  note  (pulmonary  resonance)  the 
quality  of  which  is  easily  recognisable  by  experience.  There  is  little 
to  be  gained  by  the  recognition  of  osteal  resonance  except  to  avoid 
confusing  it  with  air  resonance.  Practically,  percussion  is  employed 
to  determine  whether  there  is  more  or  less  than  the  normal  amount 
of  air  in  an  air-containing  organ,  as,  for  instance,  in  emphysema  or 
consolidation  of  the  lung ;  or  to  delimit  the  borders  of  adjacent  air- 
less and  air-containing  viscera — e.  g.,  liver,  lung ;  or  contiguous  air- 
containing  organs — e.  g.,  lung,  stomach.  The  line  of  contact  between 
two  contiguous  airless  organs  can  not  be  located  unless  by  a  very 
slight  change  in  the  quality  of  the  sound,  the  dull  percussion  sound 
over  one  being  continuous  with  that  over  the  other — e.  g.,  heart,  liver. 
One  also  detects,  by  lack  of  resonance,  the  possible  interposition  of 
fluid  or  tissue  between  the  percussed  surface  and  an  underlying  air- 
containing  organ,  as  in  pleural  effusion  or  thickening. 

(2)  Practice  of  Percussion.— (a)  Teclmic. — The  plessor  or 
striker  may  be  a  small  hammer,  or,  as  is  commonly  the  case,  a  finger 
may  be  used.  The  blow  may  be  received  upon  the  percussed  surface 
with  nothing  interposed  to  modify  the  stroke  (direct  or  immediate 
percussion),  or  a  pleximeter  may  be  employed  (indirect  or  mediate 
percussion).  Pleximeters  are  made  in  the  shape  of  a  pillar  or  plate 
of  metal,  glass,  rubber,  or  celluloid. 

With  regard  to  the  choice  of  methods  it  is  probable  that,  as  in 
other  lines  of  work,  each  practitioner  will  by  a  process  of  selection 
evolve  a  procedure  which  fits  best  to  his  special  manner  of  work. 
Personally  the  middle  finger  of  the  right  hand  is  the  best  plessor, 
and  the  middle  finger  of  the  left  hand  the  best  pleximeter.  The 
finger  pleximeter  adapts  itself  smoothly  to  the  surface  under  exami- 
nation and,  as  an  additional  and  valuable  advantage,  is  able  to  ap- 
preciate the  resistance  of  the  underlying  structures.  Sansom's  plex- 
imeter {q.  V.)  is  to  be  excepted  as  an  important  aid  in  outlining  the 
exact  limits  of  the  entire  cardiac  dulness — i.  e.,  the  size  of  the  heart. 

The  pleximeter  finger  having  been  laid  firmly  and  smoothly  upon 
the  surface  to  be  percussed  and  adapted  to  its  inequalities,  the  stroke 
is  delivered  upon  the  middle  phalanx  of  the  finger  by  the  plessor 
finger,  its  tip  striking  vertically  upon  the  pleximeter  finger.  The 
blow  should  be  given  by  a  quick,  elastic  movement  of  the  wrist  and 
finger  joints,  the  hammer  finger  rebounding  at  once  in  order  not  to 
damp  the  vibrations  which  have  been  initiated.  It  is  sometimes  serv- 
iceable to  place  the  4  fingers  of  the  left  hand  upon  the  surface  and 
percuss  from  one  to  the  other  with  successive  single  strokes.     A 


PRACTICE  OF  PERCUSSION  289 

change  from  dulness  to  resonance  is  often  thus  brought  out  with 
unusual  clearness. 

Three,  or  at  most  four,  successive  strokes  in  the  same  spot  are 
desirable,  as  a  longer  series  is  apt,  by  fatiguing  the  ear,  to  interfere 
with  a  correct  judgment  of  the  character  of  the  sounds.  Nothing  is 
gained  by  long-continued  percussion  over  one  point. 

(b)  Judging  the  Souiid. — In  estimating  the  character  of  the  per- 
cussion sound  the  elements  to  be  considered  are  pitch  (high  or  low), 
duration^  volume^  and  quality.  The  sound  produced  by  percussion 
over  a  considerable  body  of  air  in  a  simple  cavity  is  low  in  pitch,  of 
decided  duration  and  volume  and,  taking  all  the  factors  into  consid- 
eration, is  said  to  possess  a  tympanitic  quality  (e.  g.,  stomach).  At 
the  other  extreme  is  the  percussion  sound  over  a  cavity  containing 
fluid,  which,  so  far  as  it  can  be  said  to  have  pitch,  is  high,  short,  of 
little  volume,  and  is  called ^a^  (e.  g.,  pleural  effusion).  The  percus- 
sion sound  over  the  lung  has  a  distinctive  quality,  normal  pulmonary 
resonance.  Absence  of  resonance  not  amounting  to  flatness  is  called 
dulness.  There  are  two  percussion  sounds  of  peculiar  quality,  the 
"  cracked-pot "  and  amphoric  or  metallic,  which  will  be  described  in 
connection  with  the  examination  of  the  lungs  {q.  v.). 

Depending  upon  the  fact  that  in  many  instances,  as  a  surface  is 
traversed,  a  percussion  sound  of  one  kind  merges  almost  impercepti- 
bly into  another  variety,  or  that  a  given  sound  can  not  always  be 
classed  with  absolute  definiteness,  certain  qualifying  terms  are  em- 
ployed to  describe  degrees  of  difference,  their  number  in  actual  prac- 
tice varying  with  the  personal  acuteness  of  the  examiner.  The  fol- 
lowing list,  arranged  in  logical  order,  is  believed  to  comprise  as  many 
grades  as  are  desirable.  Tympanitic  resonance  possesses  the  lowest 
pitch  and  greatest  volume,  flatness  the  highest  pitch  and  least  vol- 
ume.    The  physician  inquires : 

First :  Is  this  sound  resonant  or  dull  ? 
Tympanitic  ? 
Almost  tympanitic  ? 
Dull  tympanitic  ? 
(Cracked-pot  resonance?) 
(Amphoric  resonance  ?) 
Hyperresonant  ? 
t 

Second :  Is  it — Xormal  resonance  ? 

I 
Diminished  or  impaired  resonance  ? 
Slight  dulness? 
Marked  dulness  ? 
Flatness  ? 
Third :  Is  it  normal  for  the  area  where  it  is  found  ? 


290  THE  EVIDENCES  OF  DISEASE 

(c)  Muflfting  of  the  Sounds. — The  greater  the  thickness  of  the 
tissue  (muscular,  adipose,  or  other)  which  overlies  an  air-containing 
organ,  the  greater  is  the  damping  or  muffling  of  the  vibrations  ex- 
cited by  percussion.  The  resulting  sound  is,  therefore,  more  or  less 
dull.  An  allowance,  to  be  learned  by  practice,  must  be  made  for 
this  fact  when  examining  an  obese  person  or  one  with  edematous 
thoracic  walls,  or  a  deep-seated  organ.  The  employment  of  an  un- 
usually strong  percussion  stroke  will  largely  obviate  this  difficulty. 

(d)  Strength  of  Stroke. — The  refinements  of  percussion  are  lost 
if  a  powerful  thumping  stroke  is  uniformly  employed.  Such  a  stroke 
will  easily  demonstrate  the  flatness  of  a  chest  full  of  fluid,  but  is 
entirely  unsuitable  for  such  work  as  accurately  outlining  the  heart 
or  the  lower  edge  of  the  liver.  The  strength  of  the  percussion  stroke 
should,  therefore,  be  modified  in  accordance  with  the  considerations 
about  to  be  stated. 

A  gentle  stroke  throws  the  underlying  tissues  into  vibration  to  a 
certain  depth,  while  by  a  more  powerful  blow  vibrations  are  returned 
from  structures  situated  still  farther  below  the  surface.  The  diagram 
(Fig.  64)  will  aid  in  elucidation.  The  small  triangles  represent  the 
depth  reached  by  gentle,  the  large  triangles  by  strong,  percussion 
strokes.  In  passing  from  A  to  B,  from  air-containing  lung  over 
solid  liver  to  air-containing  intestine,  it  is  desired  to  determine,  firsty 
the  upper  border  of  the  liver  ;  second,  the  lower  border  of  the  lung  ; 
third,  the  lower  border  of  the  liver,  these  organs  being  so  shaped 
and  situated  as  to  overlap  or  underlie  one  another.  Beginning  at 
the  upper  part  of  the  right  chest,  one  passes  downward,  percussing 
smartly,  until  the  normal  pulmonary  resonance  becomes  diminished, 
because  the  stroke  has  been  sufficiently  strong  to  develop  the  dulling 
effect  of  the  solid  liver,  although  covered  by  the  lung  as  at  1.  If  the 
stroke  had  been  gentle,  as  at  2,  nothing  would  have  been  elicited  ex- 
cept the  resonance  of  the  lung  tissue.  As  the  next  point  is  to  deter- 
mine the  lower  edge  of  the  gradually  thinning  lappet  of  lung,  the 
percussion  stroke  should  be  gentle  in  order  to  bring  out  lung  reso- 
nance only,  until  it  terminates  abruptly  in  the  unmistakable  dulness 
of  the  uncovered  liver  (strokes  2  and  3).  Finally,  gentle  percussion 
defines  the  lower  thin  edge  of  the  liver  (strokes  5  and  6),  a  forcible 
stroke  as  at  4  developing  too  soon  the  tympanitic  resonance  of  the 
intestines,  and  defeaj;ing  the  object  in  view.  Therefore,  to  formu- 
late the  conclusions : 

(1)  JJse  forcible percuftsion  when  the  organ,  tumour,  consolidation, 
or  fluid  is  deep-seated,  or  the  covering  walls  are  thick  (see  (c)  preced- 
ing)- 

(2)  Use  gentle  percussion  when  the  edges  of  the  organ  are  thin^ 


PRACTICE  OP   PERCUSSION 


291 


and  the  organ  superficial,  especially  when  it  is  desired  to  define  its 
limits. 

(e)  Auscultatory  Percussion.— If,  instead  of  listening  to  the  per- 
cussion sounds  as  transmitted  through  the  air,  the  stethoscope  is  em- 


LUNG 


1.  STRONG  =  pulmonary 
resonance  impaired  by 
liver  dulness 


2.  GENTLE  =  pulmonary 

resonance 

3.  GENTLE  =  liver  dulness 


4.  STRONG  -  tympanitic 

resonance 

5.  GENTLE  =  liver  dulness 

6.  GENTLE  =  tympanitic 

resonance 


INTESTIN^«-V 


f  iG.  64. — Diagram  showing  the  rationale  and  utility  of  varying  the  force  of  the  percussion 
stroke.  A  strong  stroke  as  at  1  develops  deep  dulness  and  locates  the  upper  border  of 
the  liver,  while  a  gentle  stroke  in  the  same  spot  gives  only  pulmonary  resonance.  A 
gentle  stroke  at  2  gives  pulmonary  resonance  and  the  next  gentle  stroke,  8,  gives  liver 
dulness,  thus  locating  the  lower  edge  of  the  lung,  while  a  powerful  stroke  at  2  will 
give  mainly  liver  dulness.  Gentle  stroke  5  is  slightly  dull,  and  gentle  stroke  6  is 
unmistakably  tympanitic,  thus  marking  the  boundary  line  between  thin  edge  of  liver 
and  air-containing  intestine,  while  strong  stroke  4  elicits  tympanitic  resonance. 

ployed  to  convey  the  vibrations  direct  to  the  ear,  it  constitutes  aus- 
cultatory percussion.  It  is  a  sufficiently  useful  method  to  deserve  a 
much  wider  use  than  it  has  yet  attained.  Its  particular  application 
is  to  determine  the  outlines  of  either  solid  or  air-containing  organs. 


292 


THE  EVIDENCES  OF  DISEASE 


SOUND  DISTANT 
AND  INDISTINCT. 


SOUND  DIRECT 
CLEAR  AND  LOUDER. 


\  STETHOSCOPE. 


In  practice  the  technic  consists  in  placing  the  chest  end  of  tlie 
binaural  stethoscope  upon  the  surface  overlying  the  organ  which  is 
to  be  delimited,  requesting  the  patient  or  an  assistant  to  hold  it  in 
place.  Using  the  fingers  in  the  usual  manner,  percussion  is  then 
begun  at  some  distance  out- 
side of  the  presumable  limits 
of  the  organ  and  carried  to- 
ward the  stethoscope.  When 
the  outer  border  of  the  or- 
gan is  attained  there  is  a 
noticeable  increase  in  inten- 
sity, an  elevation  in  the  pitch, 
and  perhaps  a  slight  altera- 
tion in  the  quality  of 
the  sound  (Fig.  65).  LINE  OF  BEST 
T  •      xf   XI-        CONDUCTION. 

in  percussing  the  tho- 
rax a  certain  amount  of  prac- 
tice is  required  in  order  to 
discriminate  between  the  su- 
perficial vibrations  of  its  bony 
framework  and  the  deeper 
tone  emanating  from  the  sub- 
jacent organs  and  tissues. 
Similar  percussion  lines  are 
carried  radially  from  various 
points  encircling  the  organ  to  the  stethoscope  as  a  centre.  If  the 
exact  spot  on  each  line  at  which  the  alteration  in  the  sound  occurs 

is  marked,  and  these 
marks  subsequently 

joined  by  a  continuous 
line,  an  outline  of  the 
organ  will  have  been  ob- 
tained (Fig.  66).  The 
usual  rules  for  regulat- 
ing the  strength  of  the 
percussion  stroke  should 
be  followed.  Directions 
for  the  employment  of 
this  method  in  examina- 
tions of  special   organs 

Fig.  66.-Diagram  showing  the  lines  along  which  auscul-  ^re  given  elsewhere  (e.g., 

tatory  percussion  sliould   be  carried  in  order  to  out-  j     ■,  q  ,  1, 

line  an  organ.      The  central  circle  represents  the  ^^^^^^         otomach,     per- 

chest  piece  of  the  stethoscope.  CUSSion  of). 


Fig.  65. — Diagram  showing  the  theory  of  auscul- 
tatory percussion.  The  organ  over  which 
the  stethoscope  is  placed  may  be  either  solid 
or  hollow. 


PERCUSSION— AUSCULTATION  293 

The  use  of  the  phouendoscope  in  auscultatory  percussion  has 
proved  disappointing,  as  it  gives  no  better  results  for  this  purpose 
than  the  ordinary  stethoscope,  and  its  employment  in  connection 
with  stroking  instead  of  percussion  has  proved  futile.  Since  this 
opinion  was  formed  it  has  been  confirmed  in.  published  papers  by 
Stengel,  Grote,  and  others. 

(/)  Sense  of  Resistance. — An  experienced  pleximeter  finger  will 
detect  differences  in  the  degree  of  resistance  felt  while  percussing. 
This  sense  of  resistance  is  greater  over  fluid  in  the  pleura  or  a  fibroid 
lung  than  over  hepatized  lung  tissue. 

(g)  Palpatory  and  Direct  Percussion. — Like  auscultatory  percus- 
sion, these  methods  deserve  a  more  extended  use. 

To  perform  palpatory  percussion,  the  pleximeter  finger  of  the  left 
hand  is  laid  firmly  upon  the  surface  and  struck  gently  with  three 
fingers  of  the  right  hand,  which  are  only  partly  flexed  and  held  in 
such  a  manner  that  the  pulps  of  the  fingers,  rather  than  their 
extreme  ends,  touch  the  pleximeter  finger.  The  distance  through 
which  the  percussing  fingers  move  should  not  exceed  one  inch,  and 
it  is  essential  that  they  remain  upon  the  pleximeter  finger  for  a  few 
seconds  before  the  stroke  is  repeated.  The  combination  of  pressure 
and  percussion — i.  e.,  a  palpating  stroke  — is  the  essence  of  the  method 

Direct  percussion  is  conducted  in  the  same  manner,  except  that 
the  palpating  blow  is  delivered  upon  the  surface  to  be  examined 
without  the  intervention  of  the  pleximeter  finger. 

It  is  evident  that  these  methods  involve  both  the  sense  of  hearing 
and  the  tactile  sense,  and  that  the  sound  produced  is  not  of  much 
intensity.  Consequently  one  must  listen  very  heedfully,  with  the 
ear  close  to  the  surface  examined.  By  utilizing  the  blended  impres- 
sions derived  from  touch  and  hearing,  it  is  possible  in  many  cases  to 
confirm,  extend,  or  make  more  accurate  the  results  of  ordinary  per- 
cussion. Palpatory  percussion  is  especially  useful  in  connection  with 
pleural  and  pulmonary  disease  and  in  determining  the  outlines  of  the 
liver  and  spleen.  Because  of  its  gentleness  it  may  be  employed  over 
a  tender  or  inflamed  organ — e.  g.,  in  appendicitis — or  over  the  lung  in 
cases'  of  pulmonary  hemorrhage. 

III.    AUSCULTATION 

The  restricted  technical  meaning  of  tlie  term  relates  to  sounds 
which  may  be  perceived  by  direct  application  of  the  ear  to  the  sur- 
face of  the  body  or  the  use  of  an  instrument  of  transmission.  Such 
sounds  are  those  produced  in  health  and  disease  by  the  action  of 
the  respiratory,  circulatory,  and,  to  a  limited  extent,  the  digestive 
apparatuses. 
21 


294  THE  EVIDENCES  OF  DISEASE 

Teclinic  of  Auscultation. — (l)  The  Patient. — If  practicable, 
the  patient  should  assume  a  comfortable  and  symmetrical  posture,  as 
a  twisted  or  constrained  attitude,  either  sitting  or  lying,  will  inter- 
fere with  the  respiratory  movements  and  to  some  degree  with  the 
action  of  the  heart.  The  surface  to  be  auscultated  should  be  bared, 
unless  the  ear  is  to  be  applied  directly  to  the  chest,  in  which  case  a 
handkerchief  or  thin,  soft  towel  should  be  laid  smoothly  over  the 
part.  It  is  absurd  to  apply  the  stethoscope  to  a  covered  surface,  and 
in  the  case  of  women  patients  a  false  sense  of  modesty  may  lead  to  a 
defective  diagnosis.  Women  of  the  best  social  training  exhibit  the 
least  false  shame  with  reference  to  this  point. 

As  a  physical  examination  involves  a  certain  amount  of  mental 
and  physical  fatigue  to  the  patient,  an  excess  of  diagnostic  zeal 
should  be  avoided  in  the  very  ill,  after  one  thorough  investigation 
has  afforded  satisfactory  results. 

(2)  The  Methods. — Auscultation  may  be  direct  (immediate),  the 
ear  being  applied  directly  to  the  surface ;  or  indirect  (mediate),  by 
the  use  of  a  stethoscope. 

Auscultation  without  an  instrument  is  useful  in  emergencies,  and 
in  getting  a  general  idea  of  the  sounds  which  are  present.  Some 
accomplished  auscultators  claim,  moreover,  that  by  it  one  may  hear 
certain  rales  and  cardiac  murmurs  more  readily,  and  perceive  an 
aneurismal  bruit  and  thrill  with  greater  distinctness,  than  with  tlie 
stethoscope ;  and,  furthermore,  that  it  is  easier  by  this  method  to 
determine  the  relative  nearness  or  superficiality  of  friction  sounds 
and  rales.  As  a  rule,  however,  it  may  be  said  that  the  direct  method 
compares  unfavourably  with  the  stethoscopic  examination  in  accuracy 
of  localization,  refinement  of  discrimination,  and  avoidance  of  un- 
necessary personal  contact.  The  practical  lesson  from  these  differing 
opinions  is  that  one  should  be  trained  to  the  use  of  both  methods  in 
order  to  avail  one's  self  of  either  in  a  doubtful  case. 

In  the  United  States  the  double  (binaural)  hollow  stethoscope 
with  flexible  tubes  is  almost  universally  employed.  It  is  highly 
desirable  that  the  examiner  should  become  accustomed  to  some  one 
of  the  many  patterns  of  the  instrument,  as  better  work  is  possible 
with  a  familiar  and  well-used  tool.  In  choosing  a  stethoscope  much 
care  should  be  exercised,  and  a  selection  should  be  made  by  com- 
parison between  several  kinds  with  reference  to  the  following  points  : 

First. — Its  capacity  for  transmitting  sounds.  This  is  best  done 
by  laying  a  watch  upon  the  thigh  and  placing  the  metacarpal  portion 
of  both  hands,  one  over  the  other,  palms  down,  upon  the  watch,  and 
applying  the  chest  piece  of  the  instrument  to  the  dorsal  surface  of 
the  upper  hand.     It  is  usually  easy  to  decide  by  listening  to  the- 


METHODS  OF  AUSCULTATION  295 

ticking  of  the  watch  which  instrument  conducts  sound  to  the  best 
advantage. 

Second. — The  ear  pieces  must  fit  comfortably  in  the  external 
meatus,  and  almost  entirely  exclude  extraneous  sounds. 

Third. — Durability,  simplicity,  and  convenience  in  carrying 
should  be  considered. 

Fourth. — The  chest  piece  for  ordinary  use  should  not  exceed  1^ 
inch  in  diameter.  A  larger  rigid  piece  and  one  of  soft  rubber,  the 
latter  for  use  in  much  emaciated  patients,  should  be  added. 

In  applying  the  stethoscope  to  the  surface  its  mouth  should  be 
held  easily  between  the  thumb  and  forefinger,  and  in  some  cases  it 
may  be  advantageously  steadied  by  resting  the  little  finger  of  the 
same  hand  upon  the  surface  of  the  body.  The  mouth  of  the  instru- 
ment should  be  in  firm  contact  at  all  points  of  its  circumference  in 
order  to  isolate  the  columns  of  air  in  the  tubes,  and  to  shut  off  out- 
side noises.  If  the  ribs  are  prominent  and  close  contact  can  not  be 
obtained,  the  skin  may  be  gathered  in  a  small  mass  by  the  fingers  of 
the  other  hand,  thus  furnishing  a  suflBcient  amount  of  tissue  to 
secure  the  desired  apposition,  or  the  soft-rubber  chest  piece  may  be 
used.  In  some  cases  the  skin  is  so  harsh  and  dry  that  confusing 
friction  sounds  occur  with  the  respiratory  or  other  movements  of 
the  surface  examined.  This  may  be  readily  obviated  by  wetting  or, 
better,  oiling  the  skin. 

The  phonendoscope^  in  personal  use,  has  proved  to  have  no  advan- 
tages over  the  ordinary  stethoscope  in  auscultation  of  the  lungs,  but 
it  has  certain  points  of  usefulness  in  auscultation  of  the  heart  and 
vessels.  By  its  power  of  intensifying  sound  one  is  able  to  detect 
very  faint  murmm-s  or  bruits,  slight  clicking  or  harshness  of  the 
valve  sounds,  and  the  quality  of  an  extremely  weak  first  sound  with 
greater  facility  than  by  the  ordinary  means.  One  practical  advan- 
tage in  the  hurry  of  ofl&ce  work  is  the  rapid  determination  of  the 
presence  of  coarse  cardiac  murmurs  and  venous  humming  without 
removing  the  clothing,  as  such  sounds,  even  if  of  moderate  intensity, 
are  readily  heard  with  this  instrument  through  several  thicknesses 
of  fabric. 

The  differential  stetJioscope,  an  instrument  with  two  chest  pieces 
and  separate  flexible  tubes,  one  leading  to  the  right,  the  other  to 
the  left  ear,  is  very  useful  in  comparing  the  time  relations  of  two 
sounds  heard  at  different  portions  of  the  chest.  By  placing  the  two 
chest  pieces,  one  over  each  of  the  separate  localities,  the  sounds  from 
each  area  are  heard  simultaneously,  and  it  is  possible  to  determine 
very  accurately  which  precedes  the  other,  or  to  detect  differences  in 
their  quality — e.  g.,  two  systolic  murmurs  at  different  orifices. 


296  THE  EVIDENCES  OF  DISEASE 

In  view  of  the  diflBculty  often  experienced  in  auscultating  the 
lungs  posteriorly  in  those  who  are  too  ill  to  sit  up  or  even  to  undergo 
the  fatigue  incident  to  being  rolled  over  from  one  side  to  the  other, 
a  stethoscopic  chest  piece  has  been  devised  (Smith)  which  can  be 
slipped  under  the  back  without  disturbing  the  patient.  It  is  shaped 
like  a  flattened  disk  with  the  tubes  passing  off  from  a  point  on  its 
circumference. 


SECTION   XXIX 
THE   CHEST   (THOEAX) 

lN"CLLrDED  here  are  certain  points  observed  by  inspection,  partly 
also  by  palpation  and  mensuration,  of  the  thorax.  The  importance 
of  inspection  and  palpation  of  the  thorax  can  not  be  too  strongly 
emphasized.  It  is  frequently  the  case  that  the  examiner  proceeds  at 
once  to  auscultation  and  percussion  of  the  chest,  thereby  neglecting 
to  obtain  valuable  diagnostic  evidence. 

Method  of  Inspection. — The  thorax  should  be  bared,  and  the 
patient  placed  in  a  symmetrical  and  comfortable  posture,  whether 
sitting,  standing,  or  lying.  The  light  should,  as  a  rule,  fall  directly 
on  the  surface  which  is  to  be  examined.  Altering  the  direction 
from  which  the  light  comes,  either  by  moving  the  patient  or  the 
source  of  the  illumination,  so  as  to  permit  it  to  fall  obliquely  across 
the  examined  surface,  is,  by  casting  shadows,  of  much  use  in  detect- 
ing slight  pulsations  or  abnormalities  of  shape  and  movement.  In 
inspecting  the  thorax  the  examiner  should  view  its  anterior,  lateral, 
and  posterior  aspects.  Finally,  he  should  never  omit  to  look  down 
upon  it  from  above  and  behind  the  patient.  This  view  point  gives 
practically  the  outline  of  a  horizontal  section  of  the  chest,  and  is 
very  useful  in  determining  the  amount  and  any  inequality  of  expan- 
sion ;  or  the  presence  of  lateral  curvature,  projection  of  one  or  both 
scapulae,  or  differences  in  the  size  of  the  lateral  halves  of  the  chest. 

The  Normal  Thorax. — Absolute  bilateral  symmetry  is  ex- 
tremely seldom  found.  In  most  cases  there  is  a  slight  right  lateral 
curvature,  and  the  right  side  of  the  chest  is  usually  a  little  the  more 
capacious.  A  recognition  of  the  normal  shape  of  the  chest  depends 
upon  the  familiarity  gained  by  clinical  experience. 

The  bony  cage  of  the  thorax  divested  of  the  shoulder  girdle  is 
conical  in  shape,  the  smaller  end  upward,  but  in  its  clinical  state, 
especially  in  muscular  persons,  the  circumference  at  the  level  of  the 
axilla  is  greater  than  at  the  lower  end  of  the  sternum,  because  of  the 


THE  THORAX— THORACOMETRY  297 

presence  of  the  structures  mentioned.  In  the  adult  a  horizontal 
section  of  the  chest  shows  its  transverse  diameter  to  be  greater  than 
the  antero-posterior,  in  the  proportion  of  10  to  7.5  (E.  U.  Otis).  In 
children  it  is  more  nearly  circular. 

In  the  normal  thorax,  in  addition  to  its  nearly  symmetrical  con- 
tour, it  may  be  noted — 

(1)  That  the  clavicles  may  or  may  not  be  somewhat  prominent, 
especially  the  right. 

(2)  That  there  may  be  slight  depressions  above  and  below  the 
clavicles.  The  depression  between  the  deltoid  and  greater  pectoral 
muscles  below  the  clavicle  is  Mohrenheim's  fossa. 

(3)  That  there  is  a  depression  just  above  the  upper  end  of  the 
sternum — the  episternal  notch — between  the  inner  ends  of  the  clavi- 
cles. 

(4)  That  the  line  of  junction  between  the  first  piece  of  the  ster- 
num (manubrium)  and  the  second  (gladiolus)  forms  a  projection — 
the  angle  of  Louis  (angulus  Ludovici),  which  may  frequently  be  seen 
and  almost  invariably  felt.  It  constitutes  a  valuable  guide  to  the 
second  rib,  the  cartilage  of  this  rib  articulating  at  the  line  of  junc- 
tion. 

(5)  That  the  true  ribs  are  so  shaped  and  attached  to  the  sternum 
that  the  upper  ribs  run  horizontally  outward,  the  others  passing 
downward  and  outward  with  increasing  obliquity  until  the  subcostal 
or  epigastric  angle  formed  by  the  divergence  of  the  costal  margins 
and  the  lower  end  of  the  sternum  is  usually  70°  or  80°.  The  ribs, 
except  in  thin  or  ill-developed  individuals,  are  only  visible  laterally 
and  in  the  lower  third  of  the  thorax. 

(6)  That  at  the  lower  end  of  the  sternum  there  is  the  infrasternal 
depression  {scroMculus  cordis,  pit  of  the  stomach). 

Thoracometry. — Measurement  of  the  chest  is  done  with  refer- 
ence to  its  circumference,  semi-circumference,  and  main  diameters, 
by  means  of  the  tape  measure  and  the  calipers. 

(1)  The  circumference  of  the  chest  is  usually  measured  at  the 
line  of  the  nipples,  taking  care  that  the  tape  passes  around  in  a 
horizontal  line.  The  average  circumference  in  men  is  34.3  inches 
(Otis,  Hitchcock)  ;  in  women,  29.5  inches  (Miss  Wood,  Mary  Cotton).  An 
important  use  of  the  tape  line  is  as  a  stethometer  to  determine  the 
extent  of  respiratory  expansion — the  difference  in  the  girth  of  the 
chest  at  the  end  of  forced  expiration  and  forced  inspiration  respec- 
tively. Special  stethometers  with  graduated  dials  are  unnecessary. 
Expansion  varies  normally  from  1^  to  5  inches.  The  significance  of 
variations  in  amount  will  be  discussed  in  connection  with  the  exami- 
nation of  the  lungs  {q.  v.). 


298  THE  EVIDENCES  OF   DISEASE 

(2)  The  semi-circumference  of  the  chest  may  be  determined  by 
making  a  vertical  mark  in  the  median  line  of  the  sternum,  and  an- 
other on  the  spinous  process  of  the  vertebrae  at  the  level  of  the  nip- 
ples. This  may  be  done  with  a  dermatographic  pencil  or  a  stick  of 
dark  grease  paint  (removed  by  wiping  with  a  vaselined  rag).  The 
tape  is  passed  from  one  mark  to  another,  first  around  the  right  half, 
then  around  the  left  half  of  the  chest.  In  right-handed  persons  the 
right  side  of  the  chest  frequently  exceeds  the  left  in  circumference 
by  half  an  inch. 

To  measure  the  expansion  of  the  right  and  left  halves  of  the  chest 
separately,  it  is  convenient  to  have  two  tapes  joined  so  that  the  be- 
ginning of  each  is  in  the  middle  of  their  combined  length.  The 
line  of  junction  is  placed  over  the  median  line  of  the  spine  at  the 
proper  level  and  steadied  by  the  examiner's  finger,  while  the  tapes 
are  brought  around  to  the  front  and  held  by  the  patient  with  proper 
directions  as  to  tension.  The  expansion  of  each  side  during  inspira- 
tion can  be  then  readily  noted.  It  also  serves  to  measure  simultane- 
ously the  semi-circumferences  of  the  chest. 

(3)  The  diameters  of  the  chest  are  measured  at  the  level  of  the 
nipples  by  means  of  compass  calipers  with  curved  arms  or  by  slide 
calipers,  the  use  of  which  does  not  require  special  directions.  The 
average  depth  of  the  chest — the  antero-posterior  diameter — is  7.5 
inches  in  men  (Otis),  6.9  inches  in  women  (Miss  Wood).  The  average 
breadth  of  the  chest — the  transverse  diameter — in  men  is  9.9  inches. 

Cyrtometry. — The  determination  of  the  shape  of  the  chest 
consists  practically  in  obtaining  an  outline  of  its  transverse  section 
at  any  desired  level,  usually  that  of  the  nipples. 

Several  varieties  of  cyrtometers  have  been  devised  to  attain  this 
end.  Some,  as  with  those  of  Demeny,  of  Paris,  and  Evans,  of  Brook- 
lyn, are  very  accurate,  but  too  elaborate  and  expensive  for  ordinary 
use.  A  practicable  instrument  consists  of  a  compass  with  short  arms 
to  which  are  attached  narrow  strips  of  lead  easily  bent  and  yet  able 
to  retain  their-  shape  under  ordinary  circumstances.  An  indicator 
and  set  screw  enables  the  arms  to  be  fixed  at  any  angle,  opened,  and 
set  again  at  the  same  point.  The  arms  are  set  to  lie  on  either  side 
of  the  spine  and  the  metal  strips  brought  forward  from  either  side 
and  moulded  to  the  chest  until  the  ends  meet  or  cross  over  the 
sternum.  The  compass  arms  are  then  loosened,  opened,  the  instru- 
ment removed  and  closed  again  to  the  same  angle.  It  is  then  laid 
on  a  sheet  of  paper,  the  spinal  and  sternal  points  marked  and  an  out- 
line of  the  inner  borders  of  the  strips  made  with  a  soft  pencil.  For 
clinical  purposes  two  bands  of  lead  connected  by  rubber  tubing  will 
amply  suffice.     In  many  cases  the  size  and  shape  of  the  chest  may 


CYRTOMETRY— DEFORMITIES  OP  THORAX 


299 


be  ascertained  after  sufficient  experience  by  inspection  alone,  but 
for  accuracy,  for  jjurposes  of  record,  and  in  order  to  detect  slight 
differences  the  iudtrumeutal  methods  may  be  carried  out. 

Bilateral  Deformities  of  the  Thorax. — Some  of  these  are 
of  no  significance,  others  result  from  past  disease,  and  some  may 
constitute  evidence  of  existing  pathological  states.  These  deformi- 
ties, both  general  and  local,  are  as  follows  : 

(1)  The  Flat  Chest. — The  name  is  sufficiently  descriptive.  The 
costal  cartilages  are  straight,  lacking  their  normal  forward  con- 
vexity, and  in  consequence  the  antero-posterior  diameter  of  the 
chest  is  lessened.  This  shape  of  chest  is  sometimes  normal,  but 
may  indicate  a  predisposition  to  phthisis.  If  very  well  marked,  the 
chest  being  sunken  in  on  both  sides,  it  is  an  indication  of  existing 
phthisis. 

(2)  The  Pterygoid  or  Alar  Chest. — A  long  neck,  prominent  lar- 
ynx, sloping  shoulders,  scapulae  projecting  like  wings  (hence  the 
name),  great  obliquity  of  the  ribs,  which  dip  sharply  downward  from 
the  sternum  and  then  bend  sharply  upward  and  backward  to  the 
spine,  thus  making  a  very  acute  subcostal  (epigastric)  angle,  wide 
intercostal  spaces,  and  a  thorax,  as  a  whole,  vertically  long  and  nar- 
row, constitutes  the  chest  variously  termed  phthisical,  phthisinoid, 
or  paralytic.  It  is  often  also  a  flat  chest.  It  indicates  a  tendency  to 
pulmonary  phthisis,  and  if  well  marked  is  evidence  of  the  actual 
presence  of  the  disease.  Ex- 
treme emaciation  of  the  chest, 
without  a  real  change  of 
shape,  such  as  may  be  found 
after  a  long  fever,  should  not 
be  mistaken  for  this  form  of 
chest. 

(3)  The  Emphysematous 
Chest. — If  the  antero-poste- 
rior diameter  of  the  chest  is 
increased,  if  it  appears  broad 
and  short,  if  the  sternum  is 
arched,  if  the  ribs  are  thick 
and  run  horizontally  outward^ 
making  the  subcostal  angle 
unusually  wide,  and  the  an- 

gulus  L.  is  notably  prominent,  it  is  almost  certain  evidence  of  hyper- 
trophic pulmonary  emphysema  {q.  v.).  The  enlargement  of  the  lungs 
in  this  disease  causes  a  general  expansion  of  the  chest  (Fig.  67),  so 
that  it  presents  a  permanent  inspiratory  position.    In  many  instances 


Fig.  67. — Cyrtometer  curve  of  an  emphysematous 
chest  in  a  male,  aged  seveuty-four.  Dotted  line 
shows  a  slight  difference  in  the  size  of  the  right 
and  left  sides  of  the  thorax.  Redrawn  from 
Evans. 


300  THE  EVIDENCES  OF  DISEASE 

the  middle  portion  of  the  thorax  bulges  outward,  giving  rise  to  the 
"  barrel-shaped  "  chest.  Like  phthisis  and  the  phthisical  chest,  em- 
physema, particularly  the  atrophic  form,  may  exist  without  causing 
a  characteristic  chest  shape.  It  should  be  remembered  that  kyphosis 
may  simulate  an  emphysematous  chest, 

(4)  The  Rachitic  Chest. — In  this  deformity  the  ribs  immediately 
external  to  the  sternum  are  bent  upward  during  early  life,  because 
of  their  softness,  the  lessening  of  the  intrathoracic  pressure  during 


A  B 

Fig.  68. — A,  horizontal  section  of  a  rachitic  chest,  child  two  years  old,  showing  lateral 
furrows;  B,  section  of  chest  of  healthy  child  of  the  same  age  (Holt). 

inspiration  being  sufficient  to  produce  the  change  of  shape  without 
an  existing  impediment  to  respiration.  The  ends  of  the  ribs  are  also 
enlarged  and  beaded,  the  "rachitic  rosary,"  The  result  of  these 
changes  is  to  cause  the  formation  of  a  vertical  depression  on  either 
side  of  the  sternum  (Fig,  68). 

Very  often  with  this  coexist  (6)  and  (7),  to  be  described. 

(5)  The  Pigeon  or  Keel  Breast. — In  this  form  the  chest  appears  to 
be  compressed  laterally  and  the  sternum  pressed  sharply  forward, 
especially  its  lower  portion,  thus  increasing  the  antero-posterior 
diameter  and  making  the  cross  section  of  the  chest  distinctly  trian- 
gular, apex  forward.  It  is  the  result  of  rickets  plus  respiratory 
obstruction  (even  if  slight)  from  nasal  catarrh,  adenoids,  enlarged 
faucial  tonsils,  and  sometimes  prolonged  pertussis, 

(6)  Harrison's  Sulcus. — This  is  a  zonal  constriction  beginning  at 
the  stemo-xiphoid  junction,  extending  outward  and  somewhat  down- 
ward to  the  axillary  line.  It  corresponds  to  the  line  of  attachment 
of  the  diaphragm,  and,  as  the  ribs  form  the  fixed  point  for  the  action 
of  the  diaphragm,  if  they  are  softened  by  rachitis  they  are  bent 
inward  along  this  line.  The  causes  are  the  same  as  for  pigeon 
breast  (5),  and  the  latter  almost  always  presents  Harrison's  sulcus. 


DEFORMITIES  OF  THORAX  301 

A  flaring  outward  of  the  entire  costal  margin  on  both  sides,  caus- 
ing the  lower  opening  of  the  thorax  to  be  expanded,  is  not  abnormal 
in  some  individuals,  but  may  occur  acutely,  especially  in  children, 
from  the  upward  and  outward  pressure  of  great  tympanites;  or 
slowly  from  ascites  and  large  abdominal  tumours. 

(7)  Funnel  Chest  — This  is  a  more  or  less  deep  depression  or 
foveation  of  the  lower  sternum  (improperly  termed  funnel  breast) y 
which  may  extend  upward  as  high  as  the  third  rib.  It  is  usually 
congenital  and  of  no  importance,  but  if  marked  may  interfere  with 
respiration.  It  may  be  simply  a  stigma  of  degeneration.  A  similar 
depression  of  the  ensiform  appendix  and  lower  end  of  the  sternum 
may  be  due  to  the  pressure  of  tools,  especially  in  cobblers. 

Unilateral  and  Local  Thoracic  Deformities. — (1)  Uni- 
lateral enlargement  or  bulging  of  the  thorax,  as  determined  by  inspec- 
tion or  measurement,  is  caused  by  gas  or  fluid  in  one  pleural  cavity, 
as  in  pyothorax,  haemothorax,  pneumothorax,  and  pleurisy  with  effu- 
sion. The  increased  size  may  be  due  to  compensatory  emphysema 
caused  by  disease  of  the  opposite  lung — e.  g.,  fibroid  changes.  In  this 
case  the  diseased  side  is  smaller  and  the  opposite  sida  larger  than  nor- 
mal, thus  making  the  disparity  more  noticeable.  A  tumour  of  the 
lung  or  pleura  may  also  be  considered  as  a  possible  cause  of  one- 
sided enlargement.  Bulging  of  the  intercostal  spaces  is  always 
present  in  enlargement  of  the  chest,  but  may  exist  alone  as  evidence 
of  the  same  conditions. 

(2)  Local  prominences  may  be  found  in  various  portions  of  the 
thorax.  Praicordial  bulging  is  usually  significant  of  an  enlarged 
heart,  large  pericardial  effusion,  pneumopericardium,  or  a  mediastinal 
tumour  or  aneurism  pushing  the  heart  bodily  forward.  As  the 
existence  and  extent  of  this  bulging  depends  upon  the  degree  of 
plasticity  of  the  chest  wall,  it  is  most  marked  in  children  and  young 
adults.  While  it  occurs,  as  a  rule,  gradually,  there  may  be  an  acute 
bulging  in  young  subjects  from  a  rapid  and  large  pericardial  effu- 
sion. Bulging  of  the  right  hypochondrium  may  signify  enlargement 
of  the  liver,  hepatic  abscess  or  hydatids,  subphrenic  abscess,  or  effusion 
into  the  right  pleura.  It  may  be  present  as  part  of  a  marked  dis- 
tention of  the  right  side  of  the  abdomen  resulting  from  tumours  on 
the  same  side  of  the  median  line— e.  g.,  sarcoma  of  the  kidney. 

Other  causes  of  localized  swellings  or  prominences  of  the  chest 
are : 

xVneurisms  {q.  v.) ;  knuckling  or  irregular  formation  of  one  or 
more  ribs  or  costal  cartilages,  of  congenital  or  infantile  origin,  which 
by  a  careless  examiner  may  be  mistakenly  referred  to  aneurism  or 
cardiac  disease ;  localized  emphysema,  or  encysted  fluid  in  the  pleura, 


302 


THE  EVIDENCES  OF  DISEASE 


which,  however,  is  apt  to  cause  obliteration  of  the  intercostal  spaces 
over  a  limited  space  rather  than  a  distinct  prominence ;  general 
emphysema,  which  may  give  rise  to  prominence  of  the  supraclavicular 
spaces ;  collections  of  pus  due  to  disease  of  vertebrae,  sternum,  ribs, 

soft  tissues  of  the  chest  wall, 
or  actinomycosis,  perforating 
empyema,  mediastinal  ab- 
scess, and  subphrenic  ab- 
scess ;  and  hydatids  or  tu- 
mours of  the  lung,  pleural 
growths,  and,  very  rarely, 
hernia  of  the  lung. 

(3)  Unilateral  contraction 
of  the  thorax,  one  side  of 
the  chest  being  more  or  less 

Fia.  69.-Cyrtometer  curve  of  the  thorax  (at  the  e^e^lj    shrunken,     Owing    to 

level  of  the  4th  rib)  in  tubercular  infiltration  lessened  size  of  the  lung  (Fig. 

of  the  upper  and   middle  lobes  of  the  right  gg)^    may    be     significant     of 

lung.    The  dotted  line  shows  the  difference  in  i          •         i  j.i  •   •       •    i        i -i  •   i 

^\,    ■      f^x.    •  u*     AX  f^  -A      f^\,  *u  chrome  phthisis,  interstitial 

the  size  oi  the  right  and  left  sides  of  the  thorax.  ^  ' 

Kedrawn  from  Evans.  pneumonia,    extensive   pleu- 

ritic adhesions,  collapse  of 
the  lung  from  a  foreign  body  in  the  bronchus,  or  occlusion  of  a 
bronchus  by  mediastinal  tumour  or  abscess.  It  may  follow  long- 
continued  pressure  upon  the  lung  itself  by  pleural  effusions.  The 
retracted  side  is  obviously  smaller  than  the  other,  the  shoulder  of  the 
same  side  droops,  the  spine 
is  curved  with  its  concavity 
toward  the  diseased  side,  and 
the  ribs  approach  each  other 
or  may  nearly  overlap.  These 
changes,  due  to  disease  of  the 
thoracic  viscera,  are  some- 
what similar  to  those  of  sco- 
liosis {q.  V.)  arising  from 
other  causes  (Fig  70). 

(4)  Local  depressions  of 
the  thorax  are  seen  above  and 
below  the  clavicles,  especially 
in  the  space  between  the 
deltoid  and  pectoral  muscles, 
in  phthisis.  Flattenings  or  depressions  in  other  parts  of  the  chest 
may  indicate  the  existence  of  bronchiectatic  or  phthisical  cavities, 
localized  pleuritic  adhesions  or  old  fracture  of  the  ribs.     Atrophy 


Fig.  70. — Cyrtometer  curve  of  chest  in  lateral  cur- 
vature of  the  spine  (scoliosis).  Dotted  line 
shows  the  normal  outline.  Spine  and  sternum 
in  normal  relations.     Kedrawn  from  Evans. 


MISCELLANEOUS  THORACIC  SIGNS  303 

or  removal  of  one  breast  or  atrophy  of  one  great  pectoral  muscle 
gives  rise  to  flattening  of  the  corresponding  side. 

Miscellaneous. — The  flexibility  of  the  ribs  and  their  cartilages 
should  always  be  tested  by  pressure  upon  the  sternum.  It  is  greatest 
in  children  and  progressively  decreases  as  age  advances.  The 
decrease  is  partly  due  to  changes  in  the  osseous  tissue  of  the  ribs, 
but  largely  also  to  partial  calcification  of  the  cartilages.  Increased 
rigidity  of  the  bony  cage  of  the  thorax  renders  it  a  better  resonator 
and  conductor  of  sound.  Especially  in  thin  persons,  it  may  increase 
the  intensity  of  the  percussion  sound,  and  in  some  cases  give  rise 
to  a  deceptive  transference  of  auscultatory  phenomena  beyond  the 
expected  limits — e.  g,,  the  hearing  of  bronchial  breathing  for  a  short 
distance  to  the  left  of  the  spinal  column,  the  sound  being  transmitted 
from  a  consolidated  right  lower  lobe  along  the  rigid  ribs  and  ver- 
tebrae. On  the  other  hand,  the  extreme  flexibility  of  the  ribs  in 
infants  is  partly  responsible  for  the  cracked-pot  percussion  sound, 
and  perhaps  also  for  some  of  the  obscurities  in  the  differential  diag- 
nosis between  pleural  effusion  and  pulmonary  consolidation  in  the 
very  young. 

(Edema  of  the  thorax  may  be  a  part  of  general  dropsy  ;  or,  if  local- 
ized, a  symptom  of  a  deep-seated  abscess  of  the  chest  walls  or  an 
empyema  preparing  to  perforate. 

Enlarged  veins  of  the  chest  are  seen  in  the  neighbourhood  of  the 
mammary  glands  during  lactation  and  are  sometimes  significant  of 
malignant  disease  of  the  breast.  In  an  unusually  fair  skin  they  may 
be  extremely  but  normally  conspicuous.  They  may  result  from  the 
interference  to  the  return  of  blood  from  the  breast  caused  by  the  pres- 
sure of  mediastinal  tumours  and  thoracic  aneurism.  Portal  obstruc- 
tion, by  compelling  the  blood  to  retrace  its  way  through  collateral 
paths,  and  right  ventricular  dilatation,  by  damming  it  back,  will  also 
give  rise  to  abnormal  distention.  An  arched  line  of  dilated  capil- 
laries corresponding  to  the  attachments  of  the  diaphragm  along  the 
lower  costal  margin  is  not  infrequently  noted  where  the  right  ven- 
tricle is  hard  worked. 

Respiratory  movements  of  the  chest  (see  Index — Eespiration). 

Pulsations  in  the  thorax,  visible  or  palpable  (see  Index — Thorax, 
pulsating  areas  of). 

Pain  in  the  chest  (see  Index). 


304  THE  EVIDENCES  OF   DISEASE 


SECTION   XXX 

ANATOMICAL  LANDMAEKS  AXD   TOPOGRAPHICAL 
AREAS   OF   THE   THORAX 

For  purposes  of  description,  and  to  conduct  a  proper  physical 
examination  of  the  thoracic  contents,  it  is  necessary  to  be  familiar 
with  certain  anatomical  landmarks  and  arbitrarily  fixed  surface 
areas  of  this  portion  of  the  body. 

Anatomical  Landmarks  of  the  Thorax. — (1)  Sternum. — 
The  average  length  of  the  sternum  is  6  inches.  The  upper  border 
of  the  sternum,  the  episternal  notch,  which  can  always  be  seen  and 
felt,  is  on  a  level  with  the  disk  between  the  2d  and  3d  dorsal  verte- 
brae.    The  distance  between  the  disk  and  the  notch  is  2  inches. 

Running  the  finger  downward  from  the  episternal  notch,  a  trans- 
verse ridge  may  be  felt  and  often  seen,  the  angle  of  Ludovici  (Louis). 
It  is  better  marked  in  the  male  thorax  and  is  on  a  level  with  the 
lower  border  of  the  body  of  the  5th  dorsal  vertebra. 

At  the  lower  end  of  the  sternum  identify  the  ensiform  (xiphoid) 
appendix  and  its  junction  with  the  gladiolus  (body  or  corpus)  of  the 
sternum.  This  is  often  difficult  because  of  the  chondro-xiphoid  liga- 
ments which  pass  from  the  7th  cartilage  to  the  appendix.  The 
appendix  varies  in  shape  and  size.  Its  point  is  often  curved  forward 
and  its  anterior  surface  hollowed  out,  forming  a  marked  infrasternal 
fossa  or  depression.  The  sterno-xiphoid  junction  is  on  a  level  with 
the  disk  between  the  9th  and  10th  vertebrae. 

(2)  Ribs  and  Interspaces. — Every  physical  examination  of  the 
chest  requires  identification  of  the  ribs.  The  best  routine  method  is 
to  find  the  angle  of  Louis ;  then  run  the  finger  along  its  ridge  to  the 
right  or  left,  when  it  will  pass  directly  upon  the  2d  rib,  from  which 
the  ribs  may  be  counted  in  a  line  downward  and  outward,  tracing 
those  desired  into  the  axilla  and  posteriorly,  remembering  that  each 
rib  runs  upward  as  it  passes  to  the  spine.  Furthermore,  if  the  arm 
is  raised  outward  to  a  horizontal  line,  the  lower  border  of  the  great 
pectoral  muscle  corresponds  to  the  5th  rib,  and  the  highest  digita- 
tion  of  the  serratus  magnus  lies  over  the  6th  rib,  the  next  2  below 
lying  over  the  7th  and  8th  ribs  respectively. 

Owing  to  the  downward  slope  of  the  ribs  from  spine  to  sternum, 
the  chondro-sternal  articulation  of  each  rib  is  considerably  lower 
than  its  vertebral  articulation.  The  articulation  of  the  1st  rib  in 
front  is  on  a  level  with  that  of  the  4th  rib  at  the  back.  The  corre- 
sponding relations  of  the  2d  to  the  7th  ribs  inclusive  may  be  easily 


ANATOMICAL  LANDMARKS  OF  THORAX  305 

stated  by  adding  4  to  the  number  of  the  rib  in  front — e.  g.,  the  3d 
rib  anteriorly  is  on  a  level  with  the  7th  posteriorly,  6th  with  the 
10th,  etc. 

Posteriorly  the  ribs  may  be  counted  upward,  starting  with  the  12th, 
which  can  usually  be  felt,  but,  in  fat  persons,  sometimes  only  with 
great  difficulty.  The  tips  of  the  spinous  processes  of  the  dorsal  ver- 
tebrae may  also  act  as  guides  to  the  ribs.  Owing  to  their  downward 
inclination,  the  dorsal  spines  do  not  all  lie  on  a  level  with  the  same 
numbered  rib.  Thus  the  2d  dorsal  spine  corresponds  to  the  3d  rib, 
the  3d  spine  to  the  4th  rib,  and  so  on,  down  to  and  including  the 
9th  spine,  which  corresponds  to  the  10th  rib.  The  10th  spine  lies 
midway  between  the  10th  and  11th  ribs.  The  11th  and  12th  spines 
correspond  to  the  11th  and  12th  ribs. 

The  intercostal  spaces  have  the  same  number  as  that  of  the  ribs 
below  which  they  lie.  They  are  wider  in  front  than  behind,  and  the 
3d  is  usually  the  widest,  next  the  2d,  then  the  1st.  The  identifica- 
tion of  the  ribs  identifies  the  interspaces,  but  after  some  experience 
the  examiner  is  often  able  to  recognise  at  once  the  1st  and  2d  inter- 
spaces. There  is  not  infrequently  a  noticeable  gap  between  the 
clavicle  and  1st  rib,  which  may  be  readily  taken  for  the  1st  inter- 
space, and  in  a  long  thorax  the  2d  interspace  may  be  surprisingly  low 
down. 

(3)  Nipple. — In  the  male  thorax  this  is  usually  between  the  4th 
and  5tli  ribs,  4  inches  from  the  median  line  of  the  sternum,  but  it 
may  lie  directly  upon  either  of  these  ribs,  or  in  some  few  cases 
in  the  5th  interspace.  In  the  female  chest  its  position  is  ex- 
tremely variable,  depending  on  the  size  and  pendulousness  of  the 
mammary  gland.  One  learns  to  recognise  with  some  accuracy  the 
point  where  it  should  typically  be  found. 

(4)  The  Mammary  Gland.— Vertically  this  gland  extends  from  the 
3d  to  the  6th  (or  7th)  ribs  inclusive,  and  horizontally  from  the  edge 
of  the  sternum  to  the  anterior  border  of  the  axilla. 

(5)  The  Spine  and  Back.— There  usually  is  a  median  groove  or 
furrow  in  the  back,  at  the  bottom  of  which  lie  the  spinous  processes. 
In  thin  persons  and  in  many  children  the  spinous  line  is  quite 
prominent,  largely  replacing  the  groove.  In  order  to  palpate  and 
identify  the  spines,  the  patient  should  be  made  to  double  over  to  the 
front,  thus  giving  the  spinal  column  a  curve  with  its  convexity  to 
the  rear,  and  making  the  spines  more  prominent.  Or  the  spine  may 
be  briskly  rubbed  up  and  down,  by  which  device  the  tip  of  each 
spinous  process  is  capped  by  a  spot  of  hyperaemic  redness. 

If  searching  for  or  determining  a  given  spine,  the  following  points 
are  to  be  considered :  Just  under  the  occiput  the  spine  of  the  axis 


306 


THE  EVIDENCES  OP  DISEASE 


may  be  felt.  The  spines  of  the  3d,  4th,  and  5th  cervical  vertebrae 
are  usually  distinguishable  only  as  a  line  or  ridge.  The  6th  spine 
may  frequently  be  felt,  but  the  7th  cervical,  as  its  name  (prominens) 
indicates,  is  an  unmistakable  landmark  and  from  it  one  may  count 
downward.  Or,  if  the  number  of  a  given  rib  is  known  the  number 
of  the  spine  on  a  level  with  it  may  be  inferred,  conversely  as  in  (3). 

In  a  patient  sitting  with  the  arms  hanging  easily  at  the  sides  the 
scapula  covers  the  ribs  from  the  2d  to  the  7th  (sometimes  from  the 
3d  to  the  8th)  inclusive.  In  the  same  position  the  inner  end  of  the 
spine  of  the  scapula  is  on  a  level  with  the  3d  dorsal  spine,  and  the 
inferior  angle  of  the  scapula  corresponds  to  the  7th  dorsal  spine. 

Topographical  Areas  of  the  Thorax. — Certain  arbitrary 
lines,  vertical  and  horizontal,  are  conceived  to  be  drawn  upon  the 


ANTERIOR 
AXILLARY  LINE 


1 


MAMMILLARY  LINE^ 

PARASTERNAL 
LINE 


STERNAL  LINE 


sgS^ASTRir 


i 


Fig.  71. — Showing  tlie  topographical  areas  of  tlie  thorax  an 

front,  side,  and  back  of  the  thorax,  thereby  mapping  it  into  regions 
or  areas  which  are  convenient  for  purposes  of  description  or  record 
(Figs.  71  and  72). 

The  vertical  lines  are  from  front  to  back. 

(1)  The  midsternal  line  and  its  prolongation  upward. 

(2)  The  sternal  line,  corresponding  to  the  lateral  border  of  the 
sternum. 

(3)  The  parasternal  line,  midway  between  (2)  and 


TOPOGRAPHICAL  AREAS  OP  THORAX 


307 


(4)  The  mammillary  (or  nipple)  line.,  which,  even  in  the  male 
thorax,  does  not  always  pass  through  the  nipple,  but  may  be  more 
exactly  defined  as  a  vertical  line  dropped  from  the  centre  of  the 
clavicle. 

(5)  Tllie  anterior  axillary  line,  drawn  through  the  point  at  which 
the  great  pectoral  muscle  leaves  the  chest  when  the  arm  is  raised 
sidewise  to  a  horizon- 
tal line. 

(6)  The  middle  ax- 
illary line,  drawn 
through  midway  be- 
tween (5)  and 

(7)  The  posterior 
axillary  line,  which  is 
drawn  through  the 
point  at  which  the 
latissimus  dorsi  leaves 
the  chest,  the  arm  be- 
ing raised  as  in  (5). 

(8)  The  scapular 
line,  drawn  through 
the  inferior  angle  of 
the  scapula. 

(9)  The  midspinal 
line. 

The  horizontal 
lines  are,  in  front  and 
at  the  side,  from 
above  downward : 

(1)  A  line  run- 
ning from  the  cricoid 
cartilage  to  the  outer 
end  of  the  clavicle. 

(2)  The  line  of  the 
clavicles. 

(3)  A  line  through  the  third  chondro-sternal  articulation. 

(4)  A  line  through  the  sixth  chondro-sternal  articulation. 

teriorly  they  are : 

(5)  A  line  through  the  spines  of  the  scapulae. 

(6)  A  line  through  the  inferior  angles  of  the  scapulae. 

(7)  A  line  through  the  spine  of  the  twelfth  dorsal  vertebra. 
Describing  the  Site  of  Lesions  in  the  Thorax.— (1)  One 

method  is  simply  to  state  the  area  in  which  a  given  sign  or  condi- 


Fio.  72. 


-Showing  the  t<'i>"L'iiij'hic.-al  areas  of  the  trunk, 
posterior  aspect 


Pos- 


308  THE  EVIDENCES  OP   DISEASE 

tion  is  found.     This  is  of  value  in  giving  a  somewhat  general  idea 
of  locality. 

(2)  If  it  is  desired  to  define  an  exact  point,  it  is  customary,  in 
front,  to  state  the  number  of  the  rib  or  interspace,  and  the  distance, 
in  inches  or  centimetres,  either  from  the  midsternal  or  lateral  sternal 
line  at  which  it  lies ;  laterally,  to  give  the  number  of  the  rib  and  the 
relation  of  the  point  to  the  anterior,  middle,  or  posterior  axillary 
lines ;  posteriorly,  to  record  the  rib  or  interspace,  and  the  distance 
of  the  point  from  the  midspinal  line,  or 

(3)  To  state  the  number  of  the  rib  or  interspace  and  the  vertical 
line  (e.  g.,  parasternal,  anterior  axillary)  at  which  the  condition  to 
be  noted  is  found. 


SECTION    XXXI 
EXAMINATION   OF   THE   CIRCULATORY   SYSTEM 

With  one  or  two  exceptions,  space  forbids  special  reference  to 
the  normal  physiology  of  the  circulatory  system,  a  knowledge  of 
which  is  presupposed. 

The  Cardiac  Cycle. — The  "  cardiac  cycle  "  (Curtis)  comprises 
all  the  events,  both  auricular  and  ventricular,  which  occur  during 
one  complete  auricular  cycle  (systole  and  diastole),  as  seen  in  Fig. 
73,  thus  embracing  the  two  essential  facts  of  heart  activity  and 
heart  repose. 

The  duration  of  the  cardiac  cycle,  when  the  pulse  rate  is  at  the 
normal  average  of  72  per  minute,  is  0.8  second.  The  auricular  sys- 
tole lasts  0.1  second,  the  ventricular  systole  0.3  seconds,  and  the 
period  of  repose,  when  the  heart  as  a  whole  is  at  rest,  0.4  second. 
Clinically  it  should  be  borne  in  mind  that  with  a  rapid  pulse  the 
diastole,  the  resting  time  of  the  heart,  is  greatly  shortened,  rather 
than  the  systole. 

The  Normal  Heart  Sounds. — Upon  auscultation  each  car- 
diac cycle  is  found  to  be  attended  by  two  sounds  or  tones,  first  and 
second,  differing  in  character  and  relation  to  the  events  of  the  cycle. 

The  first  sound  begins  with  the  ventricular  systole  (Fig.  73), 
but  while  of  somewhat  prolonged  duration  does  not  last  through- 
out the  systole,  nor  does  it  terminate  very  abruptly.  For  conve- 
nience' sake  it  may  be  said  to  resemble  the  syllable  "  lubb."  The 
first  sound,  with  reference  to  its  mode  of  production,  is  unques- 
tionably composed  of  two  elements,  valvular  and  muscular.  The 
valvular  element  is  the  short  flapping  closure  of  the  mitral  and  tri- 


NORMAL  HEART  SOUNDS 


309 


cuspid  valve  segments.  The  muscular  element  is  the  sound,  more 
prolonged  and  booming  in  quality,  which  is  produced  by  the  con- 
traction of  muscle  fibres  and  bundles.     In  fevers,  when  the  heart 


EVENTS 


SOUNDS 


AURICULAR  SYSTOLE/ 0.1  SEC. 


VENTRICUWR  SYSTOLE  0.3  SEC. 


CARDIAC  CYCLE 
0.8  SEC. 


REPOSE  OF  ENTIRE  HEART  0.4  SEC, 


AURICULAR 
DIASTOLE 


VENTRICULAR 
DIASTOLE 


FIRST  SOUND 
(LUBB) 

SHORT  SILENCE 
SECOND SOUND 
(OUPPJ 


LONG  SILENCE 


s 


Fig.  73. — Diagram  showing  the 
evente  of  the  cardiac  cycle 
and  the  sounds  of  the  heart, 
with  the  relations  of  the 
sounds  and  events  to  each 
other.  The  duration  is  esti- 
mated for  a  pulse  rate  of  72 
per  minute.  To  be  read 
from  above  downward. 


muscle  is  weakened,  the  first  sound  loses  its  booming  quality  and 
becomes  short  and  flapping  in  character,  very  like  the  second  sound 
to  be  presently  described.  Indeed,  this  change  in  the  first  sound  is 
one  of  the  best  clinical  evidences  of  the  weakened  heart. 

After  the  first  sound  there  is  a  very  brief  interval,  the  Jirst,  or 
short.,  silence,  followed  by  the  second  sound. 

The  second  sound  coincides  with  the  end  of  the  ventricular  sys- 
tole, is  purely  valvular  in  character,  and  is  due  to  the  sudden  closure 
of  the  aortic  and  pulmonary  valve  segments.  It  is  short,  sharp,  and 
terminates  abruptly  by  comparison  with  the  first  sound.  Conven- 
tionally it  is  represented  by  the  syllable  "  dupp." 

The  second  sound  is  followed  by  the  second,  or  long,  silence,  which 
continues  until  the  first  sound  is  again  heard — e.  g.,  lubb-dupp — lubb- 
dupji — etc. 

Comparing  the  relative  intensity  (accentuation)  of  the  two  sounds 
under  normal  conditions,  it  will  be  found  that  when  the  heart  is  aus- 
cultated at  the  apex  beat,  the  first  sound  is  the  nearer  and  more  in- 
23 


310 


THE  EVIDENCES  OP  DISEASE 


Accelerator 

^Sympathetic)  .- 


Sup.  Cerv. 
Ganglion 

Middle'^ 
Cerv.  G. 


Inhibitor 

\  (Pneumogastn'c) 

I 
I 

1  Sup.  Cerv. 

I  Cardiac 

\  Branch. 

\  Inf.  Cerv. 

Carcf.  8r 


tense  (lubb-dupp),  while,  if  listened  to  in  the  second  interspace  on 
either  side  of  the  sternnm,  the  second  sound  is  accented  (iubb-dupp). 
Innervation  of  the  Heart. — The  nerve  supply  of  the  heart 
consists  of  (1)  intracardiac  ganglion  cells,  (2)  inhibitory  nerves,  and 
(3)  augmentor  nerves  (Fig.  74). 

The  heart  contracts  at  certain  intervals  under  the  influence  of 
the  cardiac  ganglia,  and  the  rate  of  the  successive  contractions  is  the 

resultant  of  the  opposing 
action  of  the  inhibitory 
(pneumogastric),  and  accel- 
erator or  augmentor  (sym- 
pathetic) nerves. 

Arterial  Tension. — 
The  blood  is  under  high 
pressure  in  the  arteries,  a 
lower  pressure  in  the  capil- 
laries, and  a  still  lower  pres- 
sure in  the  veins.  It  thus 
moves  continuously  in  the 
direction  of  the  lowest  pres- 
sure— i.  e.,  arteries  to  veins. 
The  causes  of  the  normal 
arterial  pressure  are  the 
force  of  the  ventricle,  the 
frictional  resistance  of  the 
capillaries,  and  the  elastic- 
ity of  the  arteries. 

Thus  connecting  the  car- 
diac pump  —the  force — with 
the  capillaries — the  resist- 
ance— is  a  system  of  tubes,  the  arteries,  which  are  elastic  and  dis- 
tensible (Fig.  75). 

The  arterial  tension  or  pressure,  therefore,  is  the  resultant  of  the 
intermittent  pumping  of  fluid  into  an  elastic  tube  which  at  its  fur- 
ther end  is  split  into  many  fine  tubes,  offering  a  steady  resistance  to 
the  outflow.  The  normal  degree  of  pressure  is  maintained  when  the 
amount  of  blood  accommodated  by  the  yielding  of  the  arterial  walls 
during  each  systole  of  the  ventricle  is  equal  to  the  amount  passed 
into  the  capillaries  during  the  following  diastole  of  the  ventricle. 

Changes  in  the  arterial  pressure  are  obviously  dependent  either 
upon  variation  in  the  strength  of  the  heart  beat,  or  in  the  resistance,. 
or  in  both.  If  the  heart  is  weak,  or  the  resistance  lessened  by  dila- 
tation or  loss  of  tone  in  the  arterioles,  the  pressure  falls ;  while  if 


Fig.  74. — Diagram  showing  the  nervous  mechanism 
of  the  heart.     Section  of  heart  after  Gegenbauer. 


ARTERIAL  TENSION— INNERVATION  OF  VESSELS 


311 


HIGH 

PRESSURE 

/IRTERIES 


[CURl^ED  doubl 

RCPRCSENT 
TCNTION  AND 
CNINQ  or    THE 
AR 


/IRTERIOLI 


C/IPILL/IR 


VCNTRICULAR  SYSTOLE 


mfmf@^m 


lYiTEM 


Et^sToe 


TM^ES. 


the  heart  contracts  with  great  vigour,  or  the  vessels  are  contracted,  it 
will  rise. 

Innervation  of  the  Blood  Vessels.— While  the  blood  is  kept 
in  motion  by  the  heart,  its  distribution  to  various  portions  of  the 
body  is  regulated  by 
the  blood  vessels. 
This  regulation  of 
the  blood  supply  to 
various  areas  de- 
pends upon  the  ex- 
istence of  circular 
muscular  fibres  in 
the  middle  coat  of 
the  arteries,  particu- 
larly those  of  small 
size  (arterioles),  and 
a  nervous  mechan- 
ism (the  vasomotor 
apparatus)  which,  by 
its  action  upon  the 
muscular  coat,  con- 
trols the  calibre  of 
the  supplying  ves- 
sels, and  in  conse- 
quence the  amount 
of  blood  permitted 
to  pass  through  them 
in  a  given  space  of 
time.  The  vasomo- 
tor apparatus  (Fig. 
76)  consists  of  vaso- 
constrictor and  vaso- 
dilator nerves,  with 
centres  in  the  cord 
and  in  the  medulla. 
The  vaso-constrictor 

nerves,  when  stimulated,  cause  contraction  of  the  vessels  to  which 
they  are  distributed;  if  cut,  the  vessels  dilate.  The  vaso-dilator 
nerves,  if  stimulated,  give  rise  to  enlargement  or  dilatation,  but  sec- 
tion of  these  nerves  does  not  cause  vascular  constriction.  The  dila- 
tors are  more  easily  excited  than  the  constrictors.  It  is  to  be  borne 
in  mind  that  both  dilator  and  constrictor  fibres  may  run  side  by 
side  in  the  same  anatomical  nerve — e.  g.,  the  sciatic. 


KESISTAMCE 

{rRICTlON  IN 
CAPILLARIES, 

MAINLY.) 


VEIN5. 

IL©M 


® 


Fig.  75. — Diajirraiu  explanatory  of  arterial  tension. 


312 


THE  EVIDENCES  OF  DISEASE 


■Q^  Branches  from  Cord  Cells 


*yVasomotor  Cells  at  various  levels  in  Cord. 


Ganglion 


The  state  of  contraction  or  dilatation  of  the  vessels  is,  therefore, 
dependent  upon  the  interaction  of  the  constricting  and  dilating  por- 
tions of  the  mechanism,  by  which  more  or  less  blood  is  admitted  to 
special  areas  or  to  large  portions  of  the  body.     In  some  areas  the 

vessels   may   be   di- 

MainVasoinotorCentre  in  Medulla.         lated;  in  others,  at 

the  same  moment, 
contracted.  Much 
of  this  necessary  va- 
riability in  blood 
supply  is  dependent 
upon  reflex  influ- 
ences, the  stimulus 
or  irritation  coming 
either  from  the  blood 
vessels  themselves  or 
from  the  end  organs 
of  sensory  nerves  in 
general.  The  con- 
striction or  dilata- 
tion appears  usually 
in  the  vascular  area 
from  which  the  stim- 
ulus arises — e.  g.,  the 
redness  of  a  sinap- 
ism ;  or  in  a  part  functionally  associated  vnth  the  part  stimulated — 
e.  g.,  the  hyperasmia  attending  an  increased  secretion  from  the  sub- 
maxillary as  the  result  of  acid  placed  upon  the  tongue.  The  utility 
of  counterirritation  is  based  upon  these  facts.  It  is  also  to  be 
noted  that  when  the  blood  vessels  of  the  skin  are  constricted,  those 
of  the  interior  are  dilated  (e.  g.,  chill),  or  the  contrary.  The  vaso- 
motor apparatus  may  be  an  important  factor  in  producing  an  in- 
crease or  a  diminution  in  the  arterial  pressure.  Contraction  of  the 
peripheral  arteries  increases  friction  and,  therefore,  the  resistance  to 
the  flow  of  blood  from  arteries  into  capillaries,  and  the  pressure 
rises.     Conversely,  if  the  arteries  dilate,  the  pressure  falls. 


Arterioles. 


Fig.  76.— Diagram  showina: 
the  vasomotor  nervous 
mechanism. 


I.    PATHOLOGICAL 


PHYSIOLOGY 
DEFECTS 


OF  VALVULAR 


Direct  Effect  upon  the  Heart. — Before  proceeding  to  study 
the  evidences  of  cardiac  and  vascular  disease,  it  will  be  of  service  to 
deal  briefly  with  some  of  the  disturbances  of  the  normal  cardiac  func- 
tions which  result  from  defective  valves. 


DIRECT  EFFECTS  OP   VALVE  LESIONS 


313 


Normally  the  blood  flows  always  in  the  same  direction,  because 
the  valves  close  easily  and  accurately ;  and  it  passes  in  proper  amount, 
because  the  openings  into  and  out  of  the  ventricles  are  sufficiently 
large  to  permit  its  free  entrance  and  exit.  Defects  at  the  valvular 
openings  are  therefore  of  two  kinds :  either  the  valve  openings  are 
narrowed  (stenosis),  or  the  valves,  because  of  shrinkage,  do  not  close 
effectually  {iiicompetency,  regui-gitation).  The  valves  may  be  normal 
and  yet  incompetent,  if  the  ring  or  opening  to  the  margin  of  which 
the  valve  is  attached  becomes  stretched  and  dilated  to  such  an 
extent  that  the  valve  segments  can  not  meet  {relative  insufficiency). 

Whatever  the  nature  of  the  de- 
fect, the  final  result  is  to  hinder 
the  flow  of  blood  along  its  normal 
channels  by  causing  stagnation  or 
stasis  in  one  of  the  chambers  of 
the  heart  (Fig.  77).  The  cavity 
of  the  heart,  which,  with  refer- 
ence to  the  course  of  the  blood, 
lies  behind  the  narrowed  or  in- 
competent valve,  is  habitually 
overfilled ;  it  can  not  properly 
empty  itself,  and  because  of  its 
constant  overdistention  becomes 
dilated.  In  course  of  time  its 
muscular  walls,  having  an  exces- 
sive amount  of  work  to  perform, 
increase  in  thickness  and  strength, 
i.  e.,  undergo  hypertrophy  up  to 
a  certain  degree,  which  is  deter- 
mined by  the  gravity  of  the  lesion 
and  the  nutritional  capability  of 
the  cardiac  muscle. 

According  to  the  particular  valve  affected  and  the  nature  of  the 
lesion,  the  resulting  changes  vary  in  detail  (Figs.  78,  79). 

(1)  In  aortic  stenosis  the  valve  segments  are  most  commonly 
thickened,  rigid,  and  adherent  by  their  edges,  so  that  during  the 
systole  of  the  left  ventricle  they  refuse  to  open  out  against  the  aortic 
walls,  and  the  exit  of  blood  from  the  ventricle  is  hindered  (Fig.  78). 
Consequently  the  latter  hypertrophies,  generally  a  single  hypertro- 
phy, with  little  dilatation  until  the  disease  is  well  advanced,  when 
there  may  be  relative  mitral  insufficiency  and  its  results.  (See  (3) 
following.) 

(2)  In  aortic  incompetency  the  valve  segments  are  shrunken  and 


FiG.  77. — Semidiagranimatic  representation  of 
the  chambers,  valves,  and  vessels  of  the 
heart.    After  Page  (redrawn  and  modified). 


314 


THE  EVIDENCES  OF  DISEASE 


their  edges  curled,  so  that  they  fail  of  exact  apposition.  As  a  result, 
after  the  left  ventricle  has  delivered  its  charge  of  blood  into  the 
aorta,  the  elastic  pressure  of  the  latter  drives  a  portion  of  the  blood 
which  it  contains  back  through  the  defective  valve  into  the  ventricle. 


Obstruction  from 

stenosis  (narrow- 
ing) of  an  arterial 
opening  (aortic  or 
pulmonary  orifice  ■ 


Regurgitation  from  im- 
perfect closure  (insuffl- 
■iency)  of  an  auriculo- 
ventricular  valve  (mitral 
or  tricuspid).  Valve 
cusps  shrunken 


Fig.  78.— Diagram  representing  insufficiency  and  stenosis.     Large  arrows  =  normal  course 
of  blood;  small  arrows  =  abnormal  currents. 

During  its  diastole,  therefore,  the  left  ventricle  is  receiving  blood 
from  both  the  auricle  and  the  aorta.  Under  this  increased  pressure 
its  walls  primarily  dilate  and  secondarily  become  hypertrophied. 
Very  frequently  there  is  also  relative  mitral  insufficiency.  (See  (3) 
following.) 

(3)  Mitral  incompetency  results  either  from  shrinking  and  puck- 
ering of  the  cusps,  or  from  dilatation  of  the  left  ventricle  so  that 
the  segments  can  not  fill  in  the  enlarged  opening  (relative  insuflfi- 
ciency),  or  from  weakening  of  the  muscular  tissue  of  the  heart,  so  that 
the  papillary  muscles  do  not  act  with  accuracy,  nor  does  the  mitral 
orifice  contract  as  in  health  during  systole. 

In  consequence  of  the  imperfect  closure  of  the  mitral  valve  during 
the  systole  of  the  left  ventricle,  a  portion  of  the  blood  which  should 


VALVULAR  LESIONS-COMPENSATION  315 

"be  expelled  into  the  aorta  regurgitates  into  the  left  auricle  (Fig.  78). 
The  auricle  thus  receives  blood  during  its  diastole  from  two  sources, 
the  left  ventricle  and  the  pulmonary  veins.  It  therefore  becomes 
overdistended  and  dilates,  and,  as  it  must  do  extra  work  in  discharg- 
ing an  unusual  amount  of  blood  into  the  ventricle,  undergoes  hyper- 
trophy. The  left  ventricle,  receiving  this  unusual  amount  of  blood 
just  previous  to  its  systole,  also  dilates  and  hypertrophies.  The 
increased  pressure  in  the  left  auricle  dams  back  the  blood  succes- 
sively in  the  pulmonary  veins,  capillaries,  artery,  and  right  ventricle. 
The  right  ventricle  dilates  and  hypertrophies,  because  of  the  dis- 
tention and  increased  work  caused  by  the  obstruction  in  the  pul- 
monary circuit.  The  tricuspid  valve  may  become  relatively  insuf- 
ficient, and  regurgitation  take  place  into  the  right  auricle.  Finally, 
the  venae  cavae,  and  through  them  the  venous  side  of  the  systemic 
circulation,  may  enter  upon  a  condition  of  permanent  engorgement. 

(4)  Mitral  stenosis  may  be  due  in  varying  proportions  to  narrow- 
ing of  the  ring,  adhesion  of  the  valve  cusps  by  their  edges,  or  con- 
traction of  the  chordae  tendineae.  In  consequence  of  the  lessened 
size  of  the  mitral  orifice  the  auricle  has  difficulty  in  expelling  its 
contents  into  the  left  ventricle.  It  dilates  and  to  a  marked  extent 
undergoes  hypertrophy.  As  with  mitral  insufficiency,  the  impedi- 
ment to  the  blood  which  comes  through  the  pulmonary  veins  into 
the  left  auricle  causes  dilatation  and  hypertrophy  of  the  right  ven- 
tricle and  auricle,  and  final  systemic  venous  congestion. 

(5)  Tricuspid  incompetence  is  usually  relative  and  secondary  to 
valvular  lesions  of  the  left  side  of  the  heart.  The  right  ventricle 
and  auricle  dilate  and  undergo  hypertrophy  for  the  same  reasons  as 
the  left  chambers  in  mitral  insufficiency,  and  the  systemic  veins 
become  overfilled. 

(G)  Tricuspid  stefiosis  is  usually  secondary  to  left-side  lesions, 
the  increased  work  and  blood  pressure  imposed  by  the  latter  giving 
rise  to  sclerotic  changes.  It  may  be  of  congenital  origin.  By  a 
similar  mechanism  to  that  of  mitral  stenosis,  the  right  auricle  dilates 
and  hypertrophies.     The  systemic  veins  are  engorged. 

(7)  Pulmonary  stenosis,  a  rare  congenital  defect,  causes  hyper- 
trophy and  dilatation  of  the  right  ventricle,  and  subsequent  similar 
changes  in  the  right  auricle. 

(8)  Pulmonary  insufficiency,  another  rarity,  produces  hypertrophy 
and  dilatation  of  the  right  ventricle  and  auricle. 

Compensation  and  its  Failure.— By  compensation  is  under- 
stood the  effort  made  by  the  heart  muscle  through  hypertrophy  to 
meet  the  increased  work  thrown  upon  it.  So  long  as  the  increased 
strength  of  the  cardiac  walls  serves  to  propel  the  blood  in  sufficient 


316  THE  EVIDENCES  OF  DISEASE 

amount  and  with  sufficient  thoroughness  to  prevent  marked  stagna- 
tion in  any  portion  of  the  blood  stream,  there  are  no  subjective 
symptoms,  and  the  patient  is  to  all  intents  and  purposes  well, 
although  during  this  period  dilatation  and  hypertrophy  are  pro- 
gressing. 

If,  however,  for  any  reason  the  strength  of  the  heart  muscle 
fails  slowly  or  abruptly,  the  compensation  is  said  to  be  "  broken  '^ 
or  "  ruptured."  The  point  of  principal  clinical  interest  with  refer- 
ence to  compensation  is  that  its  completeness  depends  almost 
entirely  upon  the  condition  of  the  cardiac  muscle.  The  most 
important  question  to  be  answered  during  the  examination  of  a 
case  of  valvular  defect  is  with  reference  to  this  point.  Aside  from 
the  signs  discerned  in  the  heart  itself — the  direct  effects  of  the 
lesion  (dilatation,  hypertrophy,  etc.) — this  question  must  be  answered 
by  the  presence  or  absence  of  certain  indirect  or  peripheral  effects 
or  symptoms. 

Indirect  Effects  of  Valvular  Lesions. — With  few  excep- 
tions the  peripheral  symptoms  are  due  to  passive  (venous)  conges- 
tion of  various  organs  sequent  to  the  damming  back  of  the  blood  by 
various  valvular  defects.  The  congestion,  for  obvious  reasons,  affects 
the  pulmonary  circuit  and  the  lungs  primarily,  and  later  in  the  dis- 
ease the  organs  and  parts  drained  by  the  systemic  veins.  The  organs 
and  parts  of  the  body  and  the  symptoms  of  more  or  less  complete 
compensation  which  they  offer  are  as  follows  (see  Fig,  79) : 

(1)  Lungs. — Dyspnoea,  cough,  haemoptysis,  or  pulmonary  cedema 
demand  an  examination  of  the  heart.  So  also  do  frequent  severe 
or  protracted  attacks  of  bronchitis,  Hydrothorax  is  a  direct  result 
of  valvular  disease.  The  long-continued  pulmonary  congestion  and 
high  vascular  pressure  may  lead  to  atheromatous  changes  in  the  ves- 
sels and  brown  induration  of  the  lungs. 

(2)  Liver. — Back  pressure  in  the  inferior  vena  cava  may  show 
itself  by  congestion  and  great  swelling  of  the  liver  and,  if  there 
is  tricuspid  insufficiency,  pulsation  of  the  liver  as  well.  Long-con- 
tinued passive  hyperaemia  produces  the  nutmeg  liver. 

(3)  Stomach,  Spleen,  Intestines. — As  these  organs  must  drain 
through  the  portal  vein,  the  congested  hepatic  capillary  system  fur- 
nishes, as  compared  with  other  viscera,  an  additional  barrier  to  the 
emptying  of  their  veins.  Consequently,  the  stomach  offers  the  symp- 
toms of  a  catarrhal  gastritis,  the  spleen  becomes  somewhat  enlarged, 
and  the  intestines  become  the  seat  of  a  chronic  catarrh.  Diarrhoeal 
attacks  are  controlled  with  difficulty  or  alternate  with  constipation. 
In  advanced  cases  the  congestion  is  so  great  that  there  is  a  serous 
exudate  into  the  peritoneal  cavity  (ascites). 


INDIRECT  EFFECTS  OF  VALVE  LESIONS 


317 


(4)  Kidney.— There  is  renal  congestion ;  the  urine  is  scanty,  albu- 
minous, and  contains  tube  casts. 


ff£AD""UPPER 
EXTffEM. 

CYANOSIS  OF  FACE 

Cl  UBBED  FINCEDS 

SYSTOLIC  JUCULAR 

PULSE. 


L  t/A/GS. 

COUCH. 

OVSPNOSA. 

FRCOUENT  B/fOMCHlTIS. 
OEDEMA. 

MyooorHOOAx. 

HAEMOPTYSIS  ■ 
OK  Own  fNOt/l9. 
A  THE  POM  A  TOUS 

VESSELS. 


CEREBRAL  ANAEMIA. 

VEBTICO. 
rAINTNCSS. 

At" 

S  YNCOPC. 


OKlIFo 


OCDCMA,  LOHCR 
EXTRLMITILS. 


INTESTINAL  CATARRH. 
OBSTINATE  DIARRHOEA. 


CONSTIPATION. 
ASCITES. 


ILIAC  ARTS. 


Fig.  79. — Diagram  showini?  the  indirect  (peripheral)  efiects  of  valvular  lesions.  This 
diagram  is  also  of  service  in  tracing  the  direct  (cardiac)  changes  due  to  valvular 
defects.    The  indirect  results  are  catalogued  in  the  sign  squares. 

(5)  Venae  Cavae. — If  the  back  pressure  in  the  superior  cava  is  con- 
tinuously high,  there  is  cyanosis  of  the  lips  and  face,  clubbing  of  the 
fingers,  and,  with  tricuspid  regurgitation,  a  systolic  jugular  pulse. 
As  a  result  of  a  similar  condition  in  tlie  inferior  cava,  there  is  oedema 


518  THE  EVIDENCES  OP  DISEASE 

of  the  lower  extremities,  and,  if  the  pressure  is  extremely  high  in 
both  cavae,  general  anasarca. 

(6)  Brain. — In  some  cases  so  little  blood  is  sent  to  the  brain 
(arterial  anaemia)  that  vertigo,  or  faintness,  partial  or  amounting  to 
complete  syncope,  may  occur. 

The  foregoing  signs  and  symptoms,  if  present,  demand  on  the 
one  hand  a  search  for  cardiac  disease;  on  the  other  hand,  if  cardiac 
■disease  is  found,  these  phenomena  should  be  inquired  for  in  order  to 
make  an  estimate  of  the  manner  in  which  the  heart  is  doing  its  work 
— i.  e.,  the  condition  of  the  heart  muscle. 

n.  TOPOGRAPHICAL  ANATOMY  OF  THE  HEART 
AND  ITS  VALVES 

Shape  of  the  Heart. — The  best  recent  description  of  the  surface 
anatomy  of  the  heart  is  that  of  Keillor  (American  Journal  of  the 
Medical  Sciences,  April,  1898),  based  upon  the  models  of  His  and 
his  own  gelatin-injected  specimens.  The  present  purpose  will  be 
fully  subserved  by  describing  the  heart  as  a  whole  and  the  anterior 
surface  in  particular. 

The  heart  is  an  irregular,  four-sided  pyramid,  its  base  resting 
upon  the  diaphragm.  Its  apex  is  truncated,  thus  oflEering  a  place 
for  the  roots  of  the  upspringing  great  vessels.  It  therefore  possesses 
^ve  surfaces,  anterior,  posterior,  right,  left,  and  inferior  (the  base), 
with  well-defined  borders  separating  them. 

The  anterior  surface  is  triangular  in  shape,  slightly  curved,  and 
lies  parallel  with  the  posterior  surface  of  the  sternum.  It  includes 
from  right  to  left  the  whole  right  appendix  and  a  part  of  the  right 
auricle,  the  greater  part  of  the  right  ventricle,  and  portions  of  the 
left  appendix  and  left  ventricle.  It  is  separated  from  the  right  sur- 
face by  the  convex  and  nearly  vertical  right  anterior  border  ;  from  the 
inferior  surface  or  true  anatomical  base,  by  the  sharp,  almost  straight 
antero-inferior  border  ;  from  the  left  surface  by  the  convex,  slightly 
rounded  oblique  left  anterior  border.  The  upper  angle  of  the  anterior 
surface  is  the  anatomical  apex,  and  merges  into  the  anterior  walls  of 
the  great  arteries.     The  left  anterior  angle  is  the  clinical  apex. 

The  diagram  (Fig.  80)  is  drawn  in  accordance  with  the  facts 
just  rehearsed,  except  that  the  right  lower  angle  of  the  heart  is 
rounded.  Owing  to  the  normal  anatomical  and  functional  varia- 
tions in  the  shape  of  the  heart,  and  the  changes  in  its  position  result- 
ing from  respiratory  action,  bodily  posture,  and  the  shape  of  the 
thorax,  no  one  diagram  can  tell  the  whole  story. 

Relation  of  Heart  to  Chest  Walls. — The  projection  of  the  heart 
upon  the  anterior  chest  wall,  an  outline  corresponding  to  the  shadow 


TOPOGRAPHY  OF  THE  HEART 


319 


of  the  organ  which  would  be  cast  by  parallel  rays  of  light  passing 
from  back  to  front,  is  obtained  approximately — provided  that  the 
chest  is  well  formed — as  follows  (see  Fig.  81) : 


\-  - 


Fig.  80. — The  anterior  aspect  of  the  normal  heart  and  preat  vessels,  showin?  their  relations 
to  the  anatomical  landmarks  (ribs,  sternum,  clavicles)  of  the  front  9f  the  thorax. 

(1)  Upper  Border. — Draw  a  horizontal  line  across  the  sternum  at 
the  level  of  the  3d  costal  cartilages,  from  a  point  ^,  4  an  inch  to 
the  right  of  the  right  edge  of  the  sternum,  to  a  point  B,  1  inch  to 
the  left  of  the  left  sternal  edge.  This  is  the  dividing  line  between 
the  heart  and  the  great  vessels,  and  is  the  clinical  base  of  the  heart. 

(3)  Lo2cer  Border. — Mark  a  point  Z),  vertically  below  the  nipple, 
in  the  5th  intercostal  space  between  the  5th  and  6th  left  ribs,  just 
at  the  upper  edge  of  the  latter.  The  apex  beat  (which  is  not  made 
by  the  extreme  apex  of  the  heart)  is  usually  felt  in  the  middle  of  the 


320 


THE  EVIDENCES  OF  DISEASE 


5th  space,  and  ^  to  1  inch  inside  the  mammillary  line.  Mark  also  a 
point,  C,  at  the  junction  of  the  upper  and  middle  3ds  of  the  ensiform 
cartilage.     Point  C  is  usually  ^  an  inch  higher  than  point  D. 

The  statements  here  made  Avith  reference  to  the  position  of  the 
lower  border  of  the  heart  do  not  agree  with  those  commonly  accepted, 

which  place  this  bor- 
r"""  "  .- . -^^nm^millip  —    ^g^  ^^  ^  point  a  little 

above  the  lower  end 
of  the  sternum.  The 
ordinary  descriptions 
are  correct  for  the 
cadaver  (Sibson),  not 
for  the  living  sub- 
ject, owing  to  the  as- 
cent of  the  diaphragm 
and  heart  which  takes 
place  in  articulo 
mortis. 

Draw  a  line  con- 
necting these  points. 
(3)  Right  Border. 
— From  point  A  draw 
a     line      downward, 
curving  a  little  to  the 
right,  until  it  reaches 
the  middle  of  the  4th 
interspace,  then  curv- 
ing to  the  left  until 
it  passes  over  the  car- 
tilages of  the  6th  and 
7th  ribs,  a  little  before  they  join  the  sternum,  and  meets  point  C 
over  the  ensiform  cartilage. 

(4)  Left  Border. — Connect  points  B  and  i)  by  a  line  slightly  con- 
vex to  the  left. 

This  outline  represents  the  position  of  the  heart  in  a  well-formed 
chest.  In  an  emphysematous  thorax  (permanent  position  of  inspira- 
tion) it  lies  lower  in  relation  to  the  ribs,  its  inferior  border  descend- 
ing to  the  tip  of  or  below  the  appendix.  On  the  other  hand,  if  the 
chest  is  of  the  alar  or  phthisical  type  (permanent  position  of  expira- 
tion), its  lower  border  may  lie  half  an  inch  or  more  above  the  end  of 
the  sternum. 

Mobility  of  the  Heart. — In  addition  to  the  permanent  variations 
in   position  just  mentioned,  the   heart  is  movable  by  posture  and 


Fig.  81. — Points  upon  the  chest  by  which  the  normal  bound- 
aries of  the  heart  and  great  vessels  may  be  determined. 
Nipples  in  this  iigure  are  too  far  away  from  the  median 
line. 


EXAMINATION  OF  THE  HEART  321 

respiration.  If  the  individual  lies  in  the  left  lateral  position,  the 
apex  beat  moves  to  the  left  and  becomes  more  forcible  ;  if  flat  on  his 
back,  the  heart  recedes  from  the  chest  wall,  and  the  apex  beat  may 
become  imperceptible  ;  if  on  the  right  side,  the  impulse  moves  nearer 
to  the  median  line  ;  if  he  leans  forward  or  lies  face  downward,  the 
apex  beat  strengthens.  In  forced  inspiration  the  diaphragm  descends, 
drawing  the  heart  downward  and  toward  the  median  line  by  means 
of  the  attachment  of  the  pericardial  sac  to  its  central  tendon.  The 
ribs  move  upward,  thus  increasing  the  displacement  of  the  heart 
relatively  to  these  bony  landmarks.  In  forced  expiration  the  dia- 
phragm moves  upward,  elevating  the  heart  and  shifting  its  apex 
further  to  the  left.  The  ribs  move  downward,  increasing  relatively 
the  ascent  of  the  heart.  The  excursion  of  the  diaphragm  may 
amount  to  2  inches. 

When  the  heart  moves,  it  swings  from  its  point  of  suspension  by 
the  great  vessels  at  the  base.  Consequently,  the  excursion  of  its 
apical  portion  from  side  to  side  or  from  front  to  back  is  much  greater 
than  that  of  the  base,  except  where  there  is  a  localized  pull  by  re- 
tracting fibroid  tissue  or  pressure  by  new  growths. 

Relation  of  Cavities  and  Great  Vessels  to  Chest  Wall. — The  rela- 
tions of  the  various  cavities  of  the  heart  to  the  chest  walls  are  shown 
sufficiently  in  Fig.  80. 

The  great- vessel  area,  so  called  for  convenience,  may  be  outlined 
by  first  drawing  a  horizontal  line  across  the  junction  of  the  middle 
and  upper  3ds  of  the  manubrium.  This  line  should  lie  about  f  inch 
below  the  upper  border  of  the  manubrium  (episternal  notch).  It 
should  extend  right  and  left  sufficiently  to  permit  a  vertical  line  to 
be  drawn  downward  from  each  end  to  points  A  and  B  (Fig.  81). 
The  vessels  contained  in  this  space  are  shown  in  Fig.  80. 

III.    PHYSICAL    EXAMINATION    OF    THE    HEART    AND 
ITS    NEIGHBOURHOOD 

The  subjective  symptoms  of  cardio-vascular  disease  are  summarized 
elsewhere  (see  Synopsis  of  Examinations),  and  referred  to  in  detail 
in  various  places. 

The  objective  condition  of  the  heart  is  ascertained  by  inspection, 
palpation,  percussion,  and  auscultation.  The  patient  should  be,  pref- 
eraljly,  semirecumbent,  as  there  are  fewer  physical  difficulties  in  the 
way  than  if  sitting  or  standing. 

A.  Inspection"  and  Palpation 

By  inspection  and  palpation,  which  are  instinctively  combined, 
the  examiner  determines  the  shape  of  the  praecordium,  certain  facts 


322  THE   EVIDENCES  OF   DISEASE 

regarding  the  apex  beat  and  praecordial  pulsation,  the  presence  or 
absence  of  pulsating  or  distended  veins,  and  other  abnormal  pulsa- 
tions or  thrills. 

Elsewhere  (see  Index)  have  been  considered  the  shape  of  the  prcB- 
cordium,  distended  veins  of  chest,  and  pulsating  Jug ulars. 

Apex  Beat. — The  apex  beat  lies  normally  in  the  5th  left  inter- 
costal space,  ^  inch  inside  the  mammillary  line,  and  about  3  inches  to 
the  left  of  the  midsternal  line.  In  health  the  apex  beat  is  lim- 
ited to  a  space  1  inch  in  breadth,  occupying  one  interspace  only. 
Each  impulse  pushes  the  examining  finger  outward,  about  t  to  ^ 
inch.  It  is  somewhat  internal  to  the  apex  formed  by  the  ventricles ; 
and  if  there  is  considerable  hypertrophy  it  may  lie  much  farther  to 
the  inner  side  of  the  actual  apex,  the  right  ventricle  (not  the  apex) 
of  the  enlarged  and  rounded  heart  striking  against  the  chest  wall. 
In  this  case  the  left  and  lower  border  of  complete  cardiac  dulness. 
will  be  found  some  distance  outside  of  the  apex  beat. 

In  the  majority  of  cases  the  apex  beat  can  be  both  seen  and  felt,. 
in  many  felt  but  not  seen,  and  in  some  it  may  be  imperceptible.  In. 
palpating  the  apex  beat,  the  whole  hand  should,  first  of  all,  be  laid 
smoothly  but  firmly  over  the  praecordial  region,  the  fingers  pointing 
downward  and  to  the  left.  This  is  important,  because  the  character 
of  the  heart  action  as  well  as  the  point  of  most  marked  impulse  is- 
at  once  appreciated.  After  this  the  finger  tips  may  be  employed  to 
accurately  locate  the  apex  beat.  As  tiie  impulse  may  be  diffuse,  the 
apex  beat  should  be  considered  to  lie  at  the  point  where  the  finger 
appreciates  a  distinct  thrust  from  within.  If  a  localized  impulse 
can  not  be  felt  while  the  patient  is  recumbent,  he  should  be  re- 
quired to  sit  upright,  lean  forward,  or  turn  upon  the  face  (if  his 
condition  permits),  so  as  to  bring  the  heart  to  the  front  of  the 
thorax  by  gravity. 

Having  identified  the  apex  beat,  it  is  to  be  studied,  together  with 
the  praecordial  impulse  in  general,  with  reference  to  position,  charac- 
ter, and  extent  (Fig.  82). 

Position  of  the  Apex  Beat. — The  position  of  the  apex  beat  is  of 
extreme  importance,  as  it  furnishes  the  most  reliable  information 
with  reference  to  the  situation  of  the  heart.  As  it  coincides  with 
the  ventricular  systole,  it  also  furnishes  the  standard  for  determining 
the  time  relation  of  other  pulsations — i.  e.,  whether  they  are  systolic, 
presystolic,  or  diastolic.  Aside  from  normal  alterations  in  the  posi- 
tion of  the  heart,  the  apex  beat  may  be  moved  from  its  natural  loca- 
tion, either  by  an  actual  dislocation  of  the  entire  heart  caused  by 
pressure  or  pull,  or  by  changes  in  its  shape  due  to  hypertrophy  or 
dilatation.     It  is  to  be  borne  in  mind  that  deformities  involvins;  the 


POSITION   OF  APEX   BEAT  323 

chest,  kyphosis,  scoliosis,  et  ah,  deprive  the  position  of  the  apex  beat 
of  much  of  its  diagnostic  value,  as  it  may  be  displaced  in  any  direc- 
tion and  mistakenly  considered  a  result  of  serious  cardiac  disease  or 
as  a  marked  congenital  anomaly  of  position. 

(1)  Displacement  to  the  left  and  uptvard  is  the  result  of  varying 
lesions.  It  may  be  due  to  pericardial  effusion,  or  to  abdominal  dis- 
tention vith  upward  pressure  upon  the  diaphragm  by  gas,  fluid,  or 
tumour.  Fibroid  changes  in  the  left  lung  or  pleura,  forming  a  part 
of  chronic  phthisis,  interstitial  pneumonia,  and  extensive  pleural 
adhesions,  by  their  contraction  will  pull  the  heart  to  the  left  and  the 
diaphragm  upward,  carrying  the  apex  in  the  same  direction.  It  ia 
also  carried  to  the  left  and  upward  by  the  pressure  of  fluid  or  air  in 
the  right  pleura  or  by  mediastinal  tumour.  In  severe  cases  of  thia 
displacement  the  apex  may  beat  in  the  midaxillary  line.  It  should 
be  remembered  that  in  infants,  and  in  children  up  to  the  10th  and 
12th  year,  the  apex  beat  is  normally  in  the  4th  space,  at  or  outside 
the  mammillary  line. 

(2)  Displacement  to  the  left  in  a  horizontal  line  may  arise  from 
any  of  the  causes  mentioned  in  (1),  but  is  especially  characteristic  of 
hypertrophy  and  dilatation  of  the  right  ventricle.  It  rarely  passes, 
farther  outward  than  the  mammillary  line. 

(3)  Displacement  to  the  left  and  doivmrard  is  characteristic  of 
cardiac  hypertrophy  and  dilatation,  especially  of  the  left  ventricle,, 
in  which  case  it  may  be  carried  even  to  the  8th  space  and  midaxil- 
lary line. 

(4)  Downward  displacement  of  the  beat  may  be  induced  by 
hypertrophic  emphysema.  In  this  disease  the  chest  is  in  a  perma- 
nent inspiratory  position  and  the  ribs  move  upward  over  the  heart. 
The  lungs  become  larger  and  press  the  heart  downward,  and  the 
hypertrophied  right  ventricle  contributes  to  its  lowered  position. 
Aneurism  of  the  arch  of  the  aorta  and  tumours  in  the  upper  por- 
tion of  the  mediastinum  will,  if  of  sufficient  size,  depress  the  heart 
and  with  it  the  apex  beat.  The  weight  of  an  enlarged  liver,  by 
dragging  upon  the  central  tendon  of  the  diaphragm  to  which  is 
attached  the  pericardial  sac,  has  pulled  the  heart  downward  (Pall). 
In  the  aged  the  apex  beat  may  normally  be  found  in  the  6th  inter- 
space. 

(5)  Displacement  to  the  right,  very  rarely  further  than  the  right 
mammary  line,  may  be  caused  by  the  retracting  power  of  chronic 
fibroid  changes  in  the  right  lung,  and  adhesions  in  the  right  pleural 
cavity.  A  similar  displacement  may  be  caused  by  the  pressure  of  left- 
side pleurisy  with  effusion,  hydrothorax,  pneumothorax,  or  tumour 
of  the  left  lung. 


324  THE  EVIDENCES  OF  DISEASE 

Character  and  Extent  of  Apex  Beat. — By  constant  practice  the 
hand  learns  to  appreciate  very  correctly  any  variations  in  the  extent 
and  power  of  the  impulse  of  the  heart  against  the  thorax. 

(1)  A  somewhsit  forcible  and  extensive  apex  beat  of  a  knocking  or 
slapping  character  may  be  due  to  mental  excitement,  nervousness,  or 
physical  exertion.  It  is  important  not  to  form  a  judgment  of  the 
cardiac  status  under  these  circumstances  or,  if  unavoidable,  to  make 
proper  allowance  therefor.  Certain  drugs  (tea,  coffee,  nicotine,  alco- 
hol, etc.)  have  a  similar  effect.  In  the  early  stage  of  acute  fevers  the 
same  overaction  is  observed — indeed,  it  is  present  in  almost  all  cases 
of  palpitation  (q.  v.). 

In  persons  with  unusually  thin  chest  walls  the  impulse  of  the 
heart  is  both  visible  and  palpable  over  a  much  wider  extent  than  in 
those  whose  ribs  are  well  covered.  Another  cause  of  increase  in 
extent,  not  necessarily  in  strength,  of  the  impulse,  is  the  uncovering 
of  the  heart  to  the  left  of  the  sternum  by  retraction  of  the  corre- 
sponding lung.  In  a  well-marked  case  the  impulse  is  visible  and 
palpable  in  the  3d,  4th,  and  5th  interspaces,  sometimes  slightly  in 
the  2d,  and  the  snap  of  the  arterial  valves  may  be  very  distinct. 
This  is  excellent  evidence  of  the  pulmonary  condition,  and  should 
not  be  mistakenly  referred  to  disease  of  the  heart. 

In  all  the  foregoing  cases  the  apex  beat  is  not  displaced,  a  prime 
fact  in  determining  the  absence  of  hypertrophy. 

A  strong  lifting  or  heaving  impulse,  which  can  be  felt  over  2  or  3 
interspaces,  with  displacement  of  the  apex  beat  to  the  left  and  down- 
ward, is  a  most  valuable  sign  of  hypertrophy  of  the  left  ventricle. 

(2)  Weakness  or  absence  of  the  apex  beat  may  be  caused  by  dila- 
tation of  the  heart  subsequent  to  hypertrophy,  the  lifting  heave  of 
the  latter  giving  place  to  a  diffused  undulating  impulse  of  little 
strength,  which  is  quite  distinctive.  The  disappearance  of  a  defined 
and  easily  located  apex  beat  is  particularly  marked  in  dilatation  of 
the  right  ventricle,  the  distended  roundness  of  the  latter  pushing 
the  apex  away  from  the  chest  wall.  It  disappears  also  with  the 
onset  of  a  considerable  pericardial  effusion  which  surrounds  the  apical 
portion  of  the  heart  and  separates  it  from  the  thoracic  wall. 

Weakness  or  absence  of  the  apex  impulse  is  not  incompatible 
with  health.  It  may  be  due  to  a  thick,  fat  chest  wall,  or  to  the  fact 
that  the  apex  strikes  just  behind  a  rib.  In  some  otherwise  normal 
cases  there  is  no  discoverable  reason  for  its  absence.  If  the  heart  is 
displaced  to  the  right,  the  apex  beat  may  be  extinguished  behind  the 
lower  sternum.  If  no  apex  impulse  exists,  the  place  where  it  should 
be  found  may  be  identified  by  auscultation — i.  e.,  the  point  at  which 
the  1st  sound  is  heard  with  the  greatest  intensity.     The  excessive 


CHARACTER  OF  APEX  BEAT— OTHER  PULSATIONS         325 

overlapi)ing  of  the  heart  by  the  increased  bulk  of  the  luugs  in  emphy- 
sema may  put  a  damper  upon  the  impulse.  Extensive  or  universal 
pericardial  and  mediastinal  adhesions  may  so  limit  cardiac  mobility 
that  the  apex  does  not  strike  with  sufficient  force  to  be  felt.  In  this 
case  a  systolic  drawing  in  or  retraction,  not  alone  of  the  apex  space 
but  of  the  lower  sternum  and  several  intercostal  spaces  and  ribs, 
may  replace  the  usual  systolic  protrusion,  and  possesses  diagnostic 
value.  In  rare  cases  of  extreme  aortic  stenosis  the  ventricle  takes  so 
long  to  propel  the  blood  through  the  narrow  orifice  that  the  systole 
is  deliberate  and  the  celerity  of  movement  necessary  for  the  impulse 
lacking. 

In  general  it  may  be  said  that,  barring  a  thick  chest  wall  or 
emphysema,  a  weak  or  absent  apex  beat  indicates  a  weak  heart  from 
any  cause — e.  g.,  exhausting  disease,  shock. 

Other  Pulsations  or  Pulsating  STvellings.— Inspection 
(especially  by  oblique  illumination)  and  palpation  may  reveal  cen- 
tres of  pulsation  other  than  that  of  the  apex  beat  as  shown  by  the 
simultaneous  presence  of  an  apparent  apex  beat  elsewhere. 

A  question  frequently  arises  as  to  the  exact  rhythm  of  one  pulsa- 
tion as  compared  with  another,  comparison  usually  being  made  with 
the  apex  beat  by  placing  a  finger  on  each ;  or  with  the  first  sound,  by 
auscultation  while  palpating.  For  greater  accuracy  indicators  may 
be  employed.  The  most  convenient  of  these  is  a  bit  of  absorbent 
cotton  pulled  out  into  a  slender  cone  2  or  3  inches  long.  Its  base  is 
applied  to  the  pulsating  spot,  previously  touched  with  mucilage  or 
thick  ointment.  Having  affixed  one  of  these  to  each  spot  and  placed 
the  examining  eye  so  that  the  cones  are  in  a  line,  the  movement  of 
their  extremities,  by  exaggerating  the  pulsations,  enables  a  more 
ready  determination  of  the  rhythm  of  each  pulsation.  This  method 
is  also  of  service  in  determining  the  expansile  character  of  a  pulsat- 
ing swelling,  a  cone  being  placed  on  each  side  of  the  tumour.  If 
expansile  pulsation  is  present  the  tips  of  the  cones  will  approach  ' 
and  depart  in  an  unmistakable  fashion. 

Some  pulsations  are  visible,  others  not  visible  but  palpable,  and 
still  others  present  a  more  or  less  marked  prominence  or  bulging  of 
the  chest  wall  according  to  their  nature. 

These  pulsations  may  originate  from  the  great  arteries  (dynamic, 
aneurismal),  the  veins  (pulsating  liver),  the  heart  (hypertrophy  or 
dilatation),  or  may  be  communicated  (pulsating  empyema).  Taking 
them,  according  to  location,  from  above  downward,  and  from  right 
to  left,  they  may  be  found  as  follows :  As  a  general  rule  it  may  be 
said  that  pulsations  above  the  level  of  the  3d  rib  belong  to  the  great 
arteries,  below  that  point  to  the  heart. 
23 


326 


THE   EVIDENCES  OF  DISEASE 


(1)  Pulsations  in  the  episternal  notch  and  at  the  root  of  the  neck 
have  been  discussed  elsewhere  (page  267). 

(2)  Pulsation  in  the  right  1st  or  2d  interspace,  close  to  the  right 
of  the  sternum  (Fig.  82),  systolic  in  time,  expansile  in  character, 
may  be  due  to  aneurism  of  the  ascending  portion  of   the  arch  of 


APEX  BEAT  DISPLACED— 


I  Pulsation    due    to    RE- 

I  TRACTION  OF  LUNG 
DRAWING  GREAT  VESSELS 
AND    HEART   TO   RIGHT 


Pulsation    due    to    di- 
lated    AURICLE,     also 

to      dislocation      of 
heart  to  right 


Pulsation  due  to  dis- 
location OF  HEART  TO 
RIGHT  ^  RETRACTION 
OF  LUNG  AND  PLEURA  ; 
OH  LEFT-SIDE  EFFU- 
SION, PNEUMOTHORAX, 
OR   TUMOUR 


,  Systolic  (heart) 

Enlarged  right  ventricle 

Emphysema 

Simple  overaction  of  heart 

d.splaced  apex  b3at 


Up  and  to  Left 
Pericardial  effusion 
Abdominal  distention 
Fibrosis    or    contract- 
ing cavity,  left  lung 
Extensive  left  pleural 

adhesions 
Fluid    or  air    in    right 

PLEURA 

To  Left 
Right    ventric.    hyper- 
trophy and  dilatation 


Down  and  to  Left 
Left  ventricular  hyper- 
trophy and  dilatation 


Down 

Emphysema 
Aneurism  of  arch 
Weight  of  large  liver 
Tumour   of    upper    me- 
diastinum 


EPIGASTRIC    PULSATION 


Post-systolic  (aorta) 
Throbbing  aorta 
Thin  abdominal  walls 
Tumour  in  front  of  aorta 
Abdominal  aneurism 


Position  of  normal 
APEX  beat 


Fig.  82. — Showing  the  indications  to  be  obtained  from  the  position  of  the  apex  beat  and 
other  thoracic  and  epigastric  pulsations.  For  pulsation  in  the  episternal  notch,  see 
page  267.  /,  //,  ///,  IV,  V.  VI  =  pulsations  of  aortic  aneurism  (arch),  numbered  in 
order  of  frequency  of  occurrence.  VII  =  innominate  aneurism.  //  =  also  pulsation 
of  pulmonary  artery  (and  left  auricular  appendix  ?).  V  =  also  pulsation  of  right  ven- 
tricle (and  left  auricular  appendix  ?).  O  =  cardiac  impulses.  +  =  aneurismal  pulsa- 
tions.    a>  =  both. 

the  aorta  or,  without  expansile  character,  to  violent  heart  action.  It 
is  here  that  a  diastolic  shock  accompanying  the  closure  of  the  aortic 
valves  is  to  be  felt  in  aneurism  of  the  arch. 

(3)  Pulsation  in  the  right  2d  and  3d  interspaces,  ranging  from 
the  sternal  edge  to  the  mammillary  line,  may  be  caused  by  a  dragging 
over  of  the  heart  and  great  vessels  due  to  the  retraction  of  a  fibroid 


PULSATIONS  NEAR  THE  HEART  327 

lung.    In  one  extreme  case  of  this  kind  under  observation  the  impulse 
extended  upward  into  the  first  interspace  as  well. 

(4)  Pulsation  in  the  rigid  3d,  4th,  and  5th  interspaces  close  to  the 
edge  of  the  sternum  results  from  a  dilated  right  auricle  or  a  disloca- 
tion (displacement)  of  the  heart. 

(5)  Pulsation  in  the  right  J^th  and  5th  spaces,  at  any  point  between 
the  sternal  edge  and  the  mammillary  line,  is  produced  by  displace- 
ment of  the  heart.  This  is  the  usual  location  of  a  heart  dislocated 
by  great  fluid  or  gaseous  pressure  from  the  left  pleural  cavity,  but 
retraction  of  the  lung  may  pull  the  heart  over  so  that  it  pulsates  in 
these  spaces  as  well  as  in  the  2d  and  3d  (see  (3)  preceding). 

(6)  Pulsation  over  the  manubrium  is  significant  of  aneurism  of 
the  aorta,  especially  of  the  transverse  portion  of  the  arch,  which  has 
eroded  the  bone. 

(7)  Pulsation  in  the  2d  and  sometimes  the  3d  left  interspace  close 
to  the  sternal  edge  may  be  indicative  of  aneurism  of  the  aorta,  par- 
ticularly the  descending  portion  of  the  arch,  in  which  case  the  im- 
pulse is  systolic  ;  or  of  pulsation  of  the  pulmonary  artery,  systolic  if 
due  to  the  filling  of  the  artery  by  ventricular  systole ;  and  immedi- 
ately following  the  2d  sound  if  it  is  the  rebound  of  the  artery  follow- 
ing the  closure  of  the  pulmonary  valve.  It  may  possibly,  for  there 
is  a  difference  of  opinion  on  this  point,  be  due  to  the  impulse  of  an 
hypertrophied  left  auricular  appendix,  in  which  case  it  precedes  the 
apex  beat  and  1st  sound. 

(8)  Pulsation  in  the  3d,  ^th,  5th,  and  6th  interspaces  just  to  the 
left  of  the  sternum  is  usually  caused  by  hypertrophy  and  dilatation 
of  the  right  ventricle. 

(9)  Pulsation  in  the  3d  and  Jfth  spaces  in  the  left  mammillary 
line  is  usually  the  apex  beat  of  the  heart  displaced  up  and  to  the 
left  by  pressure  from  the  right  side,  or  fibroid  contraction  of  the 
left  lung. 

(10)  Pulsation  in  the  left  5th  space  outside  the  mammillary  line 
is  usually  the  apex  beat  of  a  right  ventricular  hypertrophy. 

(11)  Pulsation  in  the  6fh,  7th,  or  8th  left  interspaces  anywhere 
between  the  mammillary  and  midaxillary  lines  is  usually  the  apex 
beat  of  left  ventricular  hypertrophy  and  dilatation.  As  a  rule,  the 
farther  the  apex  from  the  median  line,  the  lower  the  interspace  it 
occupies. 

(12)  Pulsation  over  the  left  half  of  the  precordial  area,  and  in 
the  left  axillary  region  may  in  rather  rare  cases  be  caused  by 
"pulsating  empyema"  or,  still  more  rarely,  by  a  very  vascular 
malignant  tumour. 

Aside  from  pulsations  strictly  confined  to  the  thorax,  it  is  neces- 


328  THE  EVIDENCES  OF   DISEASE 

sary  to  ascertain  whetlier  or  not  there  is  epigastric  pulsation,  or 
throbbing  of  the  liver, 

(13)  Epigastric  p^dsation,  if  found,  should  be  tested  as  to  rhythm 
by  placing  one  hand  upon  the  apex  beat,  the  other  over  the  epigas- 
trium. The  epigastric  impulse  will  be  found  either  to  coincide  with 
the  apex  beat  (systolic),  or  to  occur  immediately  but  distinctly  after 
the  heart  beat  (post-systolic). 

If  systolic^  the  impulse  comes  directly  from  the  heart,  and  may 
indicate  enlargement  or  dilatation  of  the  right  ventricle,  from  various 
causes,  the  stroke  of  which  may  be  felt  more  distinctly  by  pushing 
the  fingers  up  under  the  ensiform  appendix  and  costal  cartilages ;  an 
apex  beat  displaced  to  the  right  behind  the  sternum,  emphysema, 
or  simple  overaction  of  the  heart  from  any  cause.  In  the  latter 
case  the  pulsation  is  hardly  more  than  a  systolic  quiver  or  trembling. 
An  abnormally  short  sternum  may  also  be  a  responsible  cause. 

If  post-systolic^  the  impulse  is  from  the  abdominal  aorta,  and  its 
most  common  cause  is  the  functional  (dynamic)  throbbing  of  the 
vessel  which  is  seen  in  many  neurotic  and  neurasthenic  individuals, 
or  in  those  suffering  with  disorders  of  gastric  digestion.  It  may  be 
present  as  a  result  of  anaemia  and  hemorrhage,  and  may  be  perceived 
with  a  little  care  in  any  person  with  thin  abdominal  walls.  A  very 
marked  pulsation  may  arise  from  the  presence  of  a  tumour — e.  g., 
enlarged  lymph  glands,  pyloric  cancer,  tumour  of  pancreas,  hyper- 
trophied  or  sclerosed  left  lobe  of  the  liver,  and  hepatic  abscess. 
Finally,  it  may  be  an  aneurism,  but  this  diagnosis  is  to  be  made  with 
much  hesitation,  and  only  when  the  pulsation  is  distinctly  expansile. 
The  pulsation  due  to  a  tumour  overlying  the  aorta  will  disappear  in 
the  knee-chest  position,  the  mass  falling  forward  and  away  from 
its  contact  with  the  artery. 

Systolic  depression  of  the  epigastrium  and  lower  sternum  is  of 
value  in  making  a  diagnosis  of  extensive  pericardial  and  mediastinal 
adhesions  (indurative  mediastino-pericarditis).  One  may  mention 
here  a  systolic  depression  of  the  left  back  in  the  region  of  the  11th 
and  13th  ribs  as  a  sign  of  extensive  pericardial  adhesions,  the  pull  of 
an  hypertrophied  heart  adherent  to  the  diaphragm  making  traction 
through  the  latter  upon  the  2  movable  lower  ribs  (Broadbext). 

(14)  Pulsation  of  the  liver  is  to  be  noted  as  present  only  when 
the  entire  organ  is  enlarged  and  pulsates,  not  when  the  pulsation  is 
limited  to  the  epigastrium.  General  hepatic  pulsation  is  best  deter- 
mined by  placing  one  hand  with  firm  pressure  over  the  riglit  hyj^o- 
chondrium,  the  other  posteriorly  so  that  the  liver  lies  between  the 
two.  The  whole  organ  is  then  felt  to  expand  and,  if  timed,  the  pul- 
sation is  found  to  immediately  follow  the  apex  beat.     This  pulsation 


THRILLS  AND  FRICTION  FREMITUS 


329 


is  clue  to  and  pathoguomonic  of  tricuspid  insufficiency,  the  regurgi- 
tant wave  being  transmitted  backward  along  the  inferior  cava  and 
hepatic  veins  (Fig.  T9). 

Thrills  and  Friction  Fremitus. — Pulsation  may  be  attended 
by  thrill.  Palpable  vibrations  produced  by  the  passage  of  blood  over 
a  roughened  surface,  through  a  narrowed  orifice  or  a  leaky  valve,  are 
called  tlirills.  A  thrill  is  discernible  as  a  fine  whizzing  or  purring 
sensation  (fremissement  cataire),  but  the  vibrations  may  be  distinctly 
coarse.  A  palpable  vibration,  due  to  the  sliding  of  two  roughened 
pleural  or  pericardial  surfaces  over  each  other,  is  termed  friction 
fremitus. 


Systolic 
Aortic  stenosis 
^   Diastolic 
'      Aortic  incompetency 

^HP^ 

^ 

Systolic  thrill  of  aortic  aneu- 
rism   ANYWHERE   WITHIN    DOTTED 
LINES 

,  J 

Systouc 

Exophthalmic  goitre 
Pulmonary  stenosis 

Diastolic 
Pulmonary  regurgitation 

i          > 

>-- 

1 

Am 

anywhere  within  shaded  area 

Presystolic 
Mitral  stenosis 

Systolic 

Mitral  incompetency 
Aortic  stenosis 

Systolic 
Tricuspid  incompetency 
Hypertrophy    and    dilatation 
^          of  right  ventricle 

Fig. 


-Diagram  showing  the  diagnostic   significance  of  the  location  and  rhytJini  of 
thrills  and  friction  fremitus. 


When  a  thrill  or  friction  fremitus  is  perceived,  it  is  necessary  to 
determine  its  position  of  maximum  intensity  and  its  time  relation  to 
the  apex  beat — i.  e.,  is  it  systolic,  diastolic,  or  presystolic? 

Friction  fremitus  is  caused  by  inflammation  of  the  pericardium, 
or  of  those  portions  of  the  pleural  surfaces  which  overlie  or  are  in 
close  contact  with  the  heart.  In  both  cases  the  inflamed  or  rough- 
ened surfaces  are  rubbed  together  by  the  movements  of  the  heart, 
and  therefore  the  vibrations  exhibit  a  rhythmic  cardiac  sequence. 
It  is  usually  easy  by  auscultation  to  distinguish  between  friction 


330  THE   EVIDENCES  OF   DISEASE 

fremitus  and  a  true  thrill.  The  former  is  to  and  fro  in  character,  and 
does  not  bear  a  constant  and  definite  relation  to  the  events  of  the 
cardiac  cycle.  The  thrills  of  most  common  occurrence  are  those 
mentioned  in  (1)  and  (4)  following. 

(1)  At  and  above  the  right  2d  cartilage  and  interspace  a  systolic 
thrill,  due  to  aortic  stenosis  (see  Fig,  83).  At  the  same  point,  and 
perhaps  felt  for  some  distance  down  the  sternum,  a  diastolic  thrill, 
due  to  aortic  incompetency. 

(2)  At  and  above  the  left  2d  cartilage  and  interspace,  a  systolic 
thrill,  which  is  not  infrequent  in  exophthalmic  goitre.  Very  rarely 
it  may  indicate  pulmonary  stenosis.  A  diastolic  thrill  in  the  same 
spot  may  be  found  as  a  symptom  of  another  rare  condition,  pulmo- 
nary incompetency. 

(3)  A  systolic  thrill  over  the  lower  part  of  the  sternum  as  a 
symptom  of  tricuspid  regurgitation  ;  or,  without  valvular  disease,  in 
hypertrophy  and  dilatation  of  the  right  ventricle. 

(4)  A  systolic  thrill  over  the  apex  beat  and  its  immediate  neigh- 
bourhood is  usually  due  to  mitral  incompetency,  sometimes  to  aortic 
stenosis. 

(5)  The  thrills  so  far  referred  to  are  fine  and  soft  in  character, 
but  a  presystolic  thrill  at  r.nd  somewhat  above  and  to  the  inner  side 
of  the  apex  beat  is  very  distinctive.  It  is  composed  of  rather  rough, 
hesitating  vibrations,  and  even  in  the  absence  of  other  symptoms 
permits  a  diagnosis  of  mitral  stenosis. 

(6)  Thrills  in  any  part  of  an  area  extending  from  the  episternal 
notch  above  to  the  level  of  the  4th  rib  below,  and  on  either  side,  for 
a  distance  of  2  inches  beyond  the  sternal  edge,  may  be  due  to  aneu- 
rism of  the  aortic  arch.  A  thrill  discerned  in  this  area  should  not  be 
referred  to  valvular  disease  unless  in  the  absence  of  a  pulsating  swell- 
ing and  the  other  signs  of  aneurism. 

(7)  Friction  fremitus,  of  pericardial  or  pleural  origin,  differs  from 
thrill  in  being  of  a  to-and-fro  character,  and  having  no  very  definite 
relation  to  the  heart  sounds.  It  is  ordinarily  found  in  that  part  of  the 
praecordium  lying  between  and  including  the  2d  and  4th  interspaces. 

B.  Percussion  of  the  Heart 

The  object  of  percussing  the  heart  is  mainly  to  determine  its 
shape,  size,  and  location.  Incidentally,  in  doing  this  we  may  dis- 
cover dulness  due  to  pericardial  effusion,  and  also,  from  the  posi- 
tion of  the  left  anterior  border  of  the  left  lung,  whether  the  latter  is 
emphysematous,  retracted,  or  normal. 

Areas  of  Cardiac  Dulness  and  their  Relative  Value.— 
Percussion  of  the  heart  under  normal  conditions  affords  two  areas  of 


PERCUSSION  OF   HEART  331 

dulness :  first,  the  absolute  or  superficial  dulness  developed  by  that 
portion  of  the  heart  which  is  not  covered  by  lung  (Plate  I)  and, 
therefore,  lies  in  close  contact  with  the  chest  wall ;  and  second,  the 
deep  or  relative  dulness  of  that  portion  of  the  heart  overlapped  by 
the  lungs.  As  in  practice  these  terms  are  apt  to  be  confused,  the 
first  will  be  called,  from  personal  preference  and  to  avoid  uncertainty, 
the  exposed  dulness  ;  the  second,  the  covered  dulness  ;  both  together, 
the  entire  dulness  of  the  heart. 

The  area  of  exposed  cardiac  dulness  in  the  normal  heart  is 
bounded  by  a  line  drawn  from  the  level  of  the  -ith  cartilage  down- 
ward along  the  left  edge  of  the  sternum,  and  a  second  line  starting 
from  the  upper  end  of  the  first  and  running  downward  to  a  point  on 
the  left  6th  rib  in  the  parasternal  line.  This  gives  an  area  of  tri- 
angular shape. 

The  size  and  shape  of  the  covered  dulness  depend  upon  the 
method  of  examination  used.  The  more  accurate  the  method  the 
more  nearly  will  the  outline  of  the  covered  dulness  correspond  to 
the  anatomical  or  projection  outline  of  the  heart. 

The  clinical  importance  of  the  exposed  cardiac  dulness  in  deter- 
mining the  size  of  the  heart  has  been  much  overrated,  and  many 
clinicians  of  to-day  pay  no  attention  to  it  in  estimating  cardiac  con- 
ditions. The  size  of  the  exposed  dulness  does  change  to  some  ex- 
tent with  the  size  of  the  heart,  but  to  a  much  greater  degree  it  varies 
with  the  position  of  the  overlapping  lung  borders.  Practically,  the 
only  utility  of  outlining  the  exposed  dulness  is  to  demonstrate  the 
condition  of  the  lung — viz.,  emphysema  versus  shrinking — and  to  ac- 
count for  an  unusual  corresponding  absence  or  increase  of  praecordial 
pulsation.  As  a  matter  of  fact,  what  the  clinician  desires  in  percuss- 
ing the  heart  is  to  delimit  upon  the  chest  wall  the  entire  (exposed 
plus  covered)  dulness  of  the  heart  (Fig.  84),  which  should  corre- 
spond, as  accurately  as  the  limitations  of  the  method  of  examination 
will  permit,  to  the  projection  of  the  heart  upon  the  anterior  wall 
of  the  thorax  (Fig.  80).  Inspection  of  the  outline  obtained  enables 
one  to  determine  the  shape,  size,  and  situation  of  the  heart,  provided 
pericardial  effusion  is  absent.  If  effusion  is  present,  one  simply 
outlines  a  bag  of  fluid,  as  in  the  abdomen  an  ovarian  cystoma  or  a 
distended  bladder  is  outlined  by  dulness  on  percussion. 

Choice  of  Percussion  Methods. — There  are  three  methods 
of  percussion  which  may  be  employed  in  ascertaining  the  areas  of 
cardiac  dulness :  first,  ordinary  percussion ;  second,  auscultatory 
percussion;  tJiird,  percussion  with  the  aid  of  Sansom's  pleximeter. 

These  methods  differ  in  accuracy,  none  being  absolutely  reliable 
in  enabling  the  observer  to  obtain  the  true  projection  outline.     The 


332 


THE  EVIDENCES  OF  DISEASE 


first  method  is  of  little  or  no  use ;  the  second  and  third  are  clinically 
trustworthy.  It  is  proper  to  state  that  in  percussing  the  heart  the 
personal  skill  of  the  examiner  has  much  to  do  with  the  result,  as 
correctness  depends  largely  upon  the  detection  of  very  slight  differ- 
ences of  sound  and  feeling. 

There  is  another  method  of  obtaining  the  projection  outline  of 
the  heart  which  is  superior  to  percussion,  and  is  as  nearly  accurate 
as  can  be  conceived,  but  which  at  present  is  in  limited  use,  largely 
on  account  of  the  expensive  apparatus  and  special  training  required 
in  its  employment — viz.,  the  Euntgen  ray  and  the  fluoroscope. 
The  extremely  interesting  work  done  by  Williams,  of  Boston,  Sat- 
terlee,  of  Xew  York,  and  others,  has  proved  its  value,  and  the  future 
will  doubtless  witness  a  simplification  and  cheapening  of  the  required 
outfit. 


Card.o-hepatic 
(Ebstein's) 

ANGLE 


Covered  CARDIAC 

DULNESS 


Exposed  cardiac 

DULNESS 


Fig.  84. — Showing  the  exposed  and  covered  duluess  of  the  normal  lieart. 


Technic  of  Cardiac  Percussion. — In  percussing  the  heart 
by  either  of  these  methods  the  general  direction  of  the  lines  along 
which  the  percussion  strokes  are  conducted  is  the  same. 

(1)  In  using  ordinary  percussion  to  determine  as  fully  as  pos- 
sible the  entire  cardiac  dulness,  first  find  the  upper  limit  of  the 
covered  hepatic  dulness  by  percussing  from  the  2d  right  interspace, 
at  or  somewhat  outside  of  the  parasternal  line,  vertically  downward 


PERCUSSION  OP  HEART 


333 


(1,   in  Fig.   85   to  which   subsequent  numbers  refer)    with   heavy- 
strokes,  until  the  dulling  effect  of  the  upper  border  of  the  liver  is 
noted,  sometimes  at  the  4th  space,  usually  at  the  5th  rib  or  inter- 
space.    Determine  also  the  line  of  exposed  (absolute)  liver  dulness, 
generally  at  the  6th  rib.     Then  percuss  successively  from  right  to 
left,  beginning  suffi- 
ciently far  out  to  get 
unmixed    pulmonary 
resonance,  along  lines 
2  and  3  until  the  first 
trace  of  impaired  or 
modified  resonance  is 
noted.     It  can  not  be 
too    strongly  empha- 
sized  that   one   docs 
not    search   for   flat- 
ness or  even  dulness, 
but  for  the  first  trace 
of  impairment  or  va- 
riation   in   the    pure 
pulmonary        sound. 
Then  on  the  left  side 
percuss    from    above 
downward  in  the  para- 
sternal   line,   5,    and 
from    left    to    right 
along  lines  6,  7,  and 
8,  in  the  3d,  4th,  and 
5th     interspaces    re- 
spectively,  noting  in 
each  case  the  points  of  beginning  impaired  resonance,  and  exercising 
care  not  to  mistake  the  muffling  of  the  pulmonary  resonance  caused 
by  the  tliick  pectoral  muscle  for  the  dulling  effect  of  the  heart.     The 
mammary  gland  must  be  held  aside  for  a  similar  reason.     Percus- 
sion is  to  be  made  along  as  many  other  additional  lines  as  the  exam- 
iner may  think  best. 

Percussion  along  line  4,  from  above  downward,  along  the  left 
half  of  the  sternum,  is  intended  to  discover  the  line  of  demarcation 
between  the  base  of  the  heart  and  the  origin  of  the  great  vessels. 
Always  compare  rib  with  rib  and  interspace  with  interspace,  in  order 
to  equalize  tlie  comparison. 

To  find  the  exposed  dulness,  percussion  with  light  strokes  is  car- 
ried still  farther  to  the  left  on  line  2,  farther  to  the  right  on  lines 


ij.  ^•J. — Showing  the  principal  lines  (numbered  in  order 
of  performance)  along  which  percussion  should  be  con- 
ducted to  ascertain  the  area  of  cardiac  dulness,  both 
covered  and  exposed.    Compare  with  Fig.  84. 


334  THE  EVIDENCES  OF  DISEASE 

7  and  8,  and  from  above  downward  about  an  inch  to  the  left  of  the 
left  sternal  edge  on  line  9  until,  on  each  line,  the  modified  pulmo- 
nary resonance  or  covered  dulness  is  replaced  by  the  absolutely  dull 
sound  of  the  exposed  heart. 

(2)  Auscultatory  percussion  and  its  technic  {q.  v.)  has  been 
described  elsewhere.  For  the  heart  the  tip  of  the  stethoscope  should 
be  placed  above  and  to  the  inner  side  of  the  apex  beat,  so  that  it 
surely  rests  over  the  heart.  Percuss  from  all  sides  toward  the  stetho- 
scope, making  one  outline  with  heavy  strokes,  and  then  repeating 
with  light  strokes,  but  never  intermingling  light  with  heavy. 

It  is  claimed  by  the  advocates  of  this  method  that  the  lower  bor- 
der of  the  heart  can  usually  be  determined  without  much  difficulty, 
except  in  cases  where  the  costal  cartilages  and  the  ensiform  appen- 
dix are  close  together  and  projecting.  The  upper  limit  under  the 
sternum  is  harder  to  obtain  on  account  of  the  osseous  resonance, 
particularly  when  the  patient  is  thin  and  the  sternum  prominent, 
but  with  repeated  trials  it  is  said  that  a  sufficient  change  of  sound 
can  be  observed  to  mark  the  line  of  separation  between  the  cardiac 
and  great-vessel  areas. 

(3)  Sansom's  method  involves  the  use  of  a  special  pleximeter,  a 
slender  vulcanite  rod,  of  square  section,  1^  inch  long,  bearing  on 
one  end  a  thin  oblong  plate,  1  inch  by  |  an  inch ;  and  on  the  other 

end,  parallel  to  the  first,  a  second  plate,  f  by  f 
of  an  inch  (Fig.  86).  The  larger  of  the  thin 
flattened  plates  is  to  be  laid  upon  the  surface 
and  held  in  position  by  the  tips  of  the  1st  and 
2d  fingers  of  the  left  hand  placed  upon  the 
plate,  one  on  either  side  of  the  vertical  rod. 
Percussion  is  then  to  be  made  upon  the  plate 
at  the  other  extremity  of  the  rod  by  the  middle 
finger  of  the  right  hand  in  the  usual  manner. 

Fig.  86. — bansom's  plex-      „,.  ,  „  ,         ,  »    .  ^i 

imeter.  With  reference  to  the  theory  of  its  use  feansom 

states  that  the  observer  should  pay  attention 
not  to  sounds,  but  to  vibrations  ;  whether  these  are  mechanical  and 
appreciated  by  the  finger  tips  resting  upon  the  instrument,  or  sono- 
rous and  appreciated  by  the  ear. 

The  pleximeter  is  used  by  applying  it  with  its  long  diameter 
parallel  to  the  sternum  at  the  right  mammillary  line  about  on  a 
level,  we  will  say,  with  the  4th  rib.  It  is  then  brought  gradually 
nearer  the  sternum,  still  parallel,  until  it  reaches  a  point  where  the 
vibrations  are  sensibly  modified,  and  is  then  inclined  slightly  toward 
the  median  line  so  that  the  vibrations  come  from  the  left  edge  of 
the  plate,  practically  a  line,  at  which  point,   indicating  the  right 


PERCUSSION  OF  THE  HEART  335 

border  of  cardiac  dulness,  a  short  line  is  drawn  upon  the  skin. 
This  process  is  repeated  at  different  levels  from  the  1st  to  the  5th 
interspaces.  The  upper  limit  of  liver  dulness  (usually  in  the  5th 
space),  if  not  ascertained  at  the  beginning,  is  now  determined. 

Similar  percussion  is  made  on  the  left  side  from  the  2d  rib  down- 
ward, and  from  the  anterior  axillary  line  inward,  inclining  the  plex- 
imeter  toward  the  median  line.  In  outlining  the  rather  sharp  curve 
of  the  apex  the  smaller  plate  may  be  used  by  reversing  the  plexime- 
ter.     The  marks  thus  obtained  are  united  (Fig.  66,  page  292). 

This  method  of  percussion  gives  an  outline  which  includes  not 
only  the  right  border,  left  border,  and  apex  of  the  heart,  but  also  the 
right  and  left  borders  of  the  great-vessel  area  above.  In  favourable 
cases  it  will  give  both  upper  and  lower  cardiac  borders. 

Limitations  of  Cardiac  Percussion. — It  is  rarely  possible 
by  ordinary  percussion,  and  always  difficult  by  any  method,  to  find 
the  entire  lower  border  of  the  heart,  owing  to  the  fact  that  its  ex- 
posed dulness  merges  with  the  dulness  of  the  left  lobe  of  the  liver, 
but  in  some  cases  a  slight  difference  in  the  sound  can  be  detected. 
A  similar  difficulty  exists  with  reference  to  the  upper  border.  For- 
tunately, the  outlines  which  can  be  obtained — viz.,  the  right  border, 
the  left  border  and,  usually,  the  outline  of  the  apex — are  sufficient  for 
most  clinical  purposes  (Fig.  87).  As  a  rule,  the  dulness  covers  a 
larger  area  of  the  chest  wall  than  would  seem  to  be  correct  upon 
first  thought.  AVilliams  states  that  not  only  are  the  outlines  of  the 
heart,  as  shown  by  the  fluoroscope,  more  complete  than  those  ob- 
tained by  percussion,  but  that  the  percussion  outlines  in  a  portion 
of  the  cases  examined  vary  as  much  as  an  inch  from  the  size  of  the 
heart  as  seen  in  the  fluoroscope,  indicating  sometimes  a  smaller  and 
sometimes  a  larger  heart  than  the  reality.  Xevertheless,  for  ordinary 
clinical  purposes  cardiac  percussion,  if  carefully  performed,  is  suffi- 
ciently accurate  in  determining  abnormal  increase  in  the  size  of  the 
heart,  especially  if  conjoined  with  equally  careful  palpation. 

Indications  from  Abnormal  Areas  of  Dulness.— Having 
determined  cardiac  and  great-vessel  dulness,  it  remains  to  discuss 
the  meaning  of  observed  variation  from  the  normal  in  shape,  size, 
and  position. 

(1)  Enlargement  of  the  Normal  Outline.— An  increase,  mainly  to 
the  left  and  dow7iward,  with  a  heaving  apex  beat  displaced  in  the 
same  direction,  is  characteristic  of  hypertrophy  and  dilatation  of  the 
left  ventricle.  The  apex  outline  is  unusually  pointed  (Fig.  88).  It 
is  quite  certain  that  if  the  entire  cardiac  dulness  is  increased,  dilatar 
tion  as  well  as  hypertrophy  is  present.  It  is  difficult  to  recognise 
enlargement  unless  the  heart  weighs  at  least  I'U  oz.  (400  grms.). 


Fig.  87.  —  Normal  area  of 
entire  cardiac  dulness. 
The  dotted  lines  above 
and  below  represent  the 
borders  which  are  diffi- 
cult to  delimit,  but  the 
apex  beat  and  the  finding 
of  tlie  solid-lined  portions 
of  tlie  borders  enable  a 
satisfactory  determina- 
tion of  the  size  and  shape 
of  the  heart 


Fig.  88. — Dulness  in  hyper- 
trophy of  the  left  ventri- 
cle. Apex  beat  heaving 
and  carried  down  and 
to  the  left,  perhaps  out- 
side of  the  apex  outline. 
Apex  pointed. 


Fig.  89. — Dulness  in  hyper- 
trophy and  dilatation  of 
the  right  heart.  Note 
apex  beat  moved  to  the 
left,  and  dulness  in- 
creased to  the  right  of 
the  sternum. 


Fig.  90.— Showing  the  dul- 
ness  due  tx>  dilatation  and 
hypertrophy  of  both  ven- 
tricles. Apex  rounded 
and  apex  beat  diffused. 
Compare  with  Figs.  88 
and  89.  Shows  also  (iirst 
and  second  right  inter- 
spaces) the  dulness  of 
aortic  aneurism. 


Fio.  91.  —  The  triangular 
area  of  dulness  due  to  a 
largie  pericardial  effusion 
is  shown  by  the  outer 
solid  line.  For  compari- 
son the  normal  cardiac 
dulness  is  shown  by  the 
inner  shaded  area.  Note 
position  of  apex  beat 
with  reference  to  the 
pericardial  dulness. 


Fio.  92.— Showing  the  dul- 
ness of  a  moderate  peri- 
cardial effusion. 


338  THE   EVIDENCES   OF   DISEASE 

Enlargement,  mainly  to  the  right  (Fig.  89),  with  a  rounded  apex 
outline,  is  significant  of  hypertrophy  and  dilatation  of  the  right  ven- 
tricle and  auricle,  especially  if  there  is  dulness  in  the  3d  and  -ith 
spaces  to  the  right  of  the  sternum.  If  the  usually  resonant 
(Ebstein's)  angle  in  the  right  5th  space,  between  the  lower  portion  of 
the  right  border  and  the  upper  limit  of  hepatic  dulness  (Fig.  84),  is 
obliterated,  it  may  be  due  to  a  dilated  right  auricle,  dilated  inferior 
vena  cava,  or  pericardial  effusion. 

Enlargement,  both  to  right  and  left,  with  a  weak  and  diffused 
apex  beat,  indicates  much  dilatation  as  well  as  hypertrophy  of  both 
ventricles  (Fig.  90). 

Enlargement  to  the  right,  left,  and  upivard  is  found  as  a  result 
of  pericardial  effusion.  It  is  somewhat  triangular  or  pear  shaped, 
with  the  small  end  upward,  often  extending  into  the  2d  interspace. 
It  is  a  diagnostic  sign  that  the  edges  of  the  dull  area  are  sharply 
marked,  the  transition  from  pulmonary  resonance  to  fluid  flatness 
being  noticeably  abrupt.  The  area  of  dulness  is  somewhat  larger 
when  the  patient  is  sitting  than  when  lying  down.  As  the  overlap- 
ping lungs  have  been  pushed  away,  there  is  uniform  dulness  over 
the  entire  area,  and  the  distinction  between  the  covered  and  exposed 
dulness  disappears.  In  very  large  effusions  there  may  be  an  area  of 
dull  tympanitic  resonance  in  the  left  axillary  region,  below  the  level 
of  the  nipples  and  over  the  left  base,  due  to  compression  of  the  left 
lung.  The  apex  beat,  or,  if  this  can  not  be  felt,  the  point  of  greatest 
intensity  of  the  first  sound,  is  well  inside  of  the  dull  area,  rarely  out- 
side of  the  mammillary  line  (Fig.  91).  It  is  at  times  difficult  and 
even  impossible  to  distinguish  between  a  moderate  pericardial  effu- 
sion and  extreme  dilatation  of  both  ventricles  (compare  Figs.  92  and 
90).  In  addition  to  the  points  above  given,  the  differential  diag- 
nosis is  discussed  elsewhere  (Index — Heart,  dilatation  of). 

An  apparent  enlargement  of  the  heart  by  inspection  alone  may 
be  due  to  retraction  of  the  lung,  or  to  a  pushing  forward  of  the  heart 
by  tumour  or  aneurism  in  the  posterior  mediastinum ;  but,  as  the  en- 
largement affects  only  the  exposed  cardiac  dulness,  a  determination 
of  the  entire  cardiac  outline  will  reveal  it  to  be  apparent  and  not 
actual. 

(2)  Diminution  of  the  Normal  Area.— This  may  be  due  to  atrophy 
of  the  heart  or  absorption  of  fat  in  wasting  diseases,  notably  con- 
sumption and  long-continued  typhoid  fever.  Left  pneumothorax, 
the  air-containing  pleural  sac  overlying  the  heart,  may  substitute  a 
tympanitic  sound  for  a  portion  of  the  normal  modified  pulmonary 
resonance ;  marked  emphysema  greatly  increases  the  difficulty  in 
obtaining  the  full  cardiac  outline ;  and  gaseous  distention  of  the 


AUSCULTATION  OF  THE  HEART  339 

stomach  may  prove  deceptive  for  similar  reasons.  Two  rare  condi- 
tions, pneumo-pericardium  and  emphysema  of  the  mediastinum,  may 
be  responsible  for  great  diminution  in  the  size  of  the  heart  dulness. 

(3)  Displacement  of  the  Area.— Dislocation  of  the  heart  does  not 
usually  alter  the  size  of  its  outlines,  but  the  causes  of  such  dis- 
placements (already  discussed,  page  322)  often  render  it  difficult  to 
properly  percuss  the  heart^e.  g.,  large  pleural  effusion.  In  such  a 
case  one  must  estimate  the  place  of  the  heart  by  the  position  of  the 
apex  beat.  In  the  infrequent  examples  of  transposition  of  the  heart 
(dextrocardia)  the  heart  dulness  gives  a  "  mirror  image "  of  the 
usual  outlines. 

(4)  Great-vessel  Dulness. — If  the  aorta  and  pulmonary  artery 
are  of  normal  size,  the  dulness  (or  modified  vibrations)  to  which  they 
give  rise  in  plessimetric  percussion  does  not  extend  beyond  the  edge 
of  the  sternum  to  either  side.  If  the  dulness  extends  to  the  right 
of  the  sternum  into  the  2d,  or  1st  and  2d  interspaces,  with  a  rounded 
projecting  outline  (Fig.  90),  it  is  good  evidence  of  aneurism  of  the 
aorta.  Lesser  degrees  of  dilatation  may  be  shown  in  a  similar  man- 
ner by  a  correspondingly  smaller  increase  in  the  area  and  alteration 
in  the  shape. 

C.   Auscultation  of  the  Heaet 

The  object  of  auscultation  is  to  determine  the  character  and 
rhythm  of  the  heart  sounds,  and  the  presence  or  absence  of  adventi- 
tious sounds. 

Position  of  Valves  and  their  Areas  of  Audibility.— In 
addition  to  the  facts  already  stated  with  reference  to  the  valvular 
element  of  the  heart  sounds  {q.  v.)  a  further  analysis  will  show  that 
each  sound  may  be  separated  into  2  components.  Thus  the  valvular 
portion  of  the  1st  sound  results  from  the  closure  of  2  valves,  the 
mitral  and  tricuspid ;  the  2d  sound  also  from  the  closure  of  2  valves, 
the  aortic  and  the  pulmonary.  The  1st,  therefore,  consists  of  1 
muscular  and  2  valvular  components  ;  the  2d  of  2  valvular  com- 
ponents alone.  Depending  upon  the  location  of  the  valves  and  the 
gi-eater  degree  of  audibility  of  their  respective  closures  in  certain 
directions,  it  is  practicable  to  auscultate  each  one  separately.  Of 
the  4  valves,  the  pulmonary  and  tricuspid,  belonging  to  the  right 
ventricle,  lie  nearer  the  surface  than  the  aortic  and  mitral,  which  are 
more  deeply  seated.  Taking  them  in  order  from  above  downward, 
their  positions  are  as  follows  (Fig.  93) : 

(1)  Pulmonary  Valve.— Mainly  behind  3d  left  costal  cartilage. 
Of  the  3  segments  comprising  this  valve,  2  are  anterior  and  1  pos- 
terior. 


340 


THE   EVIDENCES  OF   DISEASE 


(3)  Aortic  Valve. — Behind  the  left  half  of  the  sternum  on  a  level 
with  the  3d  space.     Of  the  3  segments  1  is  anterior  and  2  posterior. 


Aortic  area 
Aortic  valve 


O 


Tricuspid  valve 
Tricuspid  area 


M 


^^t^^. 


Pulmonary  area 
Pulmonary  VALVE 


fcw^lw ■!  c:si 


•i 


Fig.  93. — Showing  the  positions  of  the  valves  of  the  heart  and  the  areas  of  their  greatest 
audibility.  Solid  circles  and  blocks  =  deep  valves  (aortic  and  mitral).  Light  circles 
and  blocks  =  superficial  valves  (pulmonary  and  tricuspid). 

(3)  Mitral  Valve. — Behind  the  left  half  of  the  sternum  on  a  level 
■with  the  4th  cartilage,  4th  space,  and  upper  border  of  the  5th  carti- 
lage.   Of  the  2  segments  of  the  valve  1  is  anterior,  the  other  posterior. 

(4)  Tricuspid  Valve. — Behind  the  lower  4th  of  the  sternum,  to 
the  right  of  the  middle  line,  from  the  4th  right  cartilage  to  a  point 
hehind  the  junction  of  the  6th  right  cartilage  to  the  sternum. 

It  will  be  noted  that  a  stethoscope  placed  directly  over  the  gen- 
eral valve  area  will  receive  auditory  impressions  from  them  all,  and 
the  sounds  of  the  2  deep  valves  must  pass  through  the  cavities  of  the 
heart  which  overlie  them.  Consequently  the  separate  sound  of  each 
valve  is  sought  for  at  a  point  where  the  chamber  or  vessel  to  which 
it  belongs  approaches  most  closely  to  the  chest  wall  and  at  the  same 
time  is  most  distant  from  the  other  chambers  or  vessels.  These 
points  or  areas  of  auscultation  at  which  the  sound  of  the  correspond- 
ing valve  is  loudest  and  most  distinct  are  as  follows  : 

(1)  Pulmonary  Area. — At  the  2d  interspace  to  the  left  of  the 
sternum,  upon  the  pulmonary  artery  and  above  the  pulmonary  valve. 


AUSCULTATION  OP  THE  HEART  341 

(2)  Aortic  Area. — At  the  2d  interspace  to  the  right  of  the 
sternum,  upon  the  aorta  and  above  the  aortic  valve.  The  2d  right 
cartilage  is  often  called  the  aortic  cartilage. 

(3)  Mitral  Area. — At  the  apex  of  the  heart  where  the  tip  of  the 
left  ventricle  approaches  the  chest  wall. 

(4)  Tricuspid  Area. — Over  the  lower  end  of  the  sternum,  a  point 
at  which  the  right  ventricle  lies  close  to  the  chest  wall  and  at  the 
same  time  is  most  distant  from  the  left  ventricle. 

In  auscultating  the  heart  a  convenient  order  is,  first,  the  mitral 
area ;  then  the  aortic,  giving  the  character  of  the  left  ventricular 
valve  sounds  ;  then  the  pulmonary  and  tricuspid  areas,  belonging  to 
the  valves  of  the  right  ventricle. 

It  is  essential  during  auscultation  to  place  a  finger  upon  the 
apex  beat  or  upon  the  carotid  pulse  in  order  to  place  the  sounds 
with  reference  to  the  events  of  the  cardiac  cycle.  The  radial  pulse 
follows  the  apex  beat  at  a  slight  interval,  but  long  enough  to  make 
it  untrustworthy  for  careful  timing.  As  the  respiratory  sounds  may 
obscure  or  complicate  faint  cardiac  sounds  or  murmurs,  it  should  be 
made  a  routine  practice  to  direct  the  patient  to  suspend  breathing, 
one  or  more  times,  during  the  examination. 

Variations  in  the  Intensity  and  Character  of  the 
Heart  Sounds. — The  heart  sounds  are  to  be  studied  at  each  of 
these  points  with  reference  to  their  intensity,  quality,  and  rhythm ; 
also  the  presence  of  reduplication. 

It  is  possible  with  care  to  separate  the  muscular  component  of 
the  first  sound  into  2  portions,  1  furnished  by  the  left  ventricle, 
heard  a  little  to  the  left  of  the  apex ;  and  that  coming  from  the 
right,  heard  over  the  middle  of  the  sternum  at  the  level  of  the  3d 
interspace.  While  of  equal  intensity,  the  muscular  sound  of  the  left 
ventricle  is  appreciably  longer  than  that  of  the  right.  The  following 
modifications  of  the  heart  sounds  are  of  clinical  value,  but  require 
for  their  recognition  a  tliorough  familiarity  with  the  normal  sounds. 

(1)  Accentuation  of  Both  Sounds. — Increased  loudness  or  accen- 
tuation of  both  sounds  of  the  heart  is  very  common.  In  well-marked 
cases  the  sounds  may  be  heard  over  the  entire  chest  in  front,  and 
sometimes  over  the  back  of  the  thorax.  It  is  frequently  due  to 
mental  excitement.  An  apparent  increase  in  the  strength  of  the 
sounds  may  be  present  in  persons  with  thin  chest  walls,  or  in  whom 
the  heart  is  uncovered  by  phthisical  shrinkage  of  the  lung  ;  both  of 
these  conditions  permitting  a  more  ready  transmission  of  the  sounds. 
Overactivity  of  the  heart,  as  in  cardiac  neuroses  (e.  g.,  palpitation), 
exophthalmic  goitre  and  the  early  stage  of  fevers,  causes  an  unnat- 
ural loudness  of  both  sounds.  Certain  conditions  of  debility,  notably 
24 


342  THE   EVIDENCES  OP   DISEASE 

anaemia  and  chlorosis,  may  be  attended  by  loud  heart  sounds,  which, 
despite  their  intensity,  possess  a  short  and  flapping  quality,  indica- 
tive of  weakness  rather  than  strength.  On  the  other  hand,  the 
sounds  may  be  loud  because  of  cardiac  hypertrophy,  the  abnormally 
strong  muscular  walls  imparting  unusual  vigour  to  the  closure  of  the 
valves,  and  adding  strength  to  the  muscular  element  of  the  first 
sound.  Consolidated  lung  may,  by  acting  as  a  better  conductor  of 
sound  than  healthy  lung,  increase  the  loudness  of  the  sounds.  Ex- 
cessive distention  of  the  intestines  and  stomach,  the  latter  especially, 
and,  less  frequently,  pneumothorax  or  a  large,  smooth-walled  pulmo- 
nary cavity,  or  the  rare  condition  of  pneumopericardium  may,  by 
their  resonance,  impart  a  loud,  ringing,  metallic  quality  to  the  heart 
sounds. 

Comparison  of  the  sounds  may  show  that  one  sound,  or  one  of 
its  components,  may  predominate;  consequently,  the  observer  may 
find— 

(2)  Accentuation  of  the  First  Sound. — Normally  the  first  sound, 
when  auscultated  at  the  apex,  is  louder  than  the  second  sound.  If 
it  is  heard  more  distinctly  at  the  base  than  is  the  second  sound,  it  is 
either  accented,  or  the  second  sound  is  abnormally  weak.  An  unusu- 
ally loud,  prolonged,  thumping  first  sound  at  the  apex  is  heard  in 
hypertrophy,  especially  of  the  left  ventricle.  The  peculiar  quality 
of  this  sound  is  due  to  its  large  muscular  component.  On  the  other 
hand,  a  loud  but  short,  flapping  first  sound  having  a  marked  resem- 
blance to  the  valvular  quality  of  the  second  sound  and  lacking  the 
prolonged  dull  muscular  component,  is  associated  with  moderate 
dilatation  and  weakness  of  the  heart  chambers.  If  the  dilatation  or 
weakness  is  extreme,  the  accentuation  disappears.  An  uncommonly 
sharp  and  clear  first  sound  is  heard  in  cases  of  mitral  stenosis. 

(3)  Accentuation  of  the  Second  Sound. — Xormally  the  2d  sound 
is  louder  at  the  base  than  at  the  apex.  If  this  relation  is  reversed 
it  means  either  an  accented  2d  sound  or  a  weakened  1st  sound.  In 
judging  the  2d  sound  its  2  components,  aortic  and  pulmonary, 
should  be  carefully  compared  by  repeated  auscultation  of  the  aortic 
and  pulmonary  areas.  In  the  young  the  pulmonary  closure  is  some- 
what more  accentuated  than  the  aortic ;  in  advanced  years,  presuma- 
bly because  of  degenerative  changes  in  the  aortic  valve,  the  converse 
is  true.     It  may  be  found  that — 

Aortic  Closure  is  Accentuated. — One  of  the  principal  causes  of  a 
loud  and  sudden  aortic  2d  sound  is  the  presence  of  high  arterial 
pressure,  such  as  may  exist  in  nephritis  and  arteriosclerosis.  It  has 
been  compared  to  the  popping  of  a  cork  when  pulled  from  a  bottle. 

A  loud,  distinct,  but  somewhat  harsh  aortic  sound,  perhaps  of  a 


AUSCULTATION  OF  THE  HEART  343 

ringing  metallic  or  clicking  quality,  is  indicative  of  sclerosis  or  athe- 
roma of  the  aortic  valves  and  the  adjacent  portion  of  the  aorta,  with- 
out narrowing  or  incompetence.  The  significance  of  this  sound  is 
often  overlooked,  and  yet,  as  I  have  repeatedly  demonstrated  by 
autopsy,  it  is  a  most  reliable  sign.  It  is  most  frequently  encountered 
in  old  labouring  men.  Aneurism  of  the  aorta  causes  a  loud  aortic 
closure,  accompanied  by  a  palpable  "  diastolic  shock." 

Accentuation  of  the  aortic  closure  is  also  evidence  of  left  side 
hypertrophy.  The  strong  contraction  of  the  left  ventricle  distends 
the  aorta  so  forcibly  that  the  rebound  closes  the  aortic  valves  with 
unusual  force.  Indeed,  the  majority  of  cases  with  an  accentuated 
aortic  sound,  except  when  due  to  a  temporary  heightening  of  the 
arterial  pre:;sure,  present  also  evidences  of  left  hypertrophy.  On  the 
other  hand,  the  absence  of  accentuation  does  not  negative  the  exist- 
ence of  hypertrophy,  for,  if  the  latter  results  from  aortic  incompe- 
tency, the  valve  may  be  so  deficient  that  the  aortic  sound  may  be 
almost  nil.  If  marked  dilatation  and  muscular  weakness  succeed  to 
hypertrophy,  the  intensity  of  the  aortic  sound  will  lessen  pari  passu. 

Pulmo7iary  Closure  is  AccenUiated. — The  pulmonary  component 
of  the  2d  sound  is  an  invaluable  index  of  the  strength  of  the  right 
ventricle  and  the  competence  of  the  tricuspid  valve.  If  it  is  well 
marked  it  shows  that  the  tricuspid  valve  is  competent,  and  the  ven- 
tricle is  sufiiciently  strong  to  sustain  a  good  blood  pressure  in  the 
pulmonary  artery.  The  causes  of  an  unduly  accentuated  pulmonary 
2d  sound  are  those  conditions  which  hinder  the  flow  of  blood  through 
the  pulmonary  circuit.  Thus  pneumonia,  emphysema,  and  mitral 
regurgitation  or  stenosis  may  be  responsible  for  the  accented  sound. 
In  certain  varieties  of  pneumonia  a  well-marked  pulmonic  2d  sound 
is  a  favourable  prognostic,  and  its  disappearance  the  reverse.  It  may 
be  readily  seen  that  the  presence  of  pulmonic  accentuation  is  an  im- 
portant corroborative  sign  of  mitral  lesions,  of  right  ventricular 
hypertrophy  with  good  muscle,  and  of  the  absence  of  tricuspid  re- 
gurgitation. 

(4)  Weakening  of  Both  Sounds.— The  thick  chest  wall  of  the 
obese,  and  in  particular  the  large  mammary  gland  of  stout  women, 
may  cause  a  great  diminution  in  the  normal  intensity  of  the  heart 
sounds  as  a  whole.  For  somewhat  similar  reasons,  viz.,4;he  interposi- 
tion of  a  muffling  body  between  the  heart  and  the  stethoscope,  pul- 
monary emphysema,  pericardial  eiTusion,  or  a  large  pleural  effusion 
may  be  responsible  for  a  very  material  decrease  in  the  audibility  of 
the  sounds. 

Aside  from  these,  the  main  significance  of  weakened  heart  sounds 
is  a  weak  heart  muscle   from   various  causes,  such  as  the  broken 


344  THE  EVIDENCES  OF   DISEASE 

compensation  of  valvular  lesions,  degenerative  disease  of  the  heart 
muscle,  dilatation  of  the  heart,  exhausting  disease  (especially  long- 
continued  fevers  and  septic  affections),  hemorrhage,  shock,  and  over- 
exertion ;  or  pneumogastric  paralysis,  nuclear  or  peripheral. 

(5)  Weakening  of  the  First  Sound. — The  causes  of  a  weakened 
first  sound  are  for  the  most  part  those  which  have  just  been  enu- 
merated as  producing  weakness  of  both  sounds.  But,  as  any  weakness 
of  the  cardiac  muscles  is  apt  to  manifest  itself  primarily  by  weaken- 
ing of  the  muscular  component  of  the  1st  sound,  weakness  of  the 
2d  sound  appearing  subsequently,  the  character  of  the  1st  sound  is 
of  the  greatest  importance  in  estimating  the  strength  of  the  heart. 

In  exhausting  fevers  one  may  observe  day  by  day  a  progressive 
decline  in  the  strength  of  the  1st  sound,  its  muscular  component 
gradually  lessening  until  the  1st  sound  bears  a  close  resemblance  to 
the  2d,  or  in  bad  cases  becomes  almost  inaudible.  In  rare  instances 
nothing  but  the  short  2d  sound  may  be  heard  at  the  apex,  the  1st 
sound  practically  disappearing.  The  left  ventricle  is  usually  the 
first  to  yield.  A  less  marked  weakness  of  the  1st  sounr'  is  notice- 
able in  a  fatty  or  degenerated  heart,  and  in  anaemia  and  other  con- 
ditions of  debility. 

(6)  Weakening  of  the  Second  Sound. — In  addition  to  the  weaken- 
ing of  both  components  (aortic  and  pulmonary)  of  the  second  sound, 
by  conditions  already  mentioned  (4),  weakening  of  the  individual 
valve  sounds  under  special  circumstances  needs  a  reference. 

Aortic  Closure  Weakened. — This  is  frequently  found  in  marked 
cases  of  mitral  stenosis,  the  left  ventricle  receiving  through  the  nar- 
rowed orifice  a  charge  of  blood  which  is  inadequate  to  fully  distend 
the  aorta,  and  in  consequence  the  blood  pressure  in  the  vessel  is  not 
raised  to  the  point  required  to  close  the  valve  with  normal  sharp- 
ness. In  aortic  stenosis  the  stiffened  segments,  lacking  flexibility, 
may  not  vibrate  sufficiently  to  produce  a  closure  sound  of  proper 
intensity.  Finally,  in  aortic  insufficiency  the  defects  in  the  valve 
may  be  so  great  that  the  sound  of  valve  closure  disappears  and  noth- 
ing but  the  murmur  is  heard  over  the  aortic  area. 

Ftilmonary  Closure  Weakeiied. — This  is  a  significant,  valuable, 
and  almost  the  only  physical  sign  of  the  giving  way  of  the  right 
ventricle.  The  disappearance  of  a  good  or  accentuated  pulmonic 
second  sound  in  pneumonia  or  any  condition  attended  by  increased 
resistance  in  the  pulmonary  circuit  indicates  one  or  both  of  two 
things — failure  of  the  right  ventricle  or  tricuspid  insufficiency. 

(7)  Reduplication  of  the  Heart  Sounds. — In  certain  cases  ausculta- 
tion reveals  a  triple  instead  of  the  normal  double  sound  of  the  heart, 
due  to  a  doubling  or  reduplication  of  either  the  first  or  the  second 


AUSCULTATION  OF  THE  HEART  345 

sound.  In  rare  cases  both  sounds  may  be  doubled,  causing  four 
sounds.    If  the  first  sound  is  doubled,  the  normal  lubh-dupp  is  replaced 

by  lublubb dup})  (pronouncing  the  duplicated  syllables  quickly 

together) ;  or  by  lubb dupdupp  if  the  reduplication,  as  most 

commonly  found,  affects  the  second  sound.  If  these  sounds  are  so 
accented  as  to  resemble  the  cadenced  canter  of  a  horse,  it  is  called 
the  "  bruit  de  galop"  or  galloping  rhythm.  In  the  form  of  redupli- 
cation which  goes  under  this  name  the  doubling  usually  affects  the 
second  sound  while  the  accent  is  upon  the  first  sound,  lubb dup- 
dupp, one  long  and  two  short  (_£.  -^S)^  or  upon  the  third  (^.•^^  __). 

There  are  many  variations  in  time  and  accent,  and  quite  as  many 
largely  theoretical  explanations  of  their  exact  causation.  In  the 
presence  of  contradictory  opinions  one  may  be  permitted  to  select 
the  simplest  explanation  extant,  which  is  that  the  reduplicated 
sounds  are  due  to  non-simultaneous  closure  of  the  valves,  the  seg- 
ments of  one  coming  together  a  short  but  appreciable  time  before 
those  of  the  other.  In  the  case  of  the  mitral  and  tricuspid  valves 
the  closure  is  successive  and  not  simultaneous,  because  the  systoles 
of  the  ventricles  are  asynchronous ;  while  the  closure  of  the  aortic 
and  pulmonary  valves  is  not  synchronous  because  of  heightened 
pressure  either  in  the  pulmonary  artery  or  the  aorta,  the  valve 
exposed  to  the  higher  back  pressure  closing  first ;  but  this  theory 
does  not  fit  all  cases. 

Clinically,  reduplication  with  galloping  rhythm  is  found  not  infre- 
quently in  arteriosclerosis  and  chronic  interstitial  nephritis,  condi- 
tions in  which  there  is  heightened  arterial  pressure.  It  is  very 
characteristic  of  mitral  stenosis  and  diseases  of  the  lungs  which 
cause  an  increase  of  blood  pressure  in  the  pulmonary  circuit.  It  is 
found  especially  in  cardiac  dilatation  and  broken  compensation; 
and  in  diphtheritic  paialysis  of  the  heart,  pericardial  effusion,  and 
the  rapid  heart  action  of  exophthalmic  goitre. 

(8)  Alterations  in  the  Relative  Length  of  the  Silences.— In  a  nor- 
mally acting  heart,  the  two  sounds  and  the  long  silence  follow  one 
another  in  triple  time— i.  e.,  1st  sound  (one),  2d  sound  (two),  long 
silence  (three),  1st  sound  (one),  etc.  Even  if  the  heart  is  acting 
rapidly  this  rhythm  is  preserved. 

In  disease  there  are  two  variations  (Fig.  94)  which  are  of  impor- 
tance as  indicating  serious  weakness  of  the  cardiac  musculature. 
The  first  is  embryocardia,  so  called  because  it  approximates  the 
character  of  the  foetal  heart  sounds.  The  1st  sound  resembles  the 
2d  sound  very  closely,  and  the  short  and  long  silences  become  of 
equal  length,  so  that  the  rhythm  is  in  double  time— Ist  sound  (one), 
2d  sound  (two),  1st  sound  (one),  etc.     It  is  very  like  the  tick-tack  of 


346 


THE  EVIDENCES  OF   DISEASE 


a  watch  or  the  regular  rapid  click  of  a  short  pendulum.  It  is  a  grave 
prognostic  omen,  as  it  indicates  a  profound  enfeeblement  of  the  car- 
diac muscle,  such  as  occurs  in  the  specific  infectious  fevers  or  in 
chronic  degenerative  disease  of  the  myocardium. 


Normal 
3^  Time 


2  3  1  2  3  1  2  3 


1 

2 

1 

2 

1 

2 

1 — 1 

1 — 1 

r-i               1 

Embryocardia 

%Time 

- 

1 — 

1 

2 

3 

4 

1 

2 

3 

4 

1 

2 

3 

4 

Prolonged 
Second 

Silence 
*4Time 

Fig.  94. — Diagram  representing  two  variations  from  the  normal  cardiac  rhythm.    To  be 

read  from  left  to  risht. 


The  other  variation  is  an  undue  prolongation  of  the  second  or 
diastolic  silence.  The  1st  and  2d  sounds  are  short  and  irritably 
sharp,  and  the  interval  between  the  2d  and  1st  sounds  is  almost 
alarming  in  its  length.  One  may  say  that  it  is  in  common  (4-4) 
time,  3  and  4  representing  the  pause.  The  unusual  prolongation  of 
the  diastolic  silence  indicates  one  of  two  things :  either  an  overdose 
of  digitalis,  or  the  spasmodic  effort  of  an  overworked,  weak,  or  degen- 
erated heart  to  continue  its  labours.  In  the  latter  case  it  is  not 
of  necessity  a  fatal  prognostic.  It  has  been  met  with  more  particu- 
larly in  pneumonia. 

Adventitious  Sounds. — In  addition  to  or  in  place  of  the 
variations  in  the  ordinary  heart  sounds  which  have  been  consid- 
ered, auscultation  may  reveal  the  presence  of  certain  incidental  or 


AUSCULTATION  OF   HEART— MURMURS  347 

adventitious  sounds.  The  sounds  may  originate  within  the  heart — 
endocardial ;  or  arise  from  outside  the  heart — exocardial.  An  endo- 
cardial sound  is  called  a  murmur  or  bruit,  and  is  produced  at  one  of 
the  orifices  of  the  heart  as  a  result  of  certain  conditions  of  the  valve, 
the  orifice,  the  vessel,  the  blood,  or  the  force  and  velocity  of  the 
blood  stream.  Murmurs  caused  by  permanent  anatomical  changes 
in  the  valves  or  orifices  are  called  organic  ;  if  due  to  blood  changes 
or  modifications  of  cardiac  muscular  action, /Mnc^to/ia^  accidental,  or 
h(Bmic  murmurs.  Exocardial  sounds  for  the  most  part  originate  in 
the  pericardium,  pleura,  or  lung. 

ENDOCARDIAL  SOUNDS  (MURMURS) 

The  Physical  Explanation  of  Murmurs. — The  physical 
conditions  are  somewhat  complex.     The  most  important  factors  are : 

(1)  When  a  fluid  under  a  certain  degree  of  pressure  is  forced 
from  a  narrow  into  a  wide  channel,  or  through  a  narrowed  opening 
into  a  relatively  large  cavity,  a,  fluid  vein  is  formed,  the  particles  of 
which  are  in  a  state  of  rapid  vibration.  If  the  necessary  conditions 
are  produced  in  the  heart,  either  by  the  narrowing  of  an  orifice 
leading  into  a  larger  but  normal  cavity  or  by  a  dilatation  of  the 
cavity,  the  orifice  remaining  normal  but  relatively  narrowed,  the 
vibrations  of  the  resulting  fluid  vein  will  throw  the  walls  of  the  con- 
taining cavity  or  tube  into  lateral  vibrations  which  are  conducted  to 
the  surface  of  the  body.  In  rare  cases  the  vibrations  may  be  so 
strong  that  sound  waves  are  produced  at  the  surface  of  such  inten- 
sity as  to  be  heard  at  a  distance  of  several  inches  from  the  surface. 
Ordinarily  the  ear  must  be  placed  in  contact  with  the  surface,  or 
some  conducting  medium  (stethoscope)  used  which  will  carry  them 
to  the  ear,  in  which  they  are  translated  and  perceived  as  sounds.  If 
the  edges  of  the  opening,  as  in  the  orifices  of  the  heart,  are  fur- 
nished with  projecting  membranous  flaps  (valve  segments),  these,  by 
their  capacity  for  being  thrown  into  periodic  oscillation,  add  to  the 
number  and  intensity  of  the  vibrations,  and  consequently  modify 
very  considerably  the  character  of  the  sounds  perceived. 

As  a  rule,  vibrations  originating  in  this  manner  travel  most  rap- 
idly in  the  direction  of  the  fluid  vein.  Murmurs  due  to  a  narrowed 
orifice  move  with  the  blood  stream  (the  fluid  vein  running  in  the 
same  direction)  and  are  heard  further  along  in  its  course— e.  g., 
aortic  stenosis,  in  which  the  murmur  is  heard  also  in  the  carotids ; 
while  in  regurgitation  the  murmur  travels  backward  in  the  blood 
stream  (the  fluid  vein  opposing  the  main  current)— e.  g.,  aortic 
regurgitation,  in  which  the  murmur  is  heard  also  over  the  lower 
sternum. 


348  THE  EVIDENCES  OF  DISEASE 

(2)  The  density  or  relative  fluidity  of  the  blood  is  a  second  factor. 
The  thinner  the  blood  (the  less  its  specific  gravity),  the  more 
readily  is  it  thrown  into  vibration.  Hence,  partly  at  least,  the  great 
frequency  of  murmurs  in  anaemic  states. 

(3)  K  cerisiin  force  of  current  is  required.  Thus  a  murmur  may 
be  loudly  audible  so  long  as  the  heart  is  beating  strongly,  but  will 
diminish  or  totally  disappear  if  great  cardiac  weakness  supervenes. 

The  General  Characteristics  of  Murmurs. — It  is  neces- 
sary to  study  a  murmur  with  reference  to  its  time  relations,  tone 
and  quality,  point  of  maximum  intensity  and  lines  of  propagation ; 
and  also  endeavour  to  decide  whether  it  is  organic  or  functional. 

(a)  The  Time  of  Murmurs. — Murmurs  are  timed  with  reference  to 
the  ventricular  systole  (first  sound,  apex  beat,  or  carotid  pulse) 
and  the  ventricular  diastole  (beginning  with  the  second  sound). 
Endocardial  murmurs  always  bear  a  definite  relation  to  the  heart 
sounds.  Three  types  are  distinguished  :  Systolic,  beginning  with 
the  first  sound;  diastolic^  beginning  with  the  second  sound;  and 
presystolic,  immediately  preceding  the  first  sound. 

The  presystolic  murmur  is  in  reality  diastolic,  occurring  as  it  does 
during  the  auricular  systole,  which  takes  place  late  in  the  ventric- 
ular diastole,  but  it  is  very  desirable  to  restrict  the  term  diastolic  to 
murmurs  beginning  with  the  second  sound.  These  chronological 
types  are  represented  by  the  graphic  method  in  Fig.  95. 

{h)  The  Quality  of  Murmurs. — The  character  or  quality  of  a  mur- 
mur, while  its  diagnostic  value  is  not  great,  is  often  of  service,  and 
should  always  be  noted. 

In  general,  a  rough,  harsh,  rasping,  or  sawing  murmur  (in  mitral 
stenosis,  blubbering  or  churning)  attends  obstruction  or  stenosis  of 
an  opening  or  roughening  of  the  valve  surfaces;  while  if  the  murmur 
results  from  insufficiency  or  regurgitation  it  has  a  soft  and  blowing 
quality.  The  murmur  of  aortic  regurgitation  may  be  so  soft  as  to 
escape  detection  except  by  a  careful  examiner.  A  musical  murmur^ 
one  having  an  element  which  resembles  a  high-pitched  musical  note, 
has  no  special  significance  with  reference  to  any  particular  heart 
lesion.  It  may  be  due  to  a  perforated  valve  or  shreds  or  threads  of 
fibrin.  In  many  cases  nothing  exists  to  account  for  its  peculiar 
timbre.  Murmurs  having  a  peculiar  echoing  quality  are  due  to  the 
same  causes  as  metallic  heart  sounds  (q.  v.),  the  near  presence  of  a 
resonating  air  cavity. 

(c)  Intensity  of  Murmurs  versus  Replacement  of  Sounds. — The 
loudness  or  intensity  of  a  murmur  is  by  no  means  an  index  of  the 
gravity  of  a  valvular  lesion.  A  murmur  which  is  well-nigh  inaudible 
is  oftentimes  indicative  of  vastly  greater  damage  than  one  of  strik- 


AUSCULTATION  OF  HEART— MURMURS 


349 


ing  intensity.  A  judgment  with  reference  to  the  seriousness  of 
a  valvular  lesion  must  be  founded  on  other  evidence — e.  g.,  the 
presence  or  absence  of  hypertrophy  and  dilatation,  indirect  symp- 
toms (page  316),  etc. 


Fig.  95.— Diagram  showing  the  three  chronological  types  of  murmurs  and  their  relation 
to  the  sounds  of  the  heart.  The  events  of  the  cardiac  cycle  are  given  above  for  com- 
parison.   Murmurs  shaded  with  vertical  lines.    To  be  read  from  left  to  right 

One  of  the  principal  points  to  be  determined,  especially  with 
reference  to  regurgitant  murmurs,  is  whether  the  murmur  accom- 
panies or  replaces  the  valvular  sound  or  component.  Keplacement 
indicates  material  and  important  anatomical  changes  in  the  valve. 
In  such  a  case  the  sound  of  valve  tension  is  absent.  Thus,  if 
the  aortic  valve  is  seriously  incompetent,  the  snap  of  its  valve 
segments  will  largely  disappear  and  be  replaced  by  the  murmur. 
On  the  other  hand,  if  the  valvular  sound  is  present  and  the  murmur 
simply  trails  off  from  it,  we  may  infer  that  a  goodly  portion  of  the 
valve  action  is  preserved  and  that  the  actual  physical  alterations  in 
its  shape  and  structure  are  not  extreme. 

The  loudness  of  a  murmur  is  dependent  partly  upon  the  nature  of 
the  lesion,  partly  upon  the  strength  of  the  heart.  As  a  rule,  systolic 
murmurs  are  louder  than  diastolic,  particularly  those  originating  at 
the  aortic  orifice.     An  extremely  weak  heart  is  incapable  of  main- 


350  THE   EVIDENCES   OF   DISEASE 

taining  the  degree  of  force  of  the  blood  stream  whicli  is  requisite  to 
produce  strong  vibrations  and  a  resulting  loud  murmur.  Hence,  as 
s,  rule,  a  loud  murmur  implies  fair  compensation,  and  a  very  loud 
murmur  which  has  become  weak  may  be  restored  to  its  former 
intensity  by  rest  and  treatment  of  the  heart  muscle. 

Some  murmurs  may  be  felt  as  well  as  heard  (thrill,  q.  v.).  In 
general  it  is  the  loud  murmurs  which  give  rise  to  a  thrill,  and  the 
latter  is  usually  perceived  at  the  point  of  maximum  intensity  of  the 
murmur. 

(d)  Point  of  Maximum  Intensity  and  Lines  of  Propagation. — A 
murmur  is  heard  at  its  loudest  at  some  one  point,  the  point  of  maxi- 
mum intensity,  which  is  usually,  but  not  always,  in  the  area  of  great- 
est audibility  of  the  normal  sound  of  the  valve  at  which  the  murmur 
is  produced.  It  will  also  be  found  that  it  can  not  be  heard  equally 
well  at  equal  distances  from  this  point,  but  that  it  is  transmitted 
much  farther  in  one  direction  than  another — the  line  of  selective 
propagation. 

The  better  audibility  of  a  murmur  along  special  lines  depends 
upon  several  factors.  As  previously  stated,  the  sound  is  apt  to 
travel  in  the  direction  of  the  vibrating  fluid  vein,  either  with  or 
against  the  main  current.  Another  factor  is  the  presence  of  struc- 
tures differing  in  their  power  of  conductivity — e.  g.,  the  sternum, 
ribs,  walls  of  the  heart,  and  the  presence  or  absence  of  consolidated 
lung  or  lung  cavities.  Moreover,  the  relation  of  the  cavity  in  which 
the  murmur  originates  to  the  chest  wall  (in  contact  or  at  a  distance) 
wrll  modify  the  readiness  with  which  the  sound  reaches  the  ear. 
Special  lines  of  transmission  will  be  discussed  in  connection  with 
murmurs  arising  at  particular  orifices. 

(e)  Discrimination  between  Organic  and  Functional  Murmurs. — 
It  is  of  prime  importance  to  distinguish  between  temporary,  re- 
coverable, functional  murmurs,  not  due  to  valvular  disease ;  and 
organic  murmurs,  caused  by  permanent  and  incurable  stenosis  or 
incompetency.  The  exact  genesis  of  functional  (haemic,  anaemic, 
accidental)  murmurs  is  not  settled.  An  abnormal  fluidity  of  the 
blood  is  an  important  agency  in  their  production.  According  to 
their  location  they  are  probably  due  to  moderate  dilatation  of  the 
pulmonary  artery  giving  rise  to  a  fluid  vein ;  or  to  dilatation  of  one 
or  the  other  ventricle  in  consequence  of  a  poorly  nourished  heart 
muscle  with  resulting  relative  incompetency  at  the  mitral  or  tricuspid 
opening.  It  is  probable  that  in  some  instances  the  edges  of  the 
valve  cusps  turn  over  because  of  weakness  and  consequent  stretch- 
ing of  the  papillary  muscles,  thus  permitting  a  slight  regurgitation. 
Functional  murmurs  are  most  frequent  by  far  in  the  pulmonary  area, 


AUSCULTATION  OP   HEART— MURMURS 


351 


next  in  the  mitral,  then  in  the  tricuspid,  and  occur  more  rarely  in 
the  aortic  area.  It  is  at  times  extremely  difficult  to  determine  that 
a  murmur  is  functional,  but  the  discrimination  may  usually  be  made 
by  remembering  the  following  points  : 

(1)  The  ftmcHotial  OT  hcemic  murmur  is  almost  always,  but  not 
invariably,  systolic,  soft,  and  blowing  (sometimes  harsh),  found  most 
frequently  over  the 
pulmonic  area  where 
an  organic  murmur  is 
extremely  rare,  and  a 
venous  hum  is  heard 
in  the  veins  of  the 
neck.  Above  all,  the 
patient  is  distinctly 
anaemic  or  chlorotic. 
or  has  some  febrile  or 
wasting  disease,  and 
the  murmurs  disap- 
pear as  the  condition 
of  the  blood  improves. 
Moreover,  ventricular 
dilatation,  if  ascer- 
tained to  be  present, 
is  slight  and  unattend- 
ed by  hypertrophy  or 
secondary  symptoms. 

(2)  The  organic  murmur,  on  the  other  liand,  is  systolic  or 
diastolic,  there  may  be  marked  hypertrophy  or  dilatation,  there 
are  symptoms  referable  to  stasis  in  the  blood  current,  and  there 
is  a  history  of  rheumatism  or  other  disease  capable  of  causing 
endocarditis.  The  somewhat  sweeping  assertion  may  be  made, 
without  fear  of  serious  contradiction,  that  if  the  apex  beat  is 
not  displaced  or  altered  in  such  a  manner  as  to  indicate  hyper- 
trophy or  dilatation,  the  presence  of  a  murmur  does  not  signify 
organic  valvular  disease ;  although  it  is  possible  that  pathological 
changes  may  have  been  initiated  which  will  ultimately  lead  to  ana- 
tomical valvular  lesions  and  consequent  alterations  in  the  size  of 
the  heart. 

There  are  certain  sources  of  error.  The  history  of  rheumatism 
may  be  indefinite,  and  anaemia  alone  may  cause  dyspnoea  and  oedema 
of  the  feet.  Finally,  anajmia  may  occur  in  certain  cases  of  valvular 
disease,  notably  mitral  stenosis,  as  an  association  or  a  consequence  of 
the  valvular  affection. 


Fig.  96. — Showing  the  relative  frequency  of  anaemic  mur- 
murs at  the  various  orifices  of  the  heart.  Pereentatres 
from  Sansom. 


362 


THE  EVIDENCES  OF  DISEASE 


The  Diagnostic  Value  of  Individual  Murmurs. — Tak- 
ing the  orifices  of  the  heart  singly,  one  proceeds  to  study  the  char- 
acter and  meaning  of  the  different  murmurs  arising  at  each  opening. 
Mitral  Murmurs. — These  may  be  either  jii-esystolic  or  systolic, 
{a)  Mitral  Presystolic  Murmurs. — A  presystolic  murmur  at  this 
orifice  usually,  but  not  invariably,  indicates  : 

(1)  Mitral  Stenosis  or  Obstruction. — The  murmur  in  this  case  is 
caused  by  the  systole  of  the  left  auricle  driving  the  blood  through 
the  narrowed  opening.  The  murmur  begins  during  the  latter  part 
of  the  ventricular  diastole  with  the  systole  of  the  auricle  and  is  often 
accompanied  by  a  thrill.  It  is  harsh,  rough,  and  vibratory,  with  its 
area  of  maximum  intensity  a  little  inside  and  above  the  apex  beat 
(Fig.  97).     It  is  usually  strictly  localized,  but  it  may  be  heard  over 

an  area  beginning  at 
the  lower  end  of  the 
sternum,  passing  to 
the  left,  and  widening 
until  it  reaches  the 
midaxillary  line,  per- 
haps extending  verti- 
cally in  this  line  from 
the  3d  to  the  8th  rib 
(Griffith).  The  mur- 
mur runs  up  to  and 
terminates  in  an  ab- 
rupt 1st  sound  or 
"  snap  "  (phonetically 
"  rrup  "),  which  is  very 
characteristic.  The 
abrupt  1st  sound  has 
been  variously  ex- 
plained ;  but  the  most 
plausible  theory  is  that 
which  attributes  it  to 
a  sudden  tension  of  the  tricuspid  valve  caused  by  the  increased  pres- 
sure in  the  right  heart  consequent  upon  the  damming  back  of  the 
blood  by  the  mitral  obstruction,  the  sound  of  valve  tension  thus  pre- 
dominating over  the  muscular  component  of  the  1st  sound.  The  2d 
sound  is  frequently  reduplicated  and  its  pulmonary  component  accen- 
tuated. The  murmur  of  mitral  stenosis  is  variable,  appearing  and 
disappearing  according  to  the  strength  of  the  auricular  systole.  A 
few  moments  of  exercise  may  elicit  it  when  previously  absent.  It  is 
necessary  to  be  aware  of  the  fact  that  in  rare  instances  the  murmur 


Fig.  97. — Mitral  Presystolic  Murmur.  This  may  be  caused 
by  mitral  obstruction,  aortic  incompetence  ("  Flint "  mur- 
mur), and  slight  aortic  stenosis  and  adherent  pericardium. 
The  circle  shows  the  point  of  maximum  intensity  and 
the  usual  strict  localization  of  this  murmur.  The  radiat- 
ing lines  represent  its  possible  extent  of  audibility.  Apex 
indicated  by  the  cross. 


AUSCULTATION  OF  HEART— MURMURS 


353 


of  mitral  stenosis  may  be  diastolic,  mid-diastolic,  or  occupy  the  entire 
diastole  (Fig.  98),  the  vibrations  being  excited  at  any  time  during 
the  diastole  by  the  blood  which  begins  to  flow  into  the  ventricle 
from  the  auricle  at  the  close  of  the  ventricular  systole. 


Rrup 


^ 


Mitral  Presystolic  (Obstructive) 


(Ordinary  Type). 


li 


Mitral  Presystolic  with  Reduplicated 


Second  Sound   (Not  Uncommon). 


Mitral  Diastolic  (Uncommon). 


tt++^ 


Mitral  Diastolic-Presystolic 


(Uncommon). 


^ 


Mitral  Mid-Diastot!c 


Fig.  98.- 


(Uncommon). 


-Diagram  showing  the  chronological  varieties  of  the  murmur  of  mitral  stenosis. 
To  be  read  from  left  to  right. 


(2)  A  presystolic  mitral  murmur  is  also  caused  by  some  forms  of 
aortic  disease,  particularly  aortic  insufficiency.  This,  the  "  Flint " 
murmur,  is  attributed  to  an  extreme  dilatation  of  the  left  ventricle 
preventing  the  cusps  of  the  mitral  valve  from  folding  back  to  the 
ventricular  walls  during  diastole.  By  remaining  in  the  blood  cur- 
rent a  species  of  relative  narrowing  is  produced  and  a  vibrating 
presystolic  murmur  arises.  The  snap  of  the  first  sound  is,  however, 
absent,  and  if  the  dilatation  grows  less,  the  murmur  disappears. 

(3)  This  murmur  has  been  noted  very  infrequently  in  connection 
with  slight  aortic  stenosis  and  adherent  pericardium. 

(b)  Mitral  Systolic  3furmurs. — A  murmur  heard  in  the  mitral 
area,  beginning  with  the  first  sound  of  the  heart  (Fig.  99),  may 
indicate : 


354 


THE  EVIDENCES  OF  DISEASE 


(1)  Mitral  Insufficiency. — In  this  case  the  murmur  is  soft  and 
blowing,  either  accompanying  the  first  sound  or  replacing  its  valvu- 
lar component  more  or  less  completely.  It  is  transmitted  through 
the   left   axillary  region   and  posteriorly  to  the  angle  of  the  left 

scapula.  In  some  cases 
it  may  be  heard  over 
the  entire  chest.  Its 
maximum  intensity  is 
generally  at  the  apex, 
but  it  may  be  most 
intense  along  the  left 
edge  of  the  sternum. 
The  pulmonary  2d 
sound  is  accentuated, 
and  there  is  evidence 
of  hypertrophy  and 
dilatation.  In  the  ab- 
sence of  the  last-men- 
tioned signs  a  diag- 
nosis of  organic  or 
permanent  relative  in- 
sufficiency of  the  mi- 
tral valve  is  untenable, 
as  there  are  many  sys- 
tolic mitral  murmurs 
due  to  a  temporary  relative  insufficiency  and  caused  by  slight  dilata- 
tion, either  of  the  left  ventricle  or  the  valve  ring. 

It  is  to  be  borne  in  mind  that  a  loud  systolic  murmur,  heard  at 
the  back  as  well  as  in  front,  is  sometimes  present  in  the  dilatation 
of  the  left  ventricle  following  hypertrophy  (especially  that  due  to 
arteriosclerosis),  and  due  to  relative  insufficiency.  This  murmur 
may  totally  disappear  if  tlie  heart  regains  its  strength  and  the  dilata- 
tion is  overcome. 

(2)  The  murmur  due  to  anaemia. 

(3)  The  murmur  occurring  in  the  course  of  acute  infectious  or 
other  febrile  diseases,  especially  in  children.  In  these  cases  an  acute 
myocarditis  is  often  responsible  for  temporary  dilatation  and  conse- 
quent murmur. 

(4)  The  murmur,  varying  from  day  to  day,  of  acute  simple  or 
ulcerative,  endocarditis. 

(5)  The  intermittent  murmur,  very  rare  (cause  discovered  only 
at  autopsy)  and  due  to  a  ruptured  tendinous  cord,  or  a  pedunculated 
vegetation  floating  from  time  to  time  between  the  valve  cusps. 


Fio.  99. — Mitral  Systolic  Murmur.  This  may  indicate 
mitral  insufficiency,  anspmia,  acute  infectious  disease 
(myocarditis),  left  ventricular  dilatation,  malformation 
of  the  heart,  or  acute  endocarditis.  The  circle  indicates 
the  point  of  maximum  intensity,  the  arrow  the  line 
of  selective  transmission.  The  radiating  lines  represent 
the  area  of  audibility.  If  of  sufficient  intensity,  the 
murnmr  may  be  heard  over  the  entire  chest. 


AUSCULTATION  OF  HEART— MURMURS 


355 


(6)  A  loud  and  widely  diffused  murmur  in  the  mitral  area  of  a 
more  or  less  permanently  cyanotic  infant  may  indicate  complicated 
malformations  of  the  heart,  especially  a  defective  auricular  septum, 
patent  ductus  arteriosus,  or  transposition  of  the  great  vessels. 

Any  one  of  these  murmurs  may  disappear  if  the  heart  becomes 
sufficiently  weak,  excepting  the  murmur  mentioned  in  the  second 
paragraph  under  (1)  preceding. 

Aortic  Murmurs. — These  are  either  systolic  or  diastolic. 

{(i)  Aortic  Systolic  Miinnurs. — If  due  to  (1)  aortic  stenosis,  the 
murmur  coincides  with  the  1st  sound  (Fig.  100),  is  harsh,  accom- 
panied by  a  thrill,  heard  with  maximum  intensity  at  the  2d  right 
interspace  or  cartilage,  transmitted  into  the  carotids,  possibly  into 
the  axillary  artery,  and  the  2d  aortic  sound  is  frequently  abolished 
because  the  valve  cusps  are  too  stiff  to  vibrate  and  the  aortic  pressure 
is  lowered.  Finall3%  there  is  left  hypertrophy.  If  these  signs  occur 
in  an  elderly  person, 


a  reasonably 
diagnosis  of 
rowed  aortic 
may  be  made. 


certain 

a    nar- 

orifice 

With 


broken  compensation 
the  murmur  may  be- 
come soft  and  distant. 

(2)  If  the  presence 
of  a  systolic  aortic 
murmur  is  taken  as 
presumptive  evidence 
of  stenosis,  mistakes 
will  be  extremely  com- 
mon. In  a  majority 
of  cases  narrowing 
does  not  exist,  and 
one  of  the  following 
conditions  is  present : 
dilatation  of  the  aorta; 

roughening  or  calcification  of  the  aortic  segments  or  of  the  aorta  just 
beyond  the  valve  ring;  and  anaemia  (not  uncommon).  The  diastolic 
murmur  of  aortic  insufficiency  is  often  accompanied  by  a  systolic 
murmur  due  to  the  inequalities  of  the  valve  or  opening. 

(3)  A  systolic  murmur  heard  in  or  above  the  aortic  area,  or  to  the 
right  of  the  area,  may  be  due  to  aneurism  of  the  arch,  especially  the 
ascending  and  transverse  portions.  Careful  inspection  and  palpation 
of  the  great-vessel  area  should  be  made  to  discover  a  dull  area,  a  thrill, 


Fig.  100. — Aortic  Systolic  LIurmuk.  This  may  be  due  to 
aortic  stenosis,  anaemia,  dilatation  of  the  aorta,  roughen- 
ing of  the  aortic  segments  of  the  aorta,  inequalities  of  the 
valve  in  aortic  incompetence,  or  aneurism  of  the  arch 
of  the  aorta.  Circles  show  the  points  of  maximum  in- 
tensity and  the  arrows  the  lines  of  propagation  (into 
carotids  and  subclavians)  of  the  murmur. 


356 


THE  EVIDENCES  OF   DISEASE 


or  a  pulsating  swelling.    The  maximum  intensity  of  the  murmur  will 
in  this  case  be  over  the  dulness  or  the  swelling, 

(b)  Aortic  Diastolic  Murmur. — This  is  the  most  trustworthy  of 
all  murmurs  and  almost  invariably  signifies : 

(1)  Aortic  insufficiency,  due  to  deformation  of  the  valve  cusps. 
It  is  a  soft,  long  drawn  out,  sometimes  almost  inaudible  murmur, 
beginning  with  the  2d  sound  and  replacing  the  aortic  closure  sound 

more  or  less  complete- 
I  J^^^^^IHH^^^  I    ly.    Its  point  of  maxi- 

mum intensity  may  be 
either  at  the  aortic 
cartilage  or  over  the 
left  half  of  the  ster- 
num on  a  level  with 
the  3d  rib  or  inter- 
space (Fig.  101).  It 
is  transmitted  to  the 
lower  end  of  the  ster- 
num, and  in  some 
cases  is  very  distinct- 
ly audible  at  the  apex 
(mitral  area).  Dilata- 
tion and  hypertrophy 
always  exist.  Like 
other  heart  murmurs, 
it  may  disappear  if  the 
heart  grows  weak;  and 
vrith  great  rarity  autopsy  shows  that  the  murmur  has  ceased  because 
the  defect  in  the  valve  has  been  closed  by  a  vegetation  or  plug  of 
fibrin. 

(2)  Anaemia. — Although  its  occurrence  as  the  result  of  impover- 
ished blood  is  usually  considered  doubtful,  yet  if  the  total  disap- 
pearance of  this  murmur  following  recovery  in  2  cases  of  extreme 
anaemia  is  good  evidence,  it  may  be  said  that  its  haemic  origin  is  pos- 
sible but  infrequent. 

(3)  A  diastolic  venous  hum  originating  in  the  internal  jugular, 
or  in  the  superior  or  inferior  cava,  may  simulate  a  diastolic  aortic 
murmur,  but  in  such  a  case  there  will  be  little  if  any  evidence  of  left 
ventricular  hypertrophy  or  dilatation,  such  as  would  be  found  in 
aortic  incompetence. 

(4)  Eelative  aortic  incompetency,  the  aorta  dilating  or  the  sinuses 
of  Valsalva  yielding  because  of  atheroma,  inflammation  or  aneurism ; 
the  ventricle  dilating  as  the  result  of  fibrous  myocarditis,  general 


i'lG.  101. — AoKTic  Diastolic  Murmur.  This  may  be  due  to 
aortic  incompetency,  relative  aortic  incompetency,  or 
anaemia  (rare).  The  solid  circle  shows  the  usual  point 
of  maximum  intensity,  the  white  circles  show  the  occa- 
sional points  of  maximum  intensity,  and  the  arrow  shows 
the  direction  of  selective  transmission. 


AUSCULTATION  OP   HEART— MURMURS 


357 


arteriosclerosis,  etc.,  without  anatomical  changes  in  the  aortic  valve, 
is  perhaps  not  as  uncommon  as  is  generally  supposed  (?]uwards).  The 
simultaneous  dilatation  of  the  aorta  on  one  side  and  the  ventricle  on 
the  other  side  of  the  aortic  orifice  renders  the  aortic  valve  relatively 
incompetent.  A  musical  diastolic  murmur,  with  increase  of  dul- 
ness  over  the  great- 
vessel  area  (to  the 
right),  may  lead  to  a 
diagnosis. 

(c)    A  presystolic 

murmur  in  the  aortic 

<irea  is  a  clinical  curi- 
osity, there  being  1  or 

2  instances  on  record 

in  which  it  was  found 

in  an  infant  as  a  result 

of  a  patent  foramen 

ovale. 

Tricuspid  Murmurs. 


/ 


Fig.  102.— Tricuspid  Presystolio  MLKMLK(rare).     This  is 
due  to  tricuspid  stenosis,  congenital  or  acquired. 


-These  are  either  presystolic  or  diastolic, 
(a)   lyicuspid  Presystolic  Murmur. — This  is  a  rare  murmur  and 
indicates  tricuspid  stenosis,  either  congenital  or  acquired.     The  ac- 
quired form  is  almost  invariably  a  sequence  of  left  heart  lesions, 

especially  mitral  ste- 
nosis.     The  murmur 
(Fig.  102)   resembles 
,  that  of  mitral  narrow- 

^  A^y^     1  ing?  and  is  sometimes 

accompanied  by  a 
thrill.  Its  maximum 
intensity  is  over  the 
lower  end  of  the  ster- 
num at  the  base  of  the 
ensiform  cartilage,  or 
a  little  to  its  right. 
It  is  usually  not  trans- 
mitted. 

{h)  Tricuspid  Sys- 
tolic Murmur. — This 
murmur  is  not  uncom- 
mon and  indicates  tricuspid  regurgitation,  sometimes  from  puckering 
of  the  valves,  but  usually  on  account  of  relative  insufficiency  from 
dilatation  of  the  right  ventricle,  consequent  upon  left-side  (particu- 
larly mitral)  lesions.     The  murmur  resembles  that  of  mitral  regurgi- 


Fio.  103. — Tricuspid  Systolic  Murmur.  This  is  signiflcant 
of  relative  tricuspid  incompetency  due  to  dilatation  of 
the  right  ventricle  arising  from  left-side  disease  or  anae- 
mia. The  circle  shows  the  point  of  maximum  in- 
tensity. It  is  sometimes  heard  over  the  area  indicated 
by  the  radiating  lines. 


358 


THE  EVIDENCES  OF  DISEASE 


tation,  but  with  its  area  of  maximum  intensity  over  the  lower  end  of 
the  sternum.  It  is  usually  localized,  but  may  be  propagated  to  the 
right  as  far  as  the  anterior  axillary  line,  and  if  the  patient  is  recum- 
bent it  may  be  perceived  over  the  manubrium  (Fig.  103).  Engorged 
and  pulsating  jugulars,  and  pulsation  of  the  liver,  are  concomitant 
signs. 

This  murmur  may  also  be  significant  of  the  slight  right  ventricu- 
lar dilatation  resulting  from  anaemia,  but  when  due  to  blood  condi- 
tions the  venous  phenomena  are  not  marked  and  the  bruit  disappears 
as  the  antemia  lessens. 

Pulmonary  Murmurs. — These  may  be  systolic  or  diastolic. 

{a)  Pulmonary  Systolic  Murmurs. — In  rare  cases  this  murmur  is 
due  to — 

(1)  Congenital  malformation  of  the  heart.  In  this  case  there 
may  be  a  thrill,  and  the  pulmonary  2d  sound  is  weak  or  obliter- 
ated. The  murmur  is  loud  and  widely  diffused.  If  occurring  in  an 
infant  with  cyanosis,  the  abnormality  is  usually  a  pulmonary  stenosis ; 
without  cyanosis,  a  defective  ventricular  septum  or  a  patent  ductus 
arteriosus.     In  a  certain  proportion  of  cases  these  defects  coexist. 

(2)  In  some  instances  a  systolic  pulmonary  murmur  is  caused  by 
traction  upon  or  narrowing  of  the  pulmonary  artery  by  shrinking 
and  contraction  of  the  upper  portion  of  the  left  lung. 

(3)  Almost  invariably  this  murmur  is  not  due  to  disease  of  the 
valve,  but  is  of  anaemic  origin.    It  is  a  soft,  sometimes  slightly  rough, 

murmur,  heard  best 
in  the  2d  left  inter- 
space, 1  inch  or  more 
from  the  sternal  edge, 
and  perhaps  as  high 
as  the  1st  rib  (Fig. 
104).  It  may  be  audi- 
ble only  in  the  recum- 
bent position,  and 
may  disappear  during 
deep  inspiration.  The 
pulmonary  2d  sound 
is  accentuated. 

It  occurs  in  thin, 
nervous  children,  in 
ansmia,  and  in  con- 
ditions    of     debility 
without   notable   impoverishment  of  the  blood,  but  which   involve 
slight   dilatation    of   the  pulmonary  artery  beyond  the  valve  ring 


Fig.  104. — Pl'lmonauy  Systolic  Murmur.  This  may  be  due 
to  congenital  malformation,  traction  on  the  pulmonary 
artery,  anaemia  (very  common),  or  debility.  The  circle 
shows  the  point  of  maximum  intensity,  the  arrow  the 
line  of  transmission,  and  the  outline  the  usual  area  of 
audibility.  This  murmur,  if  due  to  malformation,  may 
be  audible  over  the  entire  chest. 


AUSCULTATION  OP  HEART— MURMURS 


359 


(relative  stenosis).  .  It  is  of  frequent  occurrence  in  exophthalmic 
goitre,  or  in  rapid  heart  action  from  fever  or  muscular  exertion.  A 
cardio-respiratory  murmur  is  often  heard  in  the  pulmonary  area ;  so 
also  is  the  transmitted  murmur  of  mitral  incompetency. 

(b)  Pulmonary  Diastolic  Murmur.  —  This  is  very  rare,  and, 
although  its  maximum  intensity  is  in  the  pulmonary  area,  it  is 
extremely  difficult  to  distinguish  it  from  the  corresponding  aortic 
diastolic  murmur.  It  may  be  due  to  (1)  congenital  malformation  of 
the  valve,  or  a  lesion  of  ulcerative  endocarditis ;  (2)  to  an  extreme 
increase  of  tension  in  the  pulmonary  artery,  the  murmur  of  high 
pressure  (Gibsox,  Steell). 

Combined  Murmurs. — When  two  or  more  murmurs  coexist  it  is 
easy  to  identify  them  if  they  occur  at  different  periods  in  the  car- 
diac cycle.  If  they  are  synchronous,  an  endeavour  must  be  made 
to  ascertain  the  point  of  maximum  intensity  and  the  line  of  prop- 


1  I  . 

1  1  1                         Aortic  Systolic  and  Diastolic 

1 1 ' 

1  1  '                                       (To  and  Fro) 

Mitral  Stenosis  and  Regurgitation 


or  Aortic  Stenosis  and  Mitral  Stenosis. 


Mitral  Stenosis  and  Aortic 


Insufficiency. 


Fig.  105. — Combined  murmurs. 


agation  of  each.  Moreover,  each  murmur  may  have  a  distinctive 
quality  of  its  own,  which  may  generally  be  ascertained  by  listening 
along  lines  connecting  the  various  orifices,  thus  finding  interme- 
diate areas  where  one  quality  ceases  and  another  begins.  The 
use  of  the  differential  stethoscope  is  helpful.  The  presence  of 
definite  circulatory  disturbances  and  the  particular  forms  of  hyper- 
trophy and  dilatation  known  to  be  due  usually  to  some  special 
lesion,  will  aid  in  the  discrimination.  The  combinations  most 
commonly  met  with,  and  in  order  of  frequency,  are  as  follows 
(Fig.  105) :  ,      . 

(1)  Aortic  Eegurgitation  and  Stenosis,  and  Mitral  Kegurgitation. 
—Systolic  murmur  at  apex  and  a  to-and-fro  murmur  at  the  aortic 
area  (Fig.  106),  the  "to"  murmur  (systolic)  running  up  to  the  2d 


360 


THE   EVIDENCES  OF   DISEASE 


sound,  almost  immediately  followed  by  the    "  fro  "  murmur  (dias- 
tolic). 

(2)  Mitral  Stenosis  and  Regurgitation.— Presystolic   murmur  at 

the  apex  terminating 
in  an  abrupt  1st 
sound,  and  followed 
immediately  by  a  sys- 
tolic murmur. 

(3)  Aortic  Steno- 
sis and  Mitral  Steno- 
sis.— Presystolic  mur- 
mur at  apex,  systolic 
at  the  base. 

(4)  Mitral  Steno- 
sis with  Aortic  In- 
sufficiency. —  Presys- 
tolic murmur  at  apex 
and  diastolic  at  base. 

Other  Adventi- 
tious Endocardial 
Sounds.  —  Not  in- 
frequently certain 
sounds,  in  some  cases 
"  qualities  "  might  be 
the  better  term,  are 
found  in  connection 
with  the  closure  of 
the  valves,  especially  the  mitral  and  aortic.  They  may  be  variously 
described  as  harsh,  grating,  rasping,  clicking,  or  murmurish.  The 
clicking  sound  may  be  mistaken  for  reduplication  of  the  1st  or  3d 
sounds ;  another  may,  as  implied  by  the  last  word  of  the  preceding 
sentence,  suggest  a  murmur  without  possessing  sufficient  duration  to 
deserve  the  name.  It  is  probable  that  in  all  cases  the  valve  cusps 
are  thickened  and  rough,  and,  when  possessing  a  murmurish  quality, 
slightly  deformed  as  well,  so  that  their  apposition  is,  for  a  brief  in- 
stant, hesitating,  imperfect,  and  with  some  friction.  A  loud  aortic 
sound  or  quality  of  the  clicking  or  harsh  variety  is  excellent  evidence 
of  atheromatous  changes. 

EXOCARDIAL   SOUNDS 

In  addition  to  the  adventitious  sounds  which  originate  in  the 
interior  of  the  heart,  others  which  arise  from  conditions  external  to 
the  heart  may  be  heard  over  the  pericardium.     Exocardial  sounds 


Fig.  106.- 


-Conibined  murmurs  of  aortic  incompetence  and 
steno.sis  and  mitral  incompetency. 


HEART— EXOCARDIAL  SOUNDS  361 

vary  considerably  in  character,  from  the  scratching  or  whiffing  peri- 
cardial friction  to  those  which  are  decidedly  "  murmurish  "  in  qual- 
ity, and  may  give  rise  to  much  perplexity  as  to  their  diagnostic 
significance.  Although  in  not  an  inconsiderable  proportion  of  indi- 
vidual cases  the  exact  mechanism  by  which  some  of  these  exocardial 
sounds  are  produced  can  not  be  positively  ascertained,  yet  it  is 
almost  always  practicable  to  determine  the  fact  of  their  exocardial 
origin.  Contrasting  them  with  intracardial  murmurs,  it  will  be  found 
that  they  do  not,  in  general,  bear  the  same  definite  relation  to  tlie 
phases  of  the  cardiac  cycle ;  they  are  notably  inconstant  and  variable, 
changing  in  intensity  with  the  phases  of  respiration,  the  position  of 
the  body,  or  pressure  upon  the  pericardium ;  and  are  for  the  most 
part  superficial — i.  e.,  convey  an  impression  of  nearness  to  the  exam- 
ining ear.  Most  important  of  all,  the  evidences  of  organic  valvular 
disease,  hypertrophy,  dilatation,  alterations  in  the  pulse,  and  circu- 
latory disturbances,  are  conspicuously  absent.  The  varieties  of  extra- 
cardial  sounds  and  their  characteristics,  arranged  as  nearly  as  possible 
in  the  order  of  frequency,  are  as  follows : 

Pericardial  Friction. — Pericardial  friction  sounds  are  variously 
described  as  scratching,  rasping,  shuffling,  rubbing,  scraping,  or  puf- 
fing, more  rarely  as  grating  or  creaking.  They  are  due  to  the  mutual 
friction  of  the  apposed  and  inflamed  surfaces  of  the  pericardium  and 
will  disappear  if  these  surfaces  are  separated  by  effusion.  They  are 
usually  double  (to  and  fro),  con-esponding  to  the  systole  and  diastole 
of  the  heart,  but  if  the  surface  of  an  auricle  is  inflamed,  a  tripling  of 
the  sound,  due  to  auricular  systole,  may  be  heard.  Although  their 
rhythm  corresponds  roughly  to  the  contraction  and  dilatation  of  the 
heart,  yet  it  may  be  perceived  that  they  do  not  bear  any  definite  and 
clear  relation  to  the  heart  sounds,  and  may  occur  during  any  portion 
of  the  cardiac  cycle. 

These  sounds  are  heard,  as  a  rule,  earliest  and  with  greatest 
intensity  at  the  base,  in  the  3d  and  4th,  not  infrequently  in  the  2d, 
left  interspaces  and  corresponding  half  of  the  sternum.  In  an  exten- 
sive pericarditis  the  point  of  greatest  audibility  is  just  internal  to 
the  left  nipple.  The  location  of  a  pericardial  friction  sound  may 
change  from  day  to  day,  but  in  all  cases  it  is  strictly  localized,  not 
transmitted.  Such  sounds  are  always  superficial,  may  be  intensified 
by  the  pressure  of  the  stethoscope  or  finger,  are  intermittent,  and,  if 
of  sufficient  intensity  and  roughness,  may  be  perceived  as  a  thrill  by 
the  palpating  hand.  In  a  patient  with  thin  chest  walls  and  a  much- 
dilated  heart  pulsating  in  the  interspaces  to  the  left  of  the  sternum, 
firm  pressure  with  the  stethoscope  may  develop  a  rubbing  sound 
somewhat  resembling  pericarditic  friction. 


362  THE  EVIDENCES  OF   DISEASE 

Pleuro-pericardial  Friction. — If  there  is  inflammation  of  the  pleu- 
ral surface  of  the  pericardium  and  the  adjoining  visceral  pleura, 
friction  sounds  synchronous  with  the  heart's  action  may  be  heard. 
They  result  from  the  rubbing  together  of  the  inflamed  surfaces  by 
the  excursions  of  the  heart.  Such  sounds  are  superficial  and  are 
most  intense  during  full  inspiration,  as  the  lung  becomes  distended, 
overlapping  the  heart  and  apposing  a  larger  area  of  roughened  sur- 
faces ;  conversely,  they  frequently  cease  during  expiration.  These 
friction  sounds  are  most  commonly  heard  over  the  4th,  oth,  and  6th 
interspaces  where  the  lingula,  or  lappet  of  lung,  overlies  the  apical 
portion  of  the  heart. 

Pleural  Friction. — Ordinarily  pleural  friction  is  synchronous  with 
the  respiration,  and  ceases  if  the  breath  is  held ;  but  in  some  cases 
of  dry  pleurisy,  affecting  the  interlobar  sulci  or  that  portion  of  the 
complementary  pleura  overlying  the  heart,  crackling  friction  sounds 
synchronous  with  the  action  of  the  latter  are  heard,  which  may  persist 
with  much  lessened  intensity  even  during  the  cessation  of  breath- 
ing. Such  friction  sounds  are  not  uncommon  in  phthisis  pulmo- 
nalis. 

Cardio-pulmonary  Murmurs.— Occasionally  a  short,  whiffing  mur- 
mur or  murmurish  sound  may  be  heard  over  and  around  the  j^r^e- 
cordial  space,  which,  in  the  absence  of  other  cardiac  signs  or  symp- 
toms, may  be  considered  as  due  to  the  action  of  the  moving  heart 
upon  the  surrounding  lung.  While  these  sounds  may  be  present 
with  apparently  normal  lungs,  it  is  probable  that  a  certain  amount 
of  emphysema,  usually  localized  or  compensatory,  is  requisite  for 
their  production.  This  murmur  may  be  produced  when  the  heart 
in  its  excursion  compresses  a  certain  portion  of  the  lung,  thereby 
driving  the  air  suddenly  from  the  air  cells  into  the  bronchioles  ;  or, 
per  contra,  when  the  heart  abruptly  recedes  from  a  portion  of  lung, 
thus  aspirating  air  into  the  alveoli.  The  cardio-pulmonary  murmur 
is  extremely  variable,  appearing  or  disappearing  during  inspiration 
or  expiration,  so  also  in  the  erect  or  recumbent  posture,  depending 
upon  the  exact  relation  of  the  portion  of  lung  in  which  the  murmur 
originates  to  the  moving  heart,  the  active  agent  in  its  production. 
I  have  more  than  once  heard  a  whiff  of  this  kind  very  distinctly  by 
auscultating  the  open  mouth  of  the  patient. 

Subphrenic  Friction. — A  friction  sound  heard  over  the  lower  end 
of  the  sternum  and  the  adjoining  costal  cartilages,  synchronous  with 
the  action  of  the  heart,  may  be  due  to  subphrenic  peritonitis  or 
abscess,  or  perhaps  to  a  diaphragmatic  pleuritis. 

Crepitation. — Fine  crepitating  rales  over  the  praecordium,  accom- 
panying the  movements  of  the  heart,  may  signify  the  rather  uncom- 


EXAMINATION  OF  BLOOD  VESSELS  363 

mon  condition  of  mediastinal  emphysema  resulting  from  traumatism 
(tracheotomy  in  particular),  pertussis,  and  diphtheria.  Pneumo- 
thorax often  coexists. 

Splashing  Sounds. — Churning,  splashing,  or  "  water-wheel "  sounds 
are  heard  in  the  rare  traumatic  hydro-pneumopericardium.  Similar 
sounds  have  been  heard  arising  from  a  large,  partly  filled  lung  cavity 
close  to  the  heart,  and  from  a  dilated  stomach  containing  air  and 
fluid.  In  all  such  cases  the  movements  of  the  heart  cause  succussion 
and  consequent  splashing  of  the  cavity  contents. 


IV.    PHYSICAL    EXAMINATION    OF    THE    BLOOD 
VESSELS    (INCLUDING    THE    PULSE) 

.  A.  Examination  of  the  Arteries 

Because  of  its  especial  importance,  the  examination  of  the  radial 
artery — i.  e.,  the  pulse — will  be  separately  considered. 

Inspection  and  Palpation  of  Arteries. — Certain  points  in  the  ex- 
amination of  the  larger  arteries  have  been  already  considered,  mainly 
with  reference  to  the  aorta — viz.,  pulsation  in  episternal  notch  (page 
267),  epigastric  pulsation  and  pulsating  liver  (page  328),  and  pulsa- 
tions in  the  neighbourhood  of  the  heart  (page  325). 

(1)  Excessive  pulsation  of  the  medium-sized  and  smaller  arteries 
is  due  to  the  same  causes  as  an  abnormally  strong  carotid  pulsa- 
tion (page  267). 

Normally  one  may  feel  pulsation  in  the  larger  accessible  arteries 
— viz.,  the  carotid,  subclavian,  brachial,  and  radial— very  frequently 
also  in  the  temporal,  femoral,  popliteal,  and  posterior  tibial.  If  the 
pulsation  is  abnormally  strong  and  extensive  it  may  be  felt  in  the 
small  arteries  of  the  lips,  fingers,  and  toes,  and  in  the  dorsalis  pedis 
artery.  In  old  people  the  pulsations  of  the  medium-sized  arteries 
are  visible  because  of  the  thickness  of  the  vessel  walls  and  the  con- 
sequent prominence  of  the  vessels. 

(2)  Palpation  of  the  accessible  arteries  furnishes  valuable  infor- 
mation with  reference  to  the  existence  of  general  arteriosclerosis. 
If  this  condition  is  present  these  arteries  are  found  to  be  hard,  cord- 
like, and  tortuous ;  and  if  calcareous  degeneration  has  taken  place, 
the  finger  tip  passed  along  the  vessel  will  perceive  a  more  or  less  dis- 
tinct sensation  of  irregular  "  beading,"  due  to  the  presence  of  the 
calcareous  plates. 

Auscultation  of  Arteries.— The  arteries  which  may  be  auscultated 
with  profit  are  the  aorta,  pulmonary,  carotid,  subclavian,  brachial, 
and  femoral  arteries,  rarely  the   radial   and  posterial  tibial.     For 


364  THE  EVIDENCES  OF   DISEASE 

sounds  and  murmurs  in  the  thoracic  aorta  and  pulmonary  artery 
see  (Index)  the  examination  of  the  heart  and  its  neighbourhood. 

In  auscultation  of  the  accessible  arteries  one  should  listen  first 
with  the  lightest  pressure  of  the  stethoscope  compatible  with  exclud- 
ing outside  noises,  then,  with  sufficient  force  to  partly,  but  not 
entirely,  occlude  the  vessel.  In  the  first  case  sounds  may  or  may 
not  be  heard  ;  in  the  second  case  a  systolic  murmur  is  developed  in 
any  artery  accessible  to  pressure.  This  murmur  arises  from  the 
vibrations  which  are  caused  by  the  rhythmic  passage  of  the  blood 
stream  through  the  narrowed  portion  of  the  vessel  and  varies  in 
intensity  with  the  degree  of  pressure. 

(1)  Carotid  and  Subclavian  Arteries. — Normally,  with  light  pres- 
sure one  can  hear  over  these  vessels  2  sounds  (not  murmurs),  sys- 
tolic and  diastolic  in  time,  which  are  the  transmitted  1st  sound  and 
aortic  2d  sound  of  the  heart.     The  1st  sound  is  sometimes  absent. 

A  harsh  systolic  murmur  heard  over  these  vessels  is  a  transmitted 
murmur  from  the  aortic  orifice,  a  roughened  aorta,  or  an  aortic  aneu- 
rism. If  softer  and  more  blowing  in  character,  especially  if  on  the 
right  side,  it  is  the  haemic  murmur  of  anaemia.  Inability  to  hear  the 
normal  diastolic  (aortic  2d)  sound  of  the  heart  over  these  vessels 
may  be  significant  of  aortic  regurgitation,  as  the  conditions  necessary 
for  its  production — viz.,  a  competent  aortic  valve — are  lacking.  A 
diastolic  murmur  in  the  carotid  and  subclavian  is  due  either  to  the 
conduction  against  the  regurgitant  blood  stream  of  the  bruit  of 
aortic  incompetency,  or  a  murmur  arising  from  a  reflex  current  in  the 
vessels  created  by  the  defective  valve. 

A  short,  whiffing  systolic  murmur  in  one  or  both  subclavian 
arteries  is  heard  in  some  healthy  individuals  when  the  chest  is  fully 
expanded  and  the  breath  held,  or  the  arms  extended  vertically  above 
the  head.  It  is  more  commonly  associated  with  apical  pulmonary 
phthisis  and  is  presumably  due  to  bending  of  the  vessel  under  the 
traction  of  adhesions  or  shrinking  lung  with  consequent  narrowing 
of  its  calibre — a  condition  equivalent  to  pressure  upon  the  vessel  by 
a  stethoscope. 

(2)  Sounds  in  Other  Arteries. — Under  normal  conditions  in  some 
persons,  with  light  pressure,  a  sitigle  systolic  sound  (not  murmur) 
may  be  heard  in  the  femoral  artery  and  the  abdominal  aorta,  the 
sound  of  systolic  tension  of  the  vessel.  In  health  this  sound  i& 
entirely  lacking  in  the  smaller  arteries.  If  single  sounds  are  heard 
with  light  pressure,  not  only  in  the  largest  but  also  in  the  smaller 
arteries  like  the  brachial,  radial,  ulnar,  posterior  tibial,  and  others 
even  less  in  size,  it  is  indicative  of  aortic  incompetency.  The  abrupt 
filling  of  the  vessels  gives  rise  to  a  sound  of  tension.     Such  sounds. 


EXAMINATION  OP  BLOOD  VESSELS  365 

may  also  be  caused  by  the  bounding  pulse  waves  of  anaemia  and  acute 
fevers. 

A  double  sound,  systolic  and  diastolic,  heard  with  light  pressure 
in  the  femoral  artery,  is  a  rare  sign  in  aortic  incompetency,  lead 
poisoning,  pregnancy,  and  mitral  stenosis,  the  second  sound  arising 
from  the  sudden  collapse  of  the  vessel.  A  double  munmir  heard 
tvith  pressure  over  the  femoral  is  found  only  in  aortic  incompe- 
tence, the  first  (systolic)  murmur  resulting  from  the  onward  rush 
of  blood  through  the  narrowed  vessel ;  the  second  (diastolic)  por- 
tion arising  from  a  backward  flow  of  the  blood  stream,  the  incom- 
petent aortic  valve  failing  to  sustain  the  peripheral  direction  of  the 
current. 

Murmurs  may  also  be  heard  in  arteries  compressed  by  enlarged 
lymph  nodes  or  other  tumours,  and  over  a  goitrous  thyroid  gland. 

B.  Capillabies 

Aside  from  the  degree  of  fulness  of  the  capillaries  as  evidenced 
by  redness  or  pallor  of  the  skin,  the  only  sign  of  importance  which 
can  be  found  by  examination  of  these  minute  vessels  is  the  "  capil- 
lary pulse  "  previously  considered  (Subungual  Pulse,  page  271). 

C.  Veins 

Inspection  and  Palpation  of  Veins. — General  and  local  venous  dis- 
tention (page  91)  has  been  considered;  so  also  has  jugular  pulsation 
(page  269).     In  addition  the  following  signs  may  be  observed  : 

(1)  A  systolic  (true)  venous  pulse  like  that  seen  in  the  jugular, 
and  occurring  under  the  same  conditions,  has  been  noted  in  the  veins 
of  the  face,  the  superficial  veins  of  the  arm,  and  the  branches  of  the 
internal  mammary  veins. 

(2)  A  centripeial  (progressive)  venous  pulse,  the  wave  passing 
from  instead  of  toward  the  periphery,  may  exist  under  certain  condi- 
tions in  the  dorsal  veins  of  the  hand  and  foot.  It  is  always  associated 
with  a  capillary  pulse  and,  like  the  latter,  is  due  to  aortic  insufficiency 
or  great  relaxation  of  the  arterioles  (as  in  anaemia,  phthisis,  neuras- 
thenia, etc.),  so  that  the  arterial  pulse  is  transmitted  through  the 
capillaries  into  the  veins.  In  rare  instances  a  direct  communication 
between  the  artery  and  vein  (aneurismal  varix)  is  responsible  for  this 
phenomenon. 

(3)  If  a  vein  is  perceived  by  palpation  to  be  /?r/«  and  cordlike  and 
cedema  of  the  extremity  coexists,  thrombosis  of  the  vein  is  present. 
It  occurs  most  frequently  in  one  or  both  femoral  veins,  extending 
perhaps  into  the  iliac  trunks,  as  the  result  of  infectious  diseases  and 
septic  processes,  more  rarely  in  the  weakness  of  age. 


366  THE  EVIDENCES  OF   DISEASE 

Auscultation  of  Veins. — (1)  Jugular  and  Innominate  Veins. — The 
only  auscultatory  evidence  of  any  importance  to  be  derived  from  the 
veins  is  the  so-called  bruit  de  diahle,  or  venous  hum.  It  is  a  con- 
tinuous humming  and  sometimes  musical  murmur,  heard  over  the 
jugular  veins  of  both  sides,  but  with  greater  loudness  over  the  right 
jugular. 

It  may  be  caused  by  the  pressure  of  the  stethoscope  or  the  con- 
striction of  the  vein  which  occurs  when  the  head  is  turned  far  to  one 
side.  Consequently,  to  determine  its  presence  as  a  real  and  not  an 
artificial  sign  the  stethoscope  must  be  applied  evenly  and  lightly,  with 
a  degree  of  pressure  just  sufficient  to  maintain  the  apposition  of  the 
mouthpiece  to  the  skin,  and  the  head  kept  in  a  symmetrical  and 
unconstrained  position.  It  occasionally  happens  that  the  tracheal 
inspiratory  sound  resembles  the  venous  hum  so  closely  that  an  error 
may  arise,  but  the  question  is  readily  solved  by  having  the  patient 
hold  his  breath.  The  maximum  intensity  of  the  bruit  is  usually  in  a 
somewhat  triangular  space  having  the  inner  third  of  the  clavicle  as 
a  base,  especially  over  the  interval  between  the  clavicular  and  sternal 
attachments  of  the  sterno-cleido-mastoid  muscle. 

The  mechanism  and  meaning  of  the  murmur  are  still  in  dispute. 
It  arises  either  from  the  formation  of  a  fluid  vein  at  the  point  where 
the  narrow  jugular  opens  into  a  wider  cavity — the  jugular  bulb— or 
from  lateral  vibrations  of  the  vessel  walls.  In  both  cases  an  abnor- 
mal fluidity  of  the  blood  is  usually  but  not  always  a  prerequisite.  The 
intensity  of  the  murmur  is  greatest  in  the  upright  position,  also 
during  inspiration  and  the  diastole  of  the  heart,  all  of  these  factors 
increasing  the  rapidity  with  which  the  blood  flows  from  the  jugulars 
through  the  innominate  veins  into  the  superior  cava.  Thus  the 
murmur,  while  continuous,  rises  and  falls  with  rhythmic  intensity. 
If  the  murmur  is  unusually  loud,  it  may  be  heard  not  only  above  the 
clavicle,  but  may  be  followed  as  far  down  as  the  2d  right  interspace 
and  rib. 

AVhile  the  venous  hum  occurs  in  some  apparently  healthy  indi- 
viduals, its  association  with  anaemia,  particularly  the  chlorotic  and 
pernicious  varieties,  is  so  frequent  and  noticeable  that  its  presence 
must  undoubtedly  be  held  as  a  very  suggestive  sign  of  this  disease. 

(2)  Sounds  in  Other  Veins. — In  extreme  grades  of  anaemia  simi- 
lar humming  murmurs  may  be  heard  in  the  subclavian  veins  and  the 
axillary  and  other  large  veins  of  the  extremities.  In  advanced  cir- 
rhosis of  the  liver  a  venous  hum  may  be  heard  over  the  lower  costal 
margin  in  the  right  hypochondrium.  In  the  jugular  veins  exhibit- 
ing the  systolic  pulse  of  tricuspid  incompetency,  a  sound  (not  a  mur- 
mur) may  usually  be  heard,  due  to  the  sudden  tension  of  the  vessel. 


THE  PULSE  367 

A  similar  sound  of  the  same  origin  may  sometimes  be  heard  in  the 
femoral  vein. 

D.  The  Pulse 

The  value  of  the  pulse  examination  depends  primarily  upon  a 
knowledge  of  the  physiology  of  the  heart  and  blood  vessels,  but  also 
very  largely  upon  the  personal  experience  of  the  examiner. 

Elements  of  the  Pulse. — The  elements  of  the  pulse  which  are 
of  clinical  value,  and  therefore  require  investigation,  are  : 

(1)  The  pulse  rate  (frequency),  (2)  the  rhythm,  (3)  the  condition 
of  the  vessel  walls  and  incidentally  the  size  of  the  vessel  itself,  (4) 
the  tension  (blood  pressure),  (5)  the  character  of  the  pulse  wave  with 
reference  to  amplitude,  duration,  and  celerity.  Finally,  (6)  the  pulse 
in  other  arteries  of  the  same  individual. 

Technic  of  Examination. — Because  of  its  accessibility,,  the 
radial  pulse  is  chosen  for  examination.  The  patient  should  be  either 
lying  or  sitting  in  an  easy  position  and,  unless  for  a  particular  ob- 
ject, should  not  have  made  any  physical  exertion  just  previous  to  the 
examination.  The  mere  act  of  taking  the  pulse  will  greatly  acceler- 
ate its  frequency  in  many  persons,  even  in  those  who  are  outwardly 
calm  and  composed. 

The  patient's  forearm  should  be  semi-pronated,  as  the  artery  is 
thus  more  readily  palpated,  and  the  arm  supported.  It  is  always 
desirable  to  examine  both  radial  arteries  in  every  patient  who  is  seen 
for  the  first  time,  in  order  to  detect  a  not  uncommon  anomaly  of  dis- 
tribution in  which  the  radial  winds  around  the  styloid  process  of  the 
radius  to  the  dorsum  of  the  bone,  while  the  superficialis  volae  pursues 
the  usual  course  of  the  radial.  Three  fingers— first,  middle,  and  ring 
— should  be  laid  upon  the  artery.  For  certain  purposes  the  simulta- 
neous employment  of  the  fingers  of  each  hand  is  desirable. 

(1)  To  Befennine  the  Pulse  Bate.— Count  the  pulse  for  15  seconds 
and  multiply  by  4.  If  it  is  irregular,  count  for  a  full  minute. 
An  extraordinarily  frequent  pulse,  200  or  over,  if  regular,  may  be 
determined  by  counting  every  2d  or  every  3d  beat  and  multiplying 
by  2  or  3  as  required ;  or  by  making  a  line  of  dots  with  pencil  on  a 
sheet  of  paper,  each  dot  corresponding  to  a  pulse  beat,  and  afterward 
enumerating  the  marks. 

(2)  Xote  the  Ehytkm.— Are  the  successive  beats  equidistant  in 
point  of  time — i.  e.,  are  they  regular  ? 

(3)  Xote  the  Condition  of  the  Vessel  Walls  and  the  Size  of  the  Ves- 
sel—Em^ty  the  vessel  by  pressure  and  roll  it  under  the  fingers,  slip- 
ping the  skin  over  the  vessel.  A  normal  artery  is  scarcely  to  be  felt 
except  in  a  very  thin  wrist,  but  one  that  is  sclerosed  is  firm,  cordlike, 


368  THE  EVIDENCES  OF  DISEASE 

and  tortuous.  While  empty,  endeavour  to  estimate  its  size.  Eun 
the  finger  along  the  vessel  in  order  to  detect  calcareous  "  beading  " — 
plates  of  lime  salts.  As  a  high-tension  artery  feels  very  much  like 
one  which  is  sclerosed,  cut  off  the  direct  blood  flow  by  firm  pressure 
with  the  finger  nearest  the  heart,  and  the  recurrent  flow  (from  pal- 
mar arch)  by  firm  pressure  with  the  finger  nearest  the  hand.  The 
middle  finger  can  then  determine  the  condition  of  the  arterial  wall, 
the  element  of  blood  pressure  having  been  eliminated. 

(4)  Estimate  the  Tension. — To  estimate  the  arterial  tension  (page 
310),  first  ascertain  the  condition  of  the  arterial  walls,  as  in  (.3),  to 
eliminate  a  deceptive  arteriosclerosis ;  then  cut  off  the  recurrent 
wave  from  the  palmar  arch  with  the  finger  nearest  the  hand,  and 
make  increasing  pressure  with  the  finger  nearest  the  heart  until  the 
direct  wave  is  no  longer  perceived  by  the  middle  of  the  3  fingers 
employed.  The  degree  of  pressure  required  to  extinguish  the  direct 
wave  is  the  measure  of  the  tension,  and  the  ability  to  gauge  it  cor- 
rectly requires  considerable  practice. 

It  is  to  be  borne  in  mind  that  while  the  pulse  wave  itself  may 
have  a  high  tension,  as  in  aortic  incompetency,  the  blood  ^essure  in 
the  intervals  between  the  beats  may  be  low,  as  it  is  in  the  same 
lesion.  It  is  only  a  continuous  or  prolonged  high-tension  pulse,  the 
blood  pressure  remaining  high  between  beats,  that  is  significant.  Its 
presence  may  be  assured  by  endeavouring  to  palpate  the  artery  be- 
tween beats,  rolling  it  from  side  to  side,  and  finding  it  firm  and  not 
easily  compressible. 

Further  assistance  may  be  derived  from  the  fact  that  a  low-ten- 
sion pulse  is  most  distinctly  felt  with  light  pressure ;  a  pulse  of  mod- 
erate tension  with  moderate  pressure,  while  a  high-tension  pulse 
develops  its  greatest  force  with  firm  pressure.  Moreover,  if  varia- 
tions in  the  size  of  the  vessel  be  excepted,  a  high-tension  pulse  is 
usually,  but  "not  always,  small,  and  conversely. 

If  with  light  pressure  upon  a  soft,  easily  compressible  artery  a 
2d  weak  rebound  is  felt,  immediately  sequent  to  the  first  expan- 
sion, it  is  the  dicrotic  wave  or  pulse,  a  sign  of  low  tension. 

(5)  Determine  the  Character  of  the  Pulse  Wave  with  Reference  to 
Amplitude,  Strength,  Duration,  and  Celerity. — The  amplitude  or  vol- 
ume of  the  individual  pulse  wave  is  measured  by  the  amount  of  ex- 
pansion of  the  artery — i.  e.,  its  increase  in  diameter — the  arterial 
diastole,  coincident  with  the  systole  of  the  heart.  The  volume  of 
the  pulse  wave  will  vary  from  large,  to  medium,  to  small.  The  pulse 
may  be  found  to  be  irregular  in  volume  and  strength  as  well  as 
rhythm. 

Here  may  be  mentioned  the  volume  or  fulness  of  the  artery  le- 


THE  PULSE  369 

tween  beats.  Palpation  between  the  successive  pulse  waves  will  show 
that  the  vessel  remains  full,  or  that  it  empties  out  more  or  less  com- 
pletely. If  full,  the  tension  may  be  high,  as  in  chronic  renal  disease, 
or  low,  as  in  the  febrile  pulse  with  relaxed  arterioles.  A  full  artery 
does  not  necessarily  imply  a  large  pulse  wave.  In  aortic  incompe- 
tence the  pulse  wave  is  extraordinarily  large,  while  the  artery  is  quite 
empty  in  the  intervals. 

It  is  hardly  possible  to  separate  the  strength  of  the  pulse  wave 
from  its  tension,  and  the  two  are  practically  synonymous. 

The  duration  and  celerity  of  the  pulse  wave  refer  to  the  manner 
of  its  ascent,  summit,  and  descent — i.  e.,  of  the  rise  of  blood  pres- 
sure, of  its  maintenance,  and  finally  its  fall.  It  is  to  be  observed, 
first,  whether  the  ascent  or  increase  of  pressure  is  sudden,  moder- 
ately rapid,  or  slow ;  second,  whether  the  pressure  is  well  sustained, 
or  whether,  having  reached  its  height,  it  falls  off  abruptly ;  third, 
whether  the  descent  or  fall  of  pressure  is  rapid,  gradual,  or  slow.  As 
a  rule,  in  a  high-tension  pulse  the  rise  is  gradual,  the  height  well 
sustained,  and  the  descent  gradual,  while  in  a  low-tension  pulse  it  is 
sudden,  brief,  and  quick. 

During  the  descent  there  may  be  perceived  a  second  slight  im- 
pulse or  secondary  wave.  If  this  is  felt  only — or  best — with  consid- 
erable pressure  in  a  high-tension  pulse,  it  is  the  tidal  or  predicrotic 
wave.  On  the  other  hand,  if  the  pulse  is  one  of  low  tension  and  the 
secondary  impulse  is  felt  only  or  best  with  very  light  pressure,  it  is 
the  dicrotic  wave  (dicrotic  pulse),  and  may  be  intensified  by  cutting 
off  the  recurrent  wave  from  the  palmar  arch.  The  dicrotic  wave  is 
much  more  frequently  observed  than  the  predicrotic. 

(6)  Compare  the  Pulse  in  Other  Arteries  in  the  Same  Individnal. 
— Compare  both  radials,  and,  if  practicable,  both  femorals,  and  both 
posterior  tibial  arteries  as  well.  It  may  be  found  that  the  pulse  wave, 
which  should  reach  symmetrical  arteries  at  the  same  instant,  is  de- 
layed in  one,  or  obliterated,  or  will  present  differences  in  amplitude, 
strength,  and  character  on  the  two  sides. 

The  Normal  Pulse. — In  an  adult  at  rest  the  frequency  of  the 
pulse  varies  from  70  to  75;  it  is  regular;  the  artery  can  be  felt 
scarcely  or  not  at  all ;  the  tension  is  moderate  ;  the  pulse  wave  is  of 
medinm  amplitude,  its  rise  and  fall  are  neither  extremely  abrupt  nor 
abnormally  slow,  and  the  pressure  is  sustained  without  undue  brevity 
or  prolongation. 

The  Significance  of  Variations  in  the  Pulse.— The  follow- 
ing variations  are  recognised  : 

Increased  Frequency  {Tachycardia^  Pulsus  frequens). — Bearing 
in  mind  the  nervous  mechanism  of  the  heart  (page  310),  it  is  evident 


370  THE  EVIDENCES  OF   DISEASE 

that  increased  frequency  of  the  pulse  may  be  due  either  to  paralysis 
of  the  pneumogastric  or  to  irritation  of  the  sympathetic  nerves  or  the 
intracardiac  ganglia.  Conversely,  a  decreased  pulse  rate  may  be  due 
to  pneumogastric  irritation  or  paralysis  of  the  cardiac  sympathetic 
nerves  and  ganglia. 

The  source  and  causes  of  irritation  or  depression  of  the  cardiac 
mechanism  are  diverse.  It  may  be  an  organic  lesion  affecting  the 
centres  in  the  medulla  or  tlie  nerves  connecting  it  with  the  heart — 
e.  g.,  tumour,  hemorrhage,  meningitis,  gumma,  exostosis,  or  neuritis — 
or  inflammation  of  the  endocardium  or  pericardium,  or  degeneration 
of  the  cardiac  muscle  containing  the  ganglia.  It  may  be  functional 
— e.  g.  reflex — from  the  cerebrum  (emotion),  or  from  connected, 
somewhat  distant  organs  (stomach,  intestines),  or  from  poisonous 
substances  circulating  in  the  blood  (alcohol,  bile),  or  from  general 
fatigue  of  the  nervous  system. 

(1)  The  pulse  rate  is  normally  more  frequent. in  infants  (140  at 
birth)  and  children  (90-100  at  3  years  of  age)  than  in  the  adult, 
slightly  more  frequent  in  women  (75)  than  in  men  (70),  is  more 
rapid  in  the  evening  than  the  morning,  in  the  erect  than  the  recum- 
bent position,  after  than  before  meals  and  the  taking  of  hot  bever- 
ages, in  hot  than  in  cold  weather,  during  exercise  than  at  rest,  and 
may  be  extremely  rapid  in  consequence  of  mental  excitement.  Eapid 
heart  action  is  usually  associated  with  a  low-tension  pulse.  Indeed, 
low  tension  is  the  most  important  factor  in  almost  all  cases  of  fre- 
quent pulse.  The  lessening  of  the  peripheral  resistance  removes  a 
check  upon  the  heart's  action,  and  therefore  permits  it  to  contract 
with  more  ease  and  consequent  increased  rapidity. 

(2)  In  all  febrile  conditions  the  pulse  rate  is  usually  increased,  8 
to  10  beats  for  each  degree  above  the  normal.  This  ratio  does  not 
always  hold,  as  in  typhoid  fever,  where  the  pulse  is  less  frequent,  and 
in  scarlet  fever,  in  which  it  is  more  frequent,  than  would  be  ex- 
pected, constituting  in  each  case  a  diagnostic  finding  of  some  value. 
If  the  fever  is  of  septic  or  suppurative  origin,  the  frequency  is  excess- 
ive as  compared  with  the  temperature. 

(3)  A  frequent  pulse  attends  all  well-marked  valvular  defects  of 
the  heart  (except  aortic  stenosis,  in  which  the  pulse  may  be  slow), 
and  is  found  in  nearly  all  cases  when  compensation  fails. 

(4)  When  a  persistently  frequent  pulse  is  encountered  in  persons 
who  are  not  at  all  or  but  slightly  febrile,  and  who  present  no  physical 
signs  of  gross  cardiac  disease,  it  should  create  suspicion  of  the  exist- 
ence of  certain  diseases  which  are  characterized  more  or  less  con- 
stantly by  this  symptom,  and  other  corroborative  evidence  should  be 
sought.     These   ailments   are   early   phthisis,   exophthalmic   goitre, 


THE  PULSE  371 

Addison's  disease,  chlorosis  and  pernicious  anaemia,  arthritis  defor- 
mans, and  locomotor  ataxia. 

(5)  It  is  also  to  be  remembered  that  neurasthenic  conditions  may 
exhibit  a  rapid  pulse  rate.  The  abuse  of  alcohol,  tobacco,  coffee,  and 
tea  may  account  for  otherwise  inexplicable  cases.  Sexual  excesses, 
lack  of  sleep,  and  disorders  of  digestion  are  not  infrequent  causes, 
and  there  is  frequently  a  tachycardia  during  convalescence  from 
acute  diseases,  and  in  hemorrhage  and  conditions  of  general  debility. 

(6)  There  is  a  peculiar  form  of  accelerated  action  of  the  heart 
which,  in  the  absence  of  demonstrable  organic  alterations,  must  be 
considered  a  neurosis.  It  consists  in  recurring  attacks  of  rapid  beat- 
ing of  the  heart  (paroxysmal  tachycardia),  lasting  for  an  hour  or  more 
and  recurring  at  varying  intervals,  in  some  cases  for  years.  The 
paroxysm  may  or  may  not  be  attended  by  nausea,  anxiety,  and  sub- 
sternal oppression.     The  pulse  rate  may  rise  to  240  or  over. 

Decreased  Frequency  {Brachycardia  or  Bradycardia^  Pulsus  rarus). 
— The  normally  slow  pulse  rate  runs  from  60  down  to  40,  while  in 
disease  the  heart  may  beat  in  very  rare  instances  but  4  times  per  min- 
ute. An  infrequent  pulse  is  usually  of  high  tension,  an  increase  of 
the  peripheral  resistance  forcing  the  heart  to  contract  more  slowly. 

(1)  The  pulse  is  slow  in  some  healthy,  usually  strong  and  large- 
bodied  individuals.  It  is  often  slow  in  old  age,  and  is  normally  infre- 
quent in  the  puerperium. 

(2)  Bradycardia  may  be  indicative  of  some  cardiac  lesion,  most 
frequently  fatty  degeneration,  chronic  myocarditis,  or  sclerosis  of  the 
coronary  arteries.  The  pulse  of  aortic  stenosis  is  usually  slow,  while 
mitral  lesions  may  also  cause  an  infrequent  pulse,  probably  because 
of  associated  changes  in  the  heart  muscles.  If  bradycardia  continues, 
notwithstanding  the  use  of  large  doses  of  atropine,  it  is  presumably 
due  to  an  affection  of  the  heart  (Dehio).  Because  of  the  impediment 
in  the  pulmonary  circuit,  the  pulse  is  slow  during  an  attack  of  spas- 
modic asthma  and  in  emphysema. 

(3)  Certain  diseases  of  the  nervous  system  may  be  responsible  for 
a  reduction  in  the  pulse  rate,  notably  cerebral  hemorrhage,  tumour, 
meningitis,  or  other  lesions  which  give  rise  to  an  increased  intra- 
cranial pressure.  It  is  also  seen  in  epilepsy,  diseases  or  injuries  of 
the  cervical  cord,  mania,  melancholia,  and  general  paralysis  of  the 
insane.  Myxoedema  with  its  general  apathy  exhibits  a  lessened 
pulse  rate. 

(4)  Poisonous  substances  circulating  in  the  blood  may,  by  acting 
upon  the  cardiac  centres  or  ganglia,  retard  the  pulse  beat  to  a  marked 
degree.  Among  these  substances  the  most  important  are  bile  (in 
jaundice),  urea  and  other  retained  excrementitious  materials   (in 


372  THE  EVIDENCES  OP   DISEASE 

uraemia),  glucose,  lead,  opium,  carbon  dioxide,  alcohol,  and  occasion- 
ally tea,  coffee,  and  tobacco. 

(5)  A  slow  pulse  is  frequently  present  in  cases  of  inanition — e.  g., 
gastric  ulcer  and  cancer;  and  it  occurs  at  times  in  convalescence 
from  certain  acute,  usually  specific  infectious,  diseases,  as  diphtheria, 
erysipelas,  pneumonia,  typhoid  fever,  malaria,  and  acute  articular 
rheumatism — possibly  an  example  of  impaired  reactive  power,  result- 
ing from  an  overtaxing  strain. 

•  (6)  Chronic  digestive  disorders,  instead  of  quickening  the  pulse 
rate,  may  slow  it  notably  in  consequence  of  mental  depression,  poi- 
sonous substances  in  the  circulating  blood,  or  reflex  influences  from 
the  digestive  organs,  one  or  all. 

(7)  There  are  cases  of  so-called  "  essential  bradycardia  "  in  which 
even  after  death  no  appreciable  lesions  can  be  found,  but  these  are 
rare.  If  the  bradycardia  be  excessive  (20  to  30),  very  alarming  syn- 
copal, apoplectiform,  or  epileptiform  attacks  may  occur  from  time  to 
time — the  Stokes-Adams  syndrome.  Such  an  attack  has  been  ascribed 
to  disease  of  the  arteries  of  the  medulla  affecting  the  pneumogastric 
centres.  The  most  common  occurrence  of  bradycardia  is  in  con- 
valescence from  acute  febrile  diseases,  next  in  chronic  digestive  dis- 
orders, then  in  diseases  of  the  heart  and  brain.  If  it  is  due  to 
cardiac  or  cerebral  disease  the  prognosis  must  be  highly  unfavour- 
able, but  in  other  cases  little  danger  need  be  apprehended.  High- 
tension  pulses  are  usually  slow. 

Intermittent  or  Irregular  Pulse  (Arrhythmia).— Intermittence 
consists  in  the  omission  of  one  or  more  beats  of  the  pulse.  The 
missing  pulsation  may  be  due  to  an  ineffectual  cardiac  systole,  the 
contraction  not  being  sufficiently  strong  to  send  a  perceptible  wave 
into  the  radial  artery,  although  a  feeble  heart  sound  may  be  heard. 
If  the  heart  actually  omits  the  systole  from  time  to  time,  the  result- 
ing intermittence  is  sometimes  referred  to  as  a  deficient  pulse.  The 
pulse  may  be  irregular,  not  only  in  time,  bnt  also  in  volume  and 
strength. 

There  are  several  varieties  of  intermittent  and  irregular  pulse. 
In  the  alternating  pulse  {pulsus  alternans)  {€',  Fig.  107)  a  strong 
beat  alternates  with  a  feeble  beat ;  in  the  bigeminal  pulse  (pulsus 
Mgeminus)  (Z),  Fig.  107),  the  beats  occur  by  twos,  and  in  the  trigemi- 
nal pulse  {pulsus  trigeminus)  by  threes.  Delirium  cordis  is  the  con- 
dition in  which  the  pulse  is  totally  irregular  both  in  time  and  strength. 
In  the  pulsus  paradoxus  the  pulse  beat  becomes  weak  or  impercep- 
tible during  inspiration. 

The  clinical  significance  of  arrhythmia  is  variable.  While  its 
presence  demands  an  examination  of  the  heart,  it  is  very  frequently 


THE  PULSE  373 

found  to  be  quite  independent  of  detectable  cardiac  disease.  It  is 
normal  in  some  individuals,  and  when  found  in  infants  or  elderly  per- 
sons is  commonly  devoid  of  diagnostic  significance.  Constant  irregu- 
larity or  intermission  is  of  greater  pathological  importance  than  occa- 
sional periods  of  arrhythmic  action,  but  cases  have  been  reported  in 
which  such  disturbed  action  has  existed  for  50  years  without  ill 
effects.  In  general  it  may  be  accepted  as  a  fact  that  arrhythmia  is 
not  of  diagnostic  value  unless  there  is  corroborative  evidence  of  asso- 
ciated disease,  nor  is  the  variety  of  the  arrhythmia  distinctive.  Search 
should  be  made  for  one  or  more  of  the  following : 

(1)  Valvular  cardiac  disease,  especially  mitral  lesions  (^andi^, 
Fig.  107),  in  which  it  is  usually,  but  not  always,  a  sign  of  beginning 
failure  of  compensation,  passing  in  many  instances  into  delirium 
cordis ;  simple  dilatation,  chronic  myocarditis,  sclerosis  of  the  coro- 
nary arteries,  and  fatty  degeneration ;  possibly  obscure  changes  in 
the  cardiac  ganglia ;  and  overstrain  or  impaired  nutrition  in  wasting 
diseases  or  long-continued  fevers.  (2)  Poisons  circulating  in  the 
blood,  such  as  alcohol,  coffee,  tea,  tobacco,  digitalis,  aconite,  and 
belladonna,  or  the  toxines  of  the  infectious  diseases,  especially  of 
typhoid  fever  and  pneumonia.  (3)  Diseases  of  the  intracranial  con- 
tents, meningitis,  hemorrhage,  abscess,  softening,  concussion,  and, 
not  infrequently,  mental  excitement.  (4)  Neurasthenic  conditions 
resulting  from  excesses  or  overstrain.  Brief  attacks  of  moderate 
arrhythmia  are  not  uncommon  in  neurotic  individuals,  following 
even  a  slight  departure  from  their  usual  habits  in  food,  drink,  or 
exertion.  (5)  Digestive  disturbances,  acute  or  chronic,  and  jaundice 
or  constipation,  particularly  if  associated  with  an  unusually  hypo- 
chondriacal frame  of  mind.  (6)  More  rarely  arthritis  deformans, 
exophthalmic  goitre,  and  renal  disease. 

With  reference  to  the  type  of  irregularity,  the  pulsus  paradoxus^ 
if  marked,  may  indicate  large  pericardial  effusion,  indurative  medias- 
tino-pericarditis,  mediastinal  tumours,  the  presence  of  some  obstruc- 
tion to  the  entrance  of  air  into  the  lungs,  or  simply  a  weak  heart. 
The  bigeminal  and  trigeminal  pulses  occur  most  frequently  in  con- 
nection with  mitral  lesions,  or  as  effects  of  digitalis. 

Thickened  Arteries.— If  the  radial  and  other  accessible  arteries 
are  found  to  be  thickened,  rigid,  tortuous,  or  calcified,  it  indicates  a 
general  arteriosclerosis  {q.  v.),  which  may  account  for  an  observed 
cardiac  hypertrophy,  and  renders  possible  the  occurrence  of  intra- 
cranial hemorrhage  or  aneurism.  This  form  of  vascular  disease  has 
widespread  relations  to  disease  of  other  organs. 

Variations  in  Tension.— (1)  High-tension  Pulse.— An  increased 
blood  pressure  and  hard  pulse  {pulsus  durus,  B,  Fig.  108)  is  some- 
2G 


APEX    OR   SUMMIT 


UPSTROKE 
PERCUSSION 

STROKE 
ASCENDING 

OR 

ANACROTIC 

LIMB 


PREDiCROTIC    OR 
TIDAL   WAVE 


DIAGRAMMATIC 
SPHYGMOGRAM 

OF  THE 
NORMAL  PULSE 


DICROTIC    OR 
RECOIL  WAVE 


VENTRIC.  SYSTOLE 


AORTIC  CLOSURE 


AORTIC    INCOMPETENCY 

Upstroke  vertical  and   high.      Pointed 

At-Ex.       Abrupt     descent.       Dicrotic 

WAVE    almost    nil. 

PULSUS    BISFERIENS 
Tidal  vi/ave  marked  and  high.     Dicrotic 

WAVE   also    present. 

IRREGULARITY 

Pulsus    alternans.       Beats    occur    in 
pairs,  every   second   beat   small. 


IRREGULARITY 
Bigeminal  pulse.      Beats    in   groups  of 


IRREGULARITY 
Mitral  incompetency. 


IRREGULARITY 
Mitral  stenosis. 


UNDULATING    BASE    LINE 
Tuberculous  meningitis. 


374 


Fig.  107. — Sphygmogranis,  diagrammatic  and  actual. 


LOW    TENSION 

Tidal  wave  absent. 
Dicrotic  wave 
prominent. 


Fully  dicrotic 


Hyperoicrotic 


HIGH    TENSION 

Tidal  wave  prominent.      Dicrotic  wave 
INDISTINCT.     Summit  broad. 


SENILE   PULSE  (Arteriosclerosis) 
Blunt  summit.    Numerous  minor  waves. 


AORTIC  STENOSIS 

Oblique  ascent.     Blunt  summit.     Slow 
DESCENT.    Secondary  waves  indistinct. 


ANEURISM    IN   COURSE    OF   VESSEL 

Slow  ascent  and  descent.     Secondary 
waves  indistinct. 


NORMAL   TRACES 

Made  by  Dudceon's  sphyg. 


Marey's  sphyg. 


Sommerbrodt's  sphyg. 


Fig.  108. — Sphygmograms,  actual. 


375 


376  THE   EVIDENCES  OF  DISEASE 

times  hereditary.  It  is  an  important  sign  in  angina  pectoris,  and 
often  exists  with  left  ventricular  hypertrophy.  Heightened  tension 
of  long  duration,  because  of  persistent  spasm  of  the  arterioles,  is 
found  in  contracted  kidney,  gout  and  lithaemia,  diabetes  in  elderly 
and  gouty  persons,  and  lead  poisoning;  also  in  arteriosclerosis, 
owing  to  arteriolar  and  capillary  obstruction.  Contrary  to  expecta- 
tion, the  tension  is  sometimes  high  in  anaemia,  perhaps  owing  to 
irritating  waste  matters  circulating  in  the  blood.  The  pulse  is  usu- 
ally hard  in  attacks  of  apoplexy.  A  small,  hard,  wiry  pulse  is  seen 
in  the  early  stage  of  peritonitis.  In  a  high-tension  pulse  the  predi- 
crotic  or  tidal  wave  may  be  felt  {pulsus  Msferiens,  B,  Fig.  107). 

(2)  Lotv-tension  Pulse. — The  pulse  is  abnormally  soft  and  com- 
pressible (pulsus  mollis)^  perhaps  dicrotic  (J,  Fig.  108),  in  all  condi- 
tions of  exhaustion  and  debility  from  whatever  cause — e.  g.,  fevers, 
anaemia,  weak  heart,  and,  in  many  persons,  during  hot  weather.  It 
may  be  an  hereditary  peculiarity,  and  is  not  uncommon  in  the  obese. 
The  supervention  of  di erotism  early  in  the  disease  is  rather  charac- 
teristic of  typhoid  fever. 

Full  Artery. — The  term  "  full "  (pulsus  plenus)  refers  to  the  con- 
dition of  the  artery  hetioeen  beats.  If  the  total  amount  of  circulating 
blood  is  large,  as  in  conditions  of  plethora,  the  vessel  will  be  full  and 
the  pulse  hard.  In  all  high-tension  pulses  the  artery  is  full,  but  not 
necessarily  large.  A  full  but  soft  and  compressible  vessel  occurs  in 
fevers  and  other  conditions  of  vascular  relaxation,  constituting  one 
feature  of  what  the  older  writers  called  a  "  gaseous  pulse." 

Empty  Artery. — The  vessel  is  empty  or  collapsed  (pulsus  vacuus) 
bettveeu  beats  in  aortic  incompetence,  that  portion  of  the  vis  a  tergo 
derived  from  the  elasticity  of  the  aorta  being  nullified  by  the  lack  of 
support  from  the  aortic  valve.  The  pulse  is  comparatively  empty  in 
malnutrition  and  wasting  diseases,  and  to  a  noticeable  extent  in 
mitral  stenosis,  in  consequence  of  the  small  quantity  of  blood  dis- 
charged from  the  left  ventricle.  An  extreme  grade  of  emptiness  as 
well  as  a  great  diminution  in  the  amplitude  of  the  pulse  wave  is  seen 
in  the  "  thready  "  or  "  running  "  pulse,  indicative  of  great  cardiac 
weakness  and  impending  death. 

Large  Pulse. — This  refers  to  a  pulse  wave  of  much  amplitude  or 
volume  (pulsus  magnus),  an  unusually  great  expansion  of  the  artery 
during  the  beat,  usually  with  low  tension.  It  is  found  in  fevers 
(bounding  pulse),  relaxation  of  the  arterioles,  aortic  incompetency, 
and  occasionally  in  left  ventricular  hypertrophy. 

Small  Pulse. — A  small  excursion  of  the  artery  during  the  beat 
(pulsus  parvus)  is  found  in  aortic  stenosis  and  mitral  lesions,  espe- 
cially mitral  narrowing,  the  quantity  of  blood  delivered  into  the  aorta 


THE  PULSE  377 

being  limited ;  in  aneurism,  if  the  dilatation  affects  the  artery  be- 
tween the  heart  and  the  palpating  finger,  thus  acting  as  a  reservoir 
to  extinguish  the  pulse  wave ;  in  cardiac  weakness  and  in  wasting 
diseases.  A  moderately  small  pulse  wave  is  not  infrequently  con- 
joined with  high  tension. 

Slow  or  Tardy  Pulse. — The  adjective  refers  to  the  character  of 
the  pulse  wave — slow  rise  and  slow  descent  {pulsus  tardus) — not  to 
the  frequency  of  the  beats.  This  form  of  pulse  wave,  also  called  a 
long  pulse,  belongs  as  a  rule  to  pulses  of  high  tension  {B,  Fig.  108), 
and  is  seen  in  contracted  kidney,  angina  pectoris,  arteriosclerosis, 
and  old  age.  A  slow  pulse  may  be  indicative  of  aortic  stenosis  (/>, 
Fig.  108),  the  blood  passing  tardily  through  the  contracted  orifice. 
If  the  ascent  of  the  pulse  wave  is  as  gradual  as  the  descent  it  is  sig- 
nificant of  an  intervening  aneurism  {E,  Fig.  108). 

Quick  Pulse. — A  pulse  wave  wdth  a  rapid  ascent  and  an  immedi- 
ate quick  falling  off  of  pressure  (pulsus  celer)  belongs  in  almost  all 
cases  to  a  pulse  of  low  tension  {A,  Fig.  108).  A  "  quick  "  pulse  must 
not  be  confused  with  a  rapid  or  frequent  pulse.  It  is  found  when 
the  arterioles  are  relaxed  as  in  fevers  and  anaemia.  Aortic  regurgi- 
tation exhibits  this  form  of  pulse  in  perfection  (Corrigan's,  shot 
pulse  or  water-hammer  pulse.  A,  Fig.  107).  One  can  not  from  the 
presence  of  this  pulse  infer  without  reserve  the  existence  of  aortic 
incompetence,  as  it  occurs  very  typically  at  times  in  anaemia  and 
other  conditions,  such  as  those  which  cause  the  subungual  or  capil- 
lary pulse  (page  371). 

Unilateral  and  Other  Abnormalities  of  the  Pulse.— Delay,  weak- 
ness, abnormal  character  or  obliteration  of  the  pulse  in  correspond- 
ing arteries  of  the  two  sides  of  the  body ;  or,  in  rare  cases,  unusual 
weakness,  extinction  or  obliteration  of  the  pulse  on  both  sides  in  par- 
ticular vessels  may  be  caused  in  general  (excluding  anatomical  varia- 
tions) by  aneurism,  embolism,  thrombosis,  pressure  from  tumours  or 
wounds  involving  the  vessels.     Particular  instances  are  : 

(1)  A  weak  or  extinct  pulse  in  the  right  radial,  indicative  of 
an  aneurism  of  the  ascending  aorta  or  innominate  artery ;  in  the  left 
radial,  of  the  descending  aorta,  and  if  delayed,  of  an  aneurism  of  the 
arch  between  the  origins  of  the  innominate  and  left  carotid  arteries ; 
in  either  radial  of  the  presence  on  the  same  side  of  pneumothorax  or 
large  pleural  effusion,  embolism,  thrombosis,  tumours  of  the  neck  or 
axilla  creating  pressure  upon  the  vessel  and,  very  rarely,  of  aneurism 
of  the  subclavian,  axillary,  or  brachial  arteries. 

(2)  Weakening  or  extinction  of  the  pulse  in  one  femoral  or  one  pos- 
terior tibial  artery  may  be  due  to  embolism,  thrombosis  or  tumour ; 
in  the  same  vessels  on  both  sides  to  similar  causes,  as  well  as  to  an 


378  THE  E\aDENCES  OP  DISEASE 

abdominal  aneurism,  or  the  excessively  rare  congenital  obliteration 
of  the  aorta. 

Pulses  Possessing  Special  Diagnostic  Value. — (1)  Mitral  Stenosis. 
— Pulse  wave  small,  its  rise  and  descent  rather  slow,  the  artery  not 
well  filled,  the  successive  beats  irregular  in  time  and  strength  {F^  Fig. 
107). 

(2)  Aortic  Stenosis. — The  pulse  is  small,  its  rise  and  fall  gradual, 
the  tidal  wave  marked  and  not  infrequently  higher  than  the  initial 
wave.  The  successive  beats  are  equal,  regular,  and  not  unduly  fre- 
quent (A  Fig.  108). 

(3)  Aortic  Incompetency. — The  pulse  wave  is  ample,  quick  (sud- 
den rise,  immediate  sudden  fall),  successive  beats  generally  regular  and 
equal,  frequency  variable  {A^  Fig.  107). 

(4)  Arteriosclerosis  and  Atheroma  of  Aorta. — A  pulse  wave  of 
good  amplitude,  of  somewhat  slow  ascent,  of  considerable  duration 
(the  artery  remaining  dilated  for  a  noticeably  long  period),  of  slow 
descent — resembling,  indeed,  the  pulse  of  aortic  stenosis,  except  that 
the  latter  is  smaller  (compare  C  and  Z>,  Fig.  108) — suggests  very 
strongly  the  existence  of  atheromatous  changes,  especially  in  the 
aorta.  The  characters  of  this  pulse  are  due  to  the  loss  of  aortic  and 
general  arterial  elasticity  which  results  from  the  degenerative  process. 
It  is  often  called  the  "  senile  pulse.'" 

(5)  Aneurism. — A  discrepancy  between  the  pulse  waves  in  sym- 
metrical arteries,  either  in  time  or  character,  is  more  significant  of 
aneurism  than  the  character  of  the  wave  in  a  single  artery.  Yet  if 
an  aneurism  lies  in  the  course  of  an  artery  the  pulse  wave  exhibits  an 
ascent  and  descent  which  depart  from  the  normal  in  being  of  nearly 
equal  duration  (E.,  Fig.  108). 

(6)  Myocarditis. — A  pulse  wave  which  is  unusually  soft  and  small, 
conjoined  with  intermittency  or  irregularity  in  force  and  strength,  and 
without  other  symptoms  of  cardiac  disease,  should  lead  one  to  suspect 
myocarditis  if  the  causative  conditions  of  the  latter  are  present. 

The  Sphygmograph. — The  sphygmograph  is  useful  in  making 
a  permanent  record  of  the  pulse  for  future  comparison  ;  in  showing 
graphically  some,  but  not  all,  of  the  elements  of  the  pulse  ;  in  teach- 
ing precision  in  the  pulse  examination ;  in  analyzing  some  of  the 
finer  details  which  may  have  been  too  delicate  or  insignificant  for 
palpation  (small  waves  or  oscillations) ;  and  in  corroborating  a  diag- 
nosis previously  made  by  palpation.  Although  there  are  some  points 
which  are  not  shown  at  all,  or  not  as  well,  by  the  sphygmograph  as 
by  palpation  (fulness  and  size  of  artery,  thickness  of  walls),  it  is 
esteemed  by  those  who  understand  how  to  use  and  interpret  it  as  a 
valuable  supplement  to  the  educated  finger. 


THE  SPHYGMOGRAPH 


379 


Technic  of  the  Sphygmograph. — The  instruments  of  Marey, 
Mahomed,  and  Sommerbrodt  are  in  use,  but  the  most  convenient  as 
well  as  reliable  form  for  clinical  use  is  that  of  Dudgeon  (Fig.  109). 

There  is  no  clinical  instrument  the  value  of  which  depends  so 
largely  upon  the  person  who  is  using  it.  Two  tracings,  taken  one 
after  the  other  from  the  same  artery  by  different  observers,  may  differ 
considerably  in  form  ;  but  each  examiner,  if  well  practised,  will  reach 
substantially  similar  conclusions.     The  technic  is  as  follows  : 

The  slips  of  paper  upon  which  the  tracing  is  to  be  made  should  be  pro- 
cured from  the  instrument  maker,  as  they  require  to  be  of  special  texture  and 
accurate  cut.  Otherwise  the  needle  does  not  play  freely  over  the  surface  or 
the  slip  binds  on  the  rollers.  To  smoke  the  slip,  place  it  in  a  holder,  a  strip  of 
tin  with  the  ends  turned  over  half  an  inch,  by  which  the  extremities  of  the  slip 
are  held  and  covered.  In  a  room 
free  from  draughts,  place  a  piece 
of  gum  camphor  on  some  suit- 
able metal  or  porcelain  surface. 
Ignite  the  camphor,  using,  if  re- 
quired, a  drop  or  two  of  alcohol 
to  facilitate  the  lighting.  Move 
the  strip  in  the  holder  to  and  fro 
over  the  ascending  column  of 
smoke,  taking  care  not  to  scorch 
the  paper,  and  endeavouring  to 
get  an  even  deposit  of  carbon 
over  its  surface.  The  makers 
furnish  a  box  in  which  half  a 
dozen  smoked  slips  can  be  car- 
ried for  outside  use. 

After  the  tracing  is  made, 
write  upon  the  smoked  surface 
with  a  pin  point  or  a  pen  with 
one  half  of  the  nib  broken  off, 

or  with  ink  upon  the  unsmoked  ends,  name,  date,  vessel  from  which  made, 
pulse,  respiration,  temperature,  and  disease.  Pour  into  a  footed  cylindrical 
jar,  6  or  7  inches  long  and  IJ  inch  in  diameter,  or  into  a  saucer,  a  quick-dry- 
ing varnish— viz.,  photographer's  negative  varnish,  or  gum  benzoin  1  ounce, 
alcohol  6  ounces,  or  gum  damar  1  ounce,  rectified  benzol  ine  6  ounces.  The 
tracing  may  be  dipped  slowly  into  the  jar,  or  slidden,  smoked  side  uppermost, 
through  the  solution  in  the  saucer,  and  allowed  to  dry.  A  second  coat  may 
be  applied  if  the  tracing  is  to  be  much  handled. 

To  Use  the  Instrument— (I)  Find  the  exact  spot  where  the  radial  beat  is 
felt  most  distinctly,  and  mark  it  accurately  (ink  or  aniline  pencil).  (2)  Wind 
the  clockwork  and  insert  the  smoked  paper.  (3)  Let  the  patient  take  an  easy 
position  and  hold  out  the  hand  toward  you.  palm  upward  and  slightly  dorsi- 
flexed,  fingers  quiet.     If  the  band  is  to  he  used:  (4)  Having  passed  the  free  end 


Fig.  109,— Dudgeon's  sphygmograph. 


380  THE  EVIDENCES  OF   DISEASE 

of  the  band  through  the  clamp,  slip  it  over  the  patient's  hand  and  tighten  it 
moderately.  (5)  Place  the  metal  pad  over  the  artery,  clock  case  nearest  elbow, 
and  steady  it  with  one  hand  while  the  other  still  further  tightens  the  band 
until  the  needle  plays  freely  at  or  about  the  central  line  of  the  paper  strip,  not 
running  off  either  edge.  If  the  band  is  not  employed,  support  the  patient's  hand 
and  wrist  on  the  arm  of  a  chair,  edge  of  bed  or  observer's  knee,  and  hold  the 
instrument  with  one  hand.  This  can  be  readily  done  after  a  little  practice, 
or  the  band  may  be  passed  around  the  wrist  and  held  from  underneath 
without  clamping.  (6)  Turn  the  milled  head  which  regulates  the  pressure  of 
the  spring  until  the  needle  attains  its  greatest  amplitude  of  movement.  The 
pressure  is  graduated  in  ounces,  but  the  nominal  reading  is  never  reliable. 
(7)  Push  over  the  projecting  lever  which  starts  the  clockwork,  and  either  stop 
it  just  before  the  slip  runs  out  or  catch  the  latter  in  the  free  hand. 

It  is  often  desirable  to  take  two  tracings  at  varying  pressures,  or,  better 
yet,  to  stop  the  clockwork  after  half  the  slip  has  been  written  upon  and  in- 
crease the  pressure  to  the  maximum,  thus  exhibiting  the  effect  of  medium  and 
heavy  pressures  upon  the  same  slip.  A  useful  wrinkle  (Daxa)  is  to  stick  2 
or  3  thicknesses  of  adhesive  plaster  upon  the  metal  pad  which  is  applied  to  the 
artery.  The  prolongation  of  this  artificial  finger  makes  it  mechanically  easier 
to  set  the  needle  in  motion. 

Interpretation  of  the  Tracing. — If  it  is  clearly  understood  that  an 
upstroke  in  the  tracing  corresponds  to  a  rise  of  pressure  in  the  ves- 
sel, and  a  downstroTce  to  a/a?Z  of  pressure,  the  interpretation  of  the 
tracing  is  relatively  easy.  After  what  has  been  said  concerning  the 
palpation  of  the  pulse,  a  study  of  the  sphygmograms  (Figs.  107,  108) 
in  connection  with  the  descriptions  about  to  be  given  will  be  suffi- 
cient without  detailed  reference. 

(1)  The  Normal  Tracing  and  its  Elements. — A  tracing  from  a 
normal  pulse  (diagram.  Fig.  107)  shows  an  almost  vertical  upstroke 
(percussion  stroke,  ascending  or  anacrotic  limb)  and  a  sloping  down- 
stroke  (descending  or  katacrotic  limb),  the  latter  interrupted  by  two 
principal  secondary  elevations,  the  first  of  which  is  the  tidal  or  pre- 
dicrotic  wave,  the  second  the  recoil  or  dicrotic  wave.  Subsequent 
to  the  dicrotic  wave  there  may  be  some  minor  elevations. 

The  percussion  stroke  or  ascending  limb  is  due  to  the  sudden  in- 
crease of  pressure  caused  by  the  transmission  of  the  force  expended 
by  the  left  ventricle  in  driving  its  contents  into  the  aorta,  along  the 
practically  incompressible  blood  columns  in  the  arteries.  The  walls 
of  the  suddenly  distended  artery  then  reactively  contract  and  again 
expand  by  virtue  of  their  elasticity,  thus  giving  rise  to  the  pretidal 
notch  and  tidal  wave,  after  which  the  pressure  again  falls  until  the 
moment  of  closure  of  the  aortic  valve.  The  blood  column,  which  has 
fallen  back  against  the  aortic  valve,  is  suddenly  checked,  and  the 
resultant  recoil  produces  an  increase  of  pressure  which  forms  the 


THE  SPHYGMOGRAPH  381 

dicrotic  wave  in  the  tracing.  Subsequent  small  elevations  are,  like 
the  tidal  wave,  due  to  elastic  oscillations  of  the  arterial  walls.  It  is 
proper  to  state  here  that  according  to  some  authorities  the  tidal 
wave  is  caused  by  the  blood  stream  coursing  through  the  artery,  but 
in  view  of  the  fact  that  the  tidal  wave  is  large  if  the  tension  of  the 
arterial  wall  is  great — i.  e.,  the  more  immediate  its  power  of  elastic 
recovery — the  foregoing  explanation  is  probably  correct. 

The  characters  of  a  normal  pulse  tracing  may  be  summarized  as 
follows :  (1)  Upstroke,  straight,  nearly  vertical,  of  moderate  ampli- 
tude ;  (2)  apex,  moderately  acute ;  (3)  descent,  gradual ;  (4)  tidal 
tvave,  small ;  (5)  dicrotic  wave,  well  marked. 

(2)  Diagnostic  Indications  from  the  Sphygmograph. — Inspect  the 
tracing  systematically  with  reference  to  the  following  points : 

Is  the  upstroke  long  or  short,  vertical  or  sloping  ? 

Is  the  apex  pointed  or  broad  and  blunt  ? 

Is  the  tidal  wave  marked,  faint,  or  absent  ? 

Is  the  dicrotic  wave  marked,  faint,  or  absent  ? 

Are  the  successive  beats  regular,  irregular,  or  intermittent  ? 

Is  the  line  of  descent  regular  or  irregular  ? 

Is  the  base  line  (the  line  connecting  the  bases  of  the  successive 
beats)  straight  or  irregular? 

As  a  whole,  of  what  is  the  trace  characteristic  or  indicative  ? 

The  significance  of  the  variations  in  the  individual  elements  of 
the  tracing  are : 

1.  Long  Upstroke. — Corresponds  to  large  volume,  and  indicates  a 
quick  systole  or  the  relaxed  arterioles,  and  free  capillary  circulation 
of  low  tension  or  aortic  regurgitation. 

2.  Short  Upstroke.— Corresponds  to  small  volume  and  indicates 
mitral  regurgitation,  aortic  stenosis,  aneurism,  or  obstructed  periph- 
eral circulation  (high  tension). 

3.  Vertical  Upstroke.— Corresponds  to  a  quick  systole  of  either  a 
weak  or  strong  heart,  or  a  large  amount  of  blood  discharged  at  each 
systole,  and  is  often  associated  with  a  long  upstroke  in  low-tension 
pulse  and  aortic  incompetency. 

4.  Oblique  or  Sloping  Upstroke.— May  be  due  to  a  considerable 
layer  of  fat  over  the  artery  or  slow  filling,  as  in  aortic  stenosis  or 
mitral  incompetency,  or  aneurism  in  the  course  of  the  vessel,  or  arte- 
riosclerosis or  high  tension ;  or,  if  these  causes  are  absent,  a  weak  left 
ventricle. 

5.  Pointed  Apex.— Indicates  an  unobstructed  peripheral  circular 
tion  (low  tension)  or  aortic  incompetency. 

6.  Blunt  or  Broad  Apex.— Indicates  strong  heart  and  obstructed 
peripheral  circulation  (high  tension),  or  aortic  stenosis,  or  arterio- 


382  THE   EVIDENCES   OF   DISEASE 

sclerosis,  or  aneurism  in  the  course  of  the  vessel,  or,  last  but  not  least, 
too  great  pressure  by  the  spring  of  the  sphygmograph. 

7.  Marked  Tidal  "Wave.  —  Indicates  strong  and  obstructed  pe- 
ripheral circulation  (high  tension),  or  aortic  stenosis,  or  arterio- 
sclerosis. 

8.  Small  or  Absent  Tidal  Wave. — Indicates  a  weak  heart,  or  a 
strong  heart  with  free  peripheral  circulation  (moderate  or  low  ten- 
sion), or  mitral  or  aortic  incompetency. 

9.  Marked  Dicrotic  Wave. — Indicates  a  weak  or  moderabely  strong 
heart  with  free  peripheral  circulation  (low  tension),  in  some  cases 
high  tension  with  a  failing  heart. 

10.  Small  or  Absent  Dicrotic  Wave.  —  Indicates  obstructed  pe- 
ripheral circulation  with  a  strong  heart  (high  tension),  arteriosclero- 
sis, aortic  stenosis,  aneurism,  or  (because  of  the  failure  of  the  recoil) 
aortic  incompetency. 

11.  Irregularity  of  the  Line  of  Descent. — Is  seen  in  mitral  steno- 
sis and  regurgitation. 

12.  Irregularity  of  the  Base  Line. — Undulations  of  the  base  line 
corresponding  to  the  respiratory  acts  occur  in  conditions  attended 
with  dyspnoea  or  irregular  breathing  from  involvement  of  the  nerve 
centres  (6^,  Fig.  107). 

13.  Irregular  or  intermittent  beats  are  graphically  illustrated  in 
the  sphygmographic  tracing,  but  require  no  further  notice  than  has 
been  given. 


SECTION    XXXII 
EXAMINATION   OF   THE  LUXGS  AXD   PLEURA 

The  lungs  are  to  be  examined  by  inspection,  palpation  (including 
mensuration  and  sometimes  spirometry),  percussion,  and  ausculta- 
tion. 

I.    TOPOGRAPHICAL   ANATOMY 

Certain  facts  regarding  the  relation  of  the  boundaries  and  lobes 
of  the  lungs  and  the  pleural  sacs  to  the  external  surface  of  the  thorax 
must  be  clearly  in  mind  preceding  an  examination  of  these  organs. 

Right  Lung. — The  apex  (see  Plates  I,  II  )  rises  from  1  to  If  inch 
above  the  level  of  the  clavicle.  From  here  the  anterior  border  runs 
downward,  forward,  and  inward,  passing  nearly  behind  the  right 
costo-sternal  articulation  to  the  midsternal  line  at  the  level  of  the  2d 
rib.     From  this  point  it  runs  vertically  downward  to  the  level  of  the 


TOPOGRAPHY  OF  LUNGS  AND  PLEURA 


383 


6th  chondro-stemal  articulation,  where  it  turns  sharply  to  the  right 
and  becomes  the  lower  border.  The  loiver  border  follows  the  6th  rib 
to  the  right  mammillary  line,  cuts  the  8th  rib  in  the  midaxillary 
line,  the  10th  rib  at  the  scapular  line,  and  the  upper  border  of  the 
11th  rib  close  to  the  spinal  column.  For  brevity,  remember,  front, 
6th ;  side,  8th ;  back,  10th  rib.  In  old  people  the  lower  borders  of 
the  lungs  extend  1  rib  farther  down,  in  children  they  lie  1  rib  higher 
than  those  just  given. 

The  right  lung  has  3  lobes  (Fig.  110).  Posteriorly  the  upper 
and  lower  lobes  are  separated  by  a  fissure  which  starts  at  the  spinal 
column,  on  a  level  with  the  spine  of  the  scapula,  and  runs  outward, 
downward,  and  forward  to 
the  4th  rib  in  the  axillary 
line,  where  it  divides  into  'I 
secondary  fissures.  The  uj)- 
permost  of  these  runs  almost 
horizontally  forward,  and 
reaches  the  anterior  border 
of  the  lung  at  about  the  level 
of  the  4th  cartilage.  The 
lower  fissure  passes  downward 
and  somewhat  forward  to  the 
lower  border  of  the  lung  in 
the  mammillary  line.  These 
two  fissures  bound  the  mid- 
dle lobe. 

Left  Lung. — The  apex  of 
the  left  lung  and  its  anterior 
border^  as  far  down  as  the  4th 
rib,  correspond  to  those  of 
the  right  lung,  except  that 
this  border  lies  farther  from  the  midstemal  line.  At  the  level  of 
the  4th  rib  the  anterior  border  curves  outward,  downward,  and  then 
moderately  inward  to  the  6th  rib,  exposing  a  somewhat  semicircular 
area  of  the  pericardium  (superficial  or  exposed  cardiac  dulness). 
From  this  point  on  the  6th  rib  the  lower  border  runs  outward  and 
around  to  the  spinal  column,  its  course  corresponding  in  all  respects 
to  that  of  the  lower  border  of  the  right  lung,  save  that  it  lies  a  trifle 
lower. 

The  left  lung  has  two  lobes  (Fig.  122),  upper  and  lower,  sepa- 
rated by  a  fissure,  which  begins  and  runs  as  in  the  right  lung,  but, 
instead  of  bifurcating,  passes  downward  and  forward  to  end  at  the 
%t\\  rib  in  the  left  mammillary  line. 


PLCUR 


Fui.  111'.— SiKiwin:.'  tlie  lobes  of  the  lung  (and 
the  lower  lintit  of  the  pleura)  on  the  right  side 
of  the  chest. 


384 


THE  EVIDENCES  OF   DISEASE 


It  will  be  seen  from  this  description  that  we  have 
Posteriorly,  on  both  sides  (Fig.  Ill),  from  above  downward,  up- 
per lobe  as  far  as  the  spine  of  the  scapula ;  below  this,  lower  lobe. 

In  fronts  on  the 
right  side,  upper  lobe 
as  far  down  as  the  4th 
rib;  from  the  4th  to 
the  6th,  middle  lobe  ; 
on  the  left  side,  upper 
lobe  alone. 

Laterally  oti  the 
right,  in  the  midaxil- 
lary  line,  upper,  be- 
ginning of  middle, 
and  the  lower  lobe. 

Laterally  on  the 
left,  in  the  midaxil- 
lary  line,  upper  and 
lower  lobes. 

PleursB.  —The 
pleural  sacs  extend 
below  the  lower  bor- 
der of  the  lungs  to  a 
very  considerable  ex- 
tent.   In  the  mammil- 


FlG.    111.- 


-Showing  the  lobes  of  the  lung  and  the  lower 
limit  of  the  pleura  posteriorly. 


lary  line  they  lie  2  inches,  in  the  midaxillary  line  d}  inches,  in  the 
scapular  line  1|  inch  lower  than  the  edges  of  the  lungs  (Fig.  111). 
The  anterior  edge  of  the  left  pleural  sac  below  the  4th  rib  lies  nearer 
the  midsternal  line  than  the  corresponding  part  of  the  anterior  bor- 
der of  the  left  lung.  The  surfaces  of  the  reflected  pleura  forming 
this  complementary  pleural  space  or  sinus  are  in  contact  except  when 
separated  by  fluid  in  the  pleural  cavities,  or  thrust  apart  by  the 
edges  of  the  lungs  as  the  latter  advance  and  retreat  during  inspira- 
tion and  expiration. 

II.    THE  PHYSIOLOGY  OF  THE  LUNGS 

Space  forbids  more  than  a  brief  reference  to  the  physiology  of  the 
respiratory  apparatus. 

Nervous  Mechanism  of  the  Respiratory  Movements.— The  nervous 
mechanism  required  to  initiate  and  regulate  the  co-ordinated  action 
of  the  numerous  muscles  which  execute  the  respiratory  movements 
consists  of  a  respiratory  centre,  with  afferent  and  efferent  nerves. 
(Fig.  112). 


PHYSIOLOGY  OP  THE  LUNGS 


385 


(1)  The  respiratory  centre  lies  in  the  lower  part  of  the  medulla 
(Reichert).  This  centre  is  divided  into  2  halves  so  closely  connected 
that  they  form  functionally  a  single  centre.  The  right  half  is  con- 
nected with  the  right  lung  and  the  respiratory  muscles  of  the  right 
side,  and  vice  versa.  Each  half  is  physiologically  again  subdivided 
into  2  portions :  an  inspiratory  or  accelerator  centre,  connected  with 
the  muscles  of  inspiration,  and  an  expiratory  or  inhibitory  centre, 
controlling  the  expiratory  muscles  in  forced  expiration. 

The  power  of  rhythmic  action  is  inherent  in  the  nerve  cells  of 
the  centre,  but  it  requires  a  continuous  excitation,  which  is  supplied 
by  the  oxygen  and  carbon  dioxide  in  the  circulating  blood  and  the 
stimulus  received  from  the  lungs  by  way  of  the  pneumogastrics. 

("2)  The  main  afferent  or  seiisory  nerves  are  the  pneumogastric, 
glosso-pharyngeal,  trigeminal,  and  cutaneous. 


Respiratory  Centre 

in 

Medulla 


Expiratory  or 

Inhibiting  Portion 

of  Centre 


Inspiratory  or 

Accelerating  Portion 

of  Centra 


MOTOR 


Glottis 


Diaphragm 


Other  Muscles 


SENSORY 


Pharynx 


Larynx 

Superior  Laiyngeal 

Nerves 


Cutaneous  Nerves 


Lungs 

Pneumogastric 

Nerves 


Fig.  112.— Diagram  of  the  respiratory  centre. 

The  pneumogastric  nerve  contains  fibres  some  of  which  convey 
impulses  to  the  inspiratory,  others  to  the  expiratory  centre.  These 
impulses  are  derived  from  the  movements  of  the  lungs,  lung  expan- 
sion giving  rise  to  expiratory,  lung  collapse  to  inspiratory,  impulses. 


386  THE  EVIDENCES  OF   DISEASE 

one  alternating  with  the  other.  The  superior  laryngeal  and  glosso- 
pharyngeal act  upon  the  inhibitory  centre — e.  g.,  arrest  of  respira- 
tion from  foreign  body  in  larynx,  or  during  the  act  of  swallowing. 
The  trigeminal  nerves  usually  arrest,  less  frequently  increase  the 
rapidity  of,  the  respiratory  movements — e.  g.,  inhalation  of  irritating 
gases ;  and  the  cutaneous  nerves  cause  primarily  accelerated  and  deep 
breathing — e.  g.,  a  dash  of  hot  or  cold  water  on  the  skin.  Other 
(psychic)  impulses  arise  from  the  centres  of  the  brain. 

(3)  The  efferent  or  motor  nerves  are :  the  inferior  or  recurrent 
laryngeal  branch  of  the  pneumogastric,  which  widens  the  glottis  dur- 
ing inspiration ;  the  very  important  phrenic  nerve,  innervating  the 
diaphragm ;  and  the  various  spinal  nerves  which  control  the  other 
respiratory  muscles. 

The  muscles  which  act  in  quiet  inspiration  are  the  diaphragm, 
quadrati  lumborum,  serrati  postici  inferiores,  scaleni,  external  inter- 
costals,  and  the  levatores  costarum.  In.  forced  inspiration  additional 
muscles  are  called  into  play — viz.,  the  sterno-cleido-mastoids,  infra- 
hyoids, greater  and  lesser  pectorals,  trapezii,  rhomboids  and  erectores 
spinae. 

In  quiet  expiration  there  is  no  muscular  action.  In  forced  expira- 
tion the  abdominal  muscles  and  the  internal  intercostals  are  at  work. 

III.  INSPECTION  AND  PALPATION  WITH  REFERENCE 
TO  THE  LUNGS 

By  sight  or  touch  (usually  conjoined)  the  rate,  rhythm,  amount 
and  manner  of  expansion,  and  general  character  of  the  breathing  are 
studied,  together  with  vocal,  rhoncal,  and  friction  fremitus.  Else- 
where {q.  V.)  have  been  considered  the  shape,  pulsations,  tenderness, 
anatomical  landmarks,  topographical  areas,  and  mensuration  of  the 
thorax. 

Frequency  of  the  Respiration. — The  respiration  rate  in  the 
newborn  is  44;  at  5  years,  26 ;  in  the  adult,  16  to  20.  In  health  it  is 
faster  standing  than  lying,  during  the  day  than  at  night,  after  meals 
than  when  fasting,  in  spring  than  at  the  end  of  summer,  and  during 
exercise  and  mental  excitement  than  when  at  rest.  The  normal 
pulse-respiration  ratio  is  1 :  4 ;  i.  e.,  1  respiration  to  4  pulse  beats.  In 
disease  the  ratio  may  vary  from  1 : 1  to  1  :  8. 

To  count  the  respirations,  one  may  watch  the  rise  and  fall  of  the 
chest  or,  better,  the  upper  abdomen ;  lay  the  hand  lightly  on  the 
lower  thorax;  or  perbaps  hear  the  breathing.  In  many  individuals 
the  consciousness  of  being  watched  will  cause  involuntary  alterations 
in  the  frequency  and  rhythm  of  the  respiration,  and  it  is  best,  if 
practicable,  to  rate  the  breathing  while  ostensibly  counting  the  pulse 


FREQUENCY  AND  TYPE  OP  RESPIRATION  387 

or  taking  the  temperature.  The  effects  of  exertion  or  mental  activity 
should  be  allowed  to  pass  off.  In  children,  when  possible,  the  breath- 
ing should  be  taken  while  asleep. 

In  disease  the  respiration  rate  may  be  increased  or  diminished. 

(1)  Rapid  Respiration. — Increased  frequency  of  breathing  may 
exist  Avithout  the  presence  of  dyspnoea  (difficult  or  laborious  breath- 
ing), although  the  two  are  frequently  associated.  Dyspnoea  (g.  v.) 
is  considered  separately. 

Muscular  exertion  causes  rapid  breathing  because  of  the  influence 
upon  the  respiratory  centre  of  certain  substances  which  enter  the 
blood  from  the  muscles  as  the  result  of  metabolic  changes.  Mental 
excitement  is  at  times  a  potent  factor  in  the  same  direction.  The 
respiration  is  accelerated  in  fever,  especially  in  children,  by  the  influ- 
ence of  the  heated  blood  upon  the  medulla.  The  breathing  may  be 
much  more  rapid  in  lobar  pneumonia  than  is  warranted  by  the  extent 
of  the  local  lesions,  suggesting  a  special  action  of  the  pneumotoxine 
upon  the  respiratory  centre. 

Hysteria  is  occasionally  responsible  for  an  extremely  high  respira- 
tion rate.  In  one  case,  that  of  a  young  girl  under  my  care,  the 
breathing  varied  from  90  to  100  per  minute  for  several  hours,  and 
the  only  subjective  complaint  was  of  fatigue  due  to  the  continued 
rapid  muscular  action. 

From  a  diagnostic  point  of  view  an  increased  respiration  rate  is 
suggestive  primarily  of  pulmonary  disease,  secondarily  of  the  condi- 
tions already  mentioned  as  well  as  those  to  be  considered  under  the 
head  of  dyspnoea. 

(2)  Slow  Respiration.— The  breathing  is  slowed  in  many  of  the 
varieties  of  coma,  also  in  collapse,  and  by  poisoning  with  aconite, 
antimony,  chloral,  chloroform,  and  opium. 

Type  of  the  Respiration. — Upon  observation  it  may  be  found 
that  the  movement  of  the  upper  thorax  during  respiration  pre- 
dominates over  that  of  the  lower  thorax  and  abdomen  or  vice 
versa. 

(1)  Thoracic  Type  Predominating.— Costal  or  thoracic  respiration 
is  normal  in  women  at  and  after  the  age  of  puberty,  largely  because 
of  heredity  and  modes  of  dress.  Costal  breathing  in  a  man  or  its 
presence  to  excess  in  a  woman  is  indicative  either  of  dyspnoea,  real  or 
subjective  {q.  r.),  or  of  some  condition  limiting  the  mobility  of  the 
diaphragm,  abdominal  respiration  depending  upon  the  full  and  free 
action  of  the  latter.  Tlie  action  of  tlie  diaphragm  is  recognised  by 
its  causing  protrusion  of  the  epigastric  region  during  inspiration. 
If  this  protrusion  is  absent,  or  if  the  epigastrium  and  upper  abdom- 
inal walls  suddenly  recede  or  are  sucked  in  during  inspiration,  it  is 


388  THE  EVIDENCES  OF  DISEASE 

godd  evidence,  in  the  absence  of  any  form  of  stenosis  of  the  upper 
air  passages,  that  the  diaphragm  is  not  working. 

Excessive  upper  costal  or  diminished  abdominal  breathing  may 
be  caused  by  pressure  upon  the  diaphragm,  by  ascites,  meteorism,  or 
abdominal  tumours  or  enlargements.  A  very  large  pericardial  effu- 
sion by  its  weight  may  act  similarly.  Inflammation  of  the  diaphrag- 
matic pleura  or  peritoneum  is  a  cause  of  increased  thoracic  breath- 
ing. Paralysis  of  the  diaphragm  affords  a  typical  example  of  absent 
abdominal  and  excessive  thoracic  respiration.  In  some  cases  it  is 
possible  by  careful  palpation  to  determine  that  the  paralysis  is  uni- 
lateral, one  side  still  acting.  In  emphysema,  although  the  actual 
expansion  of  the  chest  is  much  less  than  normal,  there  is  an  exag- 
gerated up-and-down  (vertical)  movement  of  the  thorax.  Finally,  the 
marked  superior  costal  breathing  of  the  hysterical  patient  is  familiar. 

(2)  Abdominal  Type  Predominating. — Abdominal  breathing  nor- 
mally predominates  in  children  of  both  sexes  and  the  adult  male.  If 
this  type  of  respiration  is  exaggerated  in  a  man,  or  if  it  is  present 
together  with  diminished  or  absent  thoracic  breathing  in  a  woman, 
it  is  an  abnormal  condition. 

The  causes  of  excessive  respiratory  action  of  the  abdomen — i.  e., 
of  the  diaphragm — are  found  in  conditions  which  render  movement 
of  the  thorax  painful,  such  as  pleurisy,  pleurodynia,  or  fracture  of  a 
rib,  or  which  mechanically  hinder  thoracic  expansion,  as  in  double 
pleural  effusion,  calcification  of  the  costal  cartilages,  emphysema  (per- 
manent inspiratory  form  of  the  thorax  throwing  extra  work  upon  the 
diaphragm),  the  rare  scleroderma  of  the  chest  wall,  and  ossifying 
myositis.  Inaction  of  the  thorax  may  also  be  due  to  paralysis  of  the 
muscles  of  inspiration,  as  in  injury  or  disease  of  the  cervical  portion 
of  the  cord  or  bulbar  paralysis,  or  spasm  of  the  same  muscles  in 
strychnine  poisoning  or  tetanus. 

Degree  of  Respiratory  Expansion. — The  amount  of  the 
respiratory  movement  of  the  thorax  should  be  investigated  by  inspec- 
tion, palpation,  and  mensuration.  The  chest  should  be  inspected  in 
a  good  light  from  the  front,  side,  back,  and,  last  but  not  least,  from 
above,  watching  carefully  for  defective  or  excessive  motion,  either 
general  or  local.  The  warmed  hands  should  be  laid  flat,  first  upon 
the  front  of  the  chest,  then  one  upon  each  side,  in  order  to  con- 
firm or  modify  the  results  of  inspection. 

Mensuration  {q.  v.)  should  be  employed  to  determine  with  accu- 
racy the  amount  of  expansion.  If  the  expansion  is  less  than  2  inches 
in  men  and  2\  inches  in  women,  it  is  below  the  normal  average. 

In  this  connection  the  spirometer,  if  at  hand,  is  a  useful  appa- 
ratus, of  which  there  are  several  varieties.     By  this  instrument  one 


DEGREE  OF  RESPIRATORY  EXPANSION  389 

can  measure  the  number  of  cubic  inches  of  air  exhaled.  It  consists 
essentially  of  a  bell  jar  or  capped  cylinder  submerged  in  water  and 
counterpoised,  with  a  tube  to  admit  the  expired  air  under  it.  As 
the  jar  rises,  a  properly  proportioned  scale  indicates  the  volume  of 
air  admitted.  The  only  diagnostic  fact  of  importance  to  be  obtained 
from  the  spirometer,  and  it  is  of  value,  is  a  knowledge  of  the  vital 
capacity  of  the  lungs — i.  e.,  the  volume  of  air  which  can  be  expired 
after  taking  the  deepest  possible  inspiration.  The  normal  vital 
capacity  of  a  man  22  years  old  and  5  feet  8  inches  in  height  averages 
from  230  to  240  cubic  inches,  d^  cubic  inches  for  each  inch  in  height. 
In  a  woman  of  19  years  of  age  and  5  feet  2|  inches  in  height  it  aver- 
ages 145  to  150  cubic  inches,  2.3  cubic  inches  for  each  inch  in  height. 
It  decreases  somewhat  with  age. 

(1)  Deficient  Expansion. — The  defect  in  expansion  may  be  gen- 
eral, affecting  the  thorax  as  a  whole,  or  localized  on  one  side  or  por- 
tion of  the  chest. 

If  the  vital  capacity  is  from  10  to  70  per  cent  below  what  it  should 
be  for  the  particular  individual,  the  existence  of  pulmonary  tuber- 
culosis, or  at  least  a  strong  predisposition  to  the  disease,  may  justly 
be  suspected.  Similar  conclusions  may  be  drawn  if  the  general  ex- 
pansion is  found  by  measurement  to  be  much  below  2  inches.  It  is 
claimed  that  the  expansion  is  diminished  in  exophthalmic  goitre,  but 
the  statement  lacks  confirmation. 

A  general  poor  expansion  may  be  due  to  the  limiting  effect  of  the 
chest  pain  incident  to  pleurisy,  pneumonia,  pleurodynia,  fractured 
ribs,  angina  pectoris  and  intercostal  neuralgia ;  obstructed  upper 
air  passages,  as  in  pressure  on  the  trachea  (by  mediastinal  tumours 
or  aneurism),  laryngeal  stenosis,  tumour,  paralysis,  or  spasm ;  pa- 
ralysis or  tetanic  spasm  of  the  respiratory  muscles  ;  and  asthma  and 
emphysema,  the  lungs  being  distended  to  an  extent  which  will  per- 
mit but  slight  additional  expansion.  Shallow  breathing  may  be 
simply  a  part  of  the  general  muscular  weakness  of  adynamic  condi- 
tions— e.  g.,  collapse,  syncope,  or  the  typhoid  state  in  general. 

Unilateral  deficiency  of  expansion,  one  or  the  other  lateral  halves 
of  the  chest  exhibiting  an  obvious  lack  of  inspiratory  movement,  is 
indicative  of  some  diseased  condition  which  prevents  inflation  of  the 
corresponding  lung.  It  is  a  diagnostic  symptom  of  importance,  and 
may  find  its  explanation  in  a  mechanical  hindrance  to  expansion 
upon  one  side  by  the  presence  of  fluid  or  air  in  the  pleura,  or  exten- 
sive pleural  adhesions,  or  (on  the  right  side)  by  an  enlarged  liver; 
in  obstruction  of  a  main  bronchus  by  a  foreign  body  or  the  pressure 
of  an  aneurism  or  tumour,  or  in  disease  confined  to  one  lung — tuber- 
culous, fibroid,  pneumonic,  cancerous,  hydatid,  or  atelectatic. 


390  THE  EVIDENCES  OF  DISEASE 

A  local  deficiency  in  expansion,  or  a  lagging  of  one  portion  of  the 
chest  wall  behind  the  remainder  during  inspiration,  is  suggestive  of 
circumscribed  disease  of  the  lung  or  pleura.  Deficient  expansion 
under  the  clavicle  is  seen  in  phthisis ;  of  the  upper  or  lower  portion 
of  the  thorax  in  an  apical  or  basal  pneumonia ;  of  the  pericardial 
space  in  pericardial  adhesions,  of  various  localities  with  pleural  adhe- 
sions, and,  especially  in  a  child,  in  local  atelectasis  or  collapse  of  the 
lung. 

(2)  Increased  Expansion.  —  Increased  general  expansion  occurs 
after  exercise  or  mental  excitement,  and  in  hysteria  and  some  forms 
of  dyspnoea.  Local  or  unilateral  increase  of  expansion  may  be  com- 
pensatory— i.  e.,  a  portion  or  the  whole  of  one  lung  may  expand 
beyond  its  usual  limits  in  order  to  perform  the  additional  work 
thrown  upon  it  by  disease  in  the  remaining  portion,  or  in  the  oppo- 
site lung. 

Respiratory  Bulging  and  Retraction. — Retraction  (during 
inspiration)  or  bulging  of  the  intercostal  spaces  (during  inspiration 
or  expiration)  may  be  either  general  or  circumscribed.  In  judging 
of  their  extent  it  must  be  remembered  that  the  ribs  are  ijrominent 
and  the  interspaces  marked  in  a  thin  or  emaciated  thorax,  while  the 
converse  condition  is  found  in  stout  or  muscular  persons. 

(1)  Retraction  of  the  interspaces  is  usually  associated  with  defi- 
cient expansion  and  inspiratory  dyspnoea  (difiicult  entrance  of  air). 
General  retraction  is  most  marked  in  obstruction  of  the  upjDer  air 
passages,  and  extensive  bilateral  broncho-pneumonia  (in  children). 
Unilateral  or  local  recession  indicates  obstruction  of  a  bronchus  or 
circumscribed  interference  with  expansion,  as  in  the  pulmonary  col- 
lapse of  infants,  the  affected  portion  not  distending,  pleuritic  adhe- 
hesions,  and  other  similar  conditions. 

(2)  Bulging  of  the  interspaces  during  expiration  is  usually  con- 
joined with  expiratory  dyspnoea  (difficulty  in  emptying  the  lungs), 
as  in  asthma  and  emphysema.  In  these  diseases  there  is  also  inspira- 
tory dyspnoea,  and  the  interspaces  alternately  bulge  and  retract. 
Bulging  during  inspiration  is  seen  only  above  the  clavicles,  and  is  an 
evidence  of  emphysema,  the  apex  of  the  hypertrophied  lung  protrud- 
ing above  its  normal  level. 

Rhythm  of  the  Respiration. — Normally  inspiration  passes 
into  expiration  without  an  observable  pause.  Inspiration  is  rather 
more  rapid  and  shorter,  in  the  ratio  of  5  :  6,  than  expiration.  If  the 
breathing  is  unusually  slow,  there  is  a  pause  at  the  end  of  expiration. 
While  quiet,  the  successive  respirations  are  regularly  rhythmical,  but 
this  regularity  is  subject  to  variations,  sometimes  purposive,  some- 
times involuntary.    The  breathing  is  very  irregular  in  children  while 


RHYTHM  OP  THE  RESPIRATION  391 

awake,  or  during  sleep  if  restless.    The  disturbances  of  rhythm  which 
possess  some  diagnostic  and  prognostic  value  are : 

(1)  Sighing. — An  occasional  slow,  deep  inspiration,  followed  by  a 
somewhat  rapid  expiration,  is  normal  in  many  persons  while  at  rest, 
in  order  to  more  fully  oxygenate  the  blood.  It  is  seen  as  the  result 
of  emotion,  and  in  the  hysterical,  hypochondriacal,  and  melancholic 
patient.  The  sighing  respiration  of  hemorrhage,  collapse,  or  syncope 
is  characteristic.  An  overdistended  stomach,  by  causing  pressure  on 
the  diaphragm,  may  be  responsible  for  frequent  sighing ;  it  is  seen  in 
cases  of  dilated  heart,  Addison's  disease,  meningitis,  and  lesions  of 
the  medulla,  and  is  very  common  in  typhoid  fever. 

(2)  Simple  Irregularity. — A  more  or  less  constant  irregularity  in 
the  time  intervals  and  the  depth  of  the  respirations  may  be  due  to 
collapse,  sudden  and  overwhelming  cerebral  apoplexy,  meningitis, 
brain  tumours,  especially  lesions  of  the  medulla,  and  chorea  (involve- 
ment of  the  respiratory  muscles).  A  pause  at  the  end  of  inspiration 
is  very  characteristic  of  acute  pneumonia. 

(3)  Cheyne-Stokes  Breathing. — This  is  a  peculiar  form  of  rhyth- 
mical irregularity  which  is  not  infrequently  encountered.  The  pa- 
tient ceases  to  breathe  (period  of  apnoea),  then  a  slight,  slow  respira- 
tion occurs,  followed  by  others  which  progressively  increase  in  depth 
and  rapidity,  until  an  acme  of  deep  and  hurried  breathing  is  reached 
(period  of  dyspnoea),  after  which  follows  a  corresponding  gradual 
diminution  in  rate  and  depth  until  the  respiration  again  ceases.  The 
duration  of  the  cycle  (from  apnoea  to  apnoea)  varies  from  30  seconds 
to  2  minutes.  The  Cheyne-Stokes  type  of  respiration  is  particularly 
noticeable  when  the  patient  is  quiet,  asleep  or  comatose.  If  awake 
and  talking,  its  presence  may  be  overlooked.  It  is  not  uncommon 
for  the  patient  to  be  unconscious  during  the  apnoic  period,  and  to 
wake,  move,  or  speak  with  the  onset  of  the  hurried  breathing.  The 
supervention  of  this  curious  variety  of  breathing  is  always  a  grave 
omen  and  usually  foretells  a  fatal  issue,  although  cases  are  occa- 
sionally seen  in  which  recovery  follows,  especially  if  occurring  in  the 
course  of  an  acute  and  not  a  chronic  disease.  It  may  last  for  hours, 
days,  and,  very  rarely,  even  for  months.  There  are  various  minor 
and  allied  forms— e.  g.,  sudden  deep  breathing,  following  a  cessa- 
tion (cerebral  respiration),  but  these  are  better  classed  under  (2) 
preceding. 

In  the  majority  of  instances  it  is  associated  with  apoplexy  (toward 
the  end),  chronic  nephritis  (uraemia),  tumour  of  the  brain,  tubercu- 
lous meningitis,  or  degeneration  of  the  heart  muscle.  Less  fre- 
quently it  is  observed  as  a  result  of  cardiac  valvular  defects  and  con- 
sequent embolism,  diabetes,  and  certain  acute  diseases,  notably  typhoid 


392  THE  EVIDENCES  OF  DISEASE 

fever,  pneumonia,  pertussis,  cerebro-spinal  fever,  scarlet  fever,  and 
septicaemic  conditions. 

Other  Characters  of  the  Respiration. — Certain  other  points 
of  some  clinical  importance  may  here  be  noted : 

(1)  Jerking  Respiration. — A  spasmodic  performance  of  either  in- 
spiration or  expiration  or  both  is  occasionally  seen.  Inspiration  may 
be  jerking  in  asthma,  hysteria,  and  hydrophobia ;  jerking  expiration 
is  seen  in  pleurodynia,  fractured  rib  and  the  early  stage  of  acute 
pleurisy,  because  of  the  sudden  stab  of  pain  in  the  side  which  arrests 
inspiration  and  calls  for  prompt  relief  by  expiration ;  lotli  mainly  in 
cases  where  thoracic  breathing  predominates. 

(2)  Stertorous  liespiration. — Snoring — the  sounds  arising  from 
the  vibration  of  the  soft  palate  when  breathing  through  the  mouth 
and  nose  at  the  same  time — usually  requires  unconsciousness  or  mus- 
cular relaxation  for  its  production.  Aside  from  its  frequent  occur- 
rence during  sleep  in  healthy  individuals,  especially  if  overtired,  it  is 
observed  as  a  symptom  in  profound  coma  (apoplectic,  ursemic,  dia- 
betic, etc.),  narcotic  poisoning,  and  paralysis  of  the  soft  palate.  It 
is  also  a  prominent  and  continuous  attendant  of  postnasal  adenoids 
and  enlarged  tonsils  in  children,  because  of  the  necessary  existence 
of  mouth  breathing  during  sleep. 

(3)  Stridulous  Respiration. — AVhen  the  air  in  passing  through 
the  larynx,  particularly  during  inspiration,  is  accompanied  by  a 
sound  variously  described  as  whistling,  harsh,  shrill,  creaking,  or 
screechy,  it  is  termed  stridor  or  stridulous  breathing.  It  is  always 
of  laryngeal  origin,  and  is  due  either  to  a  mechanical  obstruction  in 
the  larynx  (inflammatory  swelling,  oedema,  membrane,  tumour,  for- 
eign body)  or  to  spasm  or  paralysis  of  certain  laryngeal  muscles 
with  a  consequent  defective  opening  of  the  glottis — e.  g.,  spasmodic 
croup,  laryngismus  stridulus,  strychnine  poisoning,  tetanus,  hydro- 
phobia, pressure  upon  the  inferior  laryngeal  nerve  by  aneurism, 
mediastinal  tumour  or  enlarged  bronchial  glands,  and  in  rare  cases 
displacement  of  the  heart  or  the  trachea.  In  certaiii  forms,  because 
of  the  peculiar  character  of  the  breathing,  it  is  spoken  of  as  "  chok- 
ing "  respiration. 

(4)  Wavy  Respiration. — A  lack  of  evenness  in  the  movement  of 
inspiration  or  expiration,  one  part  of  the  chest  expanding  or  con- 
tracting before  another,  giving  rise  to  a  peculiar  undulating- or  wavy 
motion  of  the  chest  walls,  as  if  the  ribs  had  lost  their  firmness,  is  seen 
in  certain  adynamic  (typhoid)  conditions,  particularly  pneumonia. 

Dyspnoea. — Dyspncea  may  be  defined  as  difficult,  laborious,  or 
painful  breathing.  The  definition  implies  in  the  majority  of  cases  a 
subjective  sense  of  breathlessness ;  in  patients'  parlance,  "  shortness 


DYSPNCEA  393 

of  breath."  The  objective  symptoms  are  rapid  or  laboured  respira- 
tion and  more  or  less  cyanosis  {q.  v.),  according  to  the  cause  and 
severity  of  the  dyspnoea.  The  face  wears  an  anxious  expression ;  the 
pupils  are  dilated.  The  nostrils  expand  and  contract,  the  mouth 
opens  with  each  inspiration,  the  thorax  and  abdomen  heave  more  or 
less  violently,  the  skin  is  cold  and  wet,  and  if  the  dyspnoea  is  extreme 
the  patient  sits  upright  (orthopncea)  and  leans  upon  the  hands,  thus 
supporting  the  shoulders  so  that  the  extraordinary  muscles  of  respi- 
ration may  work  to  better  advantage.  In  dyspnoea  any  of  the  varia- 
tions from  the  normal  manner  of  breathing  which  have  previously 
been  considered  may  be  present  in  varying  number  and  intensity — 
e.  g.,  the  respiration  may  be  rapid  or  slow,  thoracic  or  abdominal, 
deep  or  shallow,  etc. 

Primarily,  dyspnoea  is  due,  with  few  exceptions,  either  to  lack  of 
oxygen,  excess  of  carbon  dioxide,  or  the  presence  in  the  blood  of  cer- 
tain products  of  muscular  activity  (dyspnoea  of  exercise). 

The  diseased  conditions  which  may  be  responsible  for  dyspnoea 
are  in  general :  obstruction  or  obstructive  disease  of  the  nose,  throat, 
larynx,  trachea,  and  bronchi,  causing  hindrance  to  the  entrance  of 
air  into  the  lungs ;  diseases  of  the  lungs  which  diminish  the  avail- 
able air  space ;  diseases  of  the  pleura  hindering  lung  expansion  ;  dis- 
eases of  the  heart  which  cause  pulmonary  stasis ;  pressure  upon  the 
diaphragm  by  fluid,  gas  or  tumour  in  the  abdomen ;  diminished 
amount  of  hgemoglobin  in  the  blood,  poisonous  materials  circulating 
in  it,  or  an  increase  of  its  temperature;  paralysis  or  spasm  of  the 
muscles  of  respiration;  and  pain  in  such  localities  as  to  interfere 
with  respiration. 

The  most  common  causes  of  dyspnoea  are  debility  or  anaemia,  car- 
diac, pulmonary,  or  renal  disease.  Therefore  always  examine  the 
heart,  lungs,  blood,  and  urine.  The  dyspnoea  most  commonly  seen 
is  felt  during  both  phases  of  the  respiratory  act.  It  is  helpful  to 
recognise  certain  clinical  varieties  of  this  symptom  and  their  usual 
disease  associations  as  follows  : 

(1)  Simple  Accelerated  Respiration.— Thh  usually  occurs  in  fever, 
particularly  if  the  patient  is  an  infant  or  a  neurotic  adult.  The 
breathing  is  shallow  and  a  physical  examination  does  not  reveal 
lesions  capable  of  causing  dyspnoea. 

(2)  Dyspnoea  on  Exertion.— ^\\ovine%&  of  breath  observed  only  after 
physical  exertion  is  characteristic  of  obesity,  debility,  anasmia ;  valvu- 
lar defects,  well,  but  not  perfectly,  compensated ;  moderately  weak 
heart,  disease  of  the  blood  vessels,  severe  bronchitis  of  the  larger 
tubes,  emphysema,  and  incipient  tuberculosis  or  latent  pleurisy  with 
effusion. 


394  THE  EVIDENCES  OF   DISEASE 

(3)  Dyspncea  which  is  Constant. — If  the  breath  is  short,  even  while 
at  rest,  it  may  be  due  to  a  severer  grade  or  more  advanced  stage  of 
the  conditions  mentioned  in  (2),  or  to  laryngeal  stenosis,  fibrinous 
bronchitis,  broncho-pneumonia,  lobar  pneumonia,  fibroid  or  ulcera- 
tive phthisis,  acute  pleural  effusion  or  large  pericardial  effusion. 

(4)  Dyspncea  which  is  Paroxysmal. — Sudden  attacks  of  dyspnoea, 
usually  of  sufficient  severity  to  cause  orthopnoea,  may  be  accounted 
for  by  acute  indigestion,  bronchial  asthma,  spasm  of  the  laryngeal 
adductors  (spasmodic  croup),  chronic  nephritis  (uraemic  asthma),  dis- 
ease of  heart  (cardiac  asthma),  angina  pectoris,  or  the  pressure  of  a 
tumour  or  aneurism  upon  the  pneumogastric. 

(5)  Dyspnma  ivhich  is  Inspiratory. — When  there  is  difficult  en- 
trance of  air  into  the  lungs,  as  evidenced  by  retraction  or  recession  of 
the  supraclavicular,  intercostal  and  subcostal  spaces,  with  a  compara- 
tively easy  expiration,  one  may  suspect  foreign  body  in  the  larynx  or 
trachea,  spasm  of  the  adductors  (croup,  laryngismus  stridulus)  or 
paralysis  of  the  dilators  of  the  glottis,  oedema,  inflammatory  swelling 
of  or  membrane  in  the  larynx,  or  a  movable  tumour  above  the  glottis 
acting  as  a  ball  valve. 

(6)  Dyspncea  ivhich  is  Uxpiratory. — If  expiration  is  hindered, 
which  is  proved  by  expiratory  bulging  and  excessive  action  of  the 
abdominal  muscles,  while  inspiration  is  reasonably  easy,  the  causative 
disease  is  most  frequently  pulmonary  emphysema,  next  bronchial 
asthma.  Bronchitis  with  viscid  mucus  in  the  tubes,  and  a  movable 
tumour  below  the  glottis,  so  placed  and  attached  as  to  swing  up  be- 
tween the  cords  during  expiration,  are  additional  causes. 

(7)  Dyspnoea  which  is  Subjective. — There  is  a  form  of  dyspnoea 
met  with  in  nervous  and  hysterical  women  which  appears  to  be 
purely  subjective.  The  dyspnoic  sensation  is  the  subject  of  bitter 
complaint ;  indeed,  there  may  be  orthopnoea,  but  there  is  no  blue- 
ness  of  the  lips  and  finger  nails,  and  a  thorough  search  for  cardiac, 
pulmonary,  haemic,  renal,  or  other  possible  causal  conditions  will 
afford  negative  results.     It  is  apparently  a  psychic  phenomenon. 

Vocal  Fremitus. — If  a  hand  is  laid  upon  the  chest  wall  while 
the  patient  speaks  with  ordinary  or  more  than  ordinary  loudness,  a 
peculiar  buzzing  or  vibrating  sensation  is  perceived  by  the  palpating 
fingers — the  vocal  fremitus.  The  vibrations  originate  in  the  vocal 
cords,  and  are  conducted  by  the  columns  of  air  in  the  trachea  and 
large  and  small  bronchial  tubes  through  the  substance  of  the  lungs 
to  the  chest  wall.  The  intensity  of  the  vocal  fremitus  depends  upon 
two  factors :  first,  the  loudness  and  pitch  of  the  voice ;  second,  the 
varying  conductivity  and  thickness  of  the  media  through  which  the 
vibrations  must  pass.     To  study  the  vocal  fremitus  the  patient  is 


VOCAL  AND  FRICTION  FREMITUS  395 

told  to  articulate  certain  words — e.  g.,  "  one,  two,  three,"  "  ninety- 
nine  " — while  one,  preferably  always  the  same,  warmed  hand  is  laid 
upon  various  parts  of  the  thorax.  Some  experience  with  different 
voices  and  chests  is  requisite  to  be  assured  of  variations  from  what 
may  be  considered  normal  for  the  individual  under  examination. 

(1)  Marked  or  Increased  Fremitus.— If  the  patient  has  a  loud, 
low-pitched,  or  harsh  voice,  especially  if  the  chest  walls  are  thin,  the 
fremitus  will  be  marked.  It  is  consequently  much  more  distinct  in 
men  than  in  women  and  children.  It  is  normally  more  intense  over 
the  upper  half  of  the  right  lung,  partly  because  the  right  bronchus 
exceeds  the  left  in  diameter  and  therefore  affords  a  larger  vibration- 
conveying  column  of  air,  partly  because  the  primary  bronchus  enter- 
ing the  right  upper  lobe  is  given  off  nearer  the  main  bronchus  and 
at  a  higher  level  than  that  entering  the  left  upper  lobe  (Carey). 

If  the  lung  substance  is  consolidated  or  infiltrated  it  conducts  the 
sound  vibrations  with  greater  facility ;  consequently  the  vocal  fremi- 
tus is  increased  in  pneumonia,  tuberculous  lung,  etc.  If  there  is  a 
solid  tumour  in  the  chest,  lying  between  a  large  bronchus  and  the 
chest  wall,  and  of  suflBcient  size  to  leave  little  lung  tissue  between  it 
and  them,  the  vocal  fremitus  is  increased  over  its  site.  Pulmonary 
cavities,  if  thin  walled  and  near  the  surface  of  the  chest,  may  afford 
a  very  distinct  fremitus,  the  cavity  acting  as  a  resonator  for  the 
sound  of  the  voice.  If  bands  of  adhesion  stretch  from  lung  to  pleura 
the  fremitus  may  be  conducted  and  perceived,  even  if  there  is  a  con- 
siderable pleural  effusion. 

(2)  Diminislied  or  Absent  Fremitus. — The  vocal  fremitus  is  slight 
in  women,  children,  men  with  feeble,  high-pitched  voices,  and  stout 
persons.  It  is  normally  less  on  the  left  side  than  on  the  right. 
Absence  of  vocal  fremitus,  where  it  should  exist,  is  significant  of  air 
or  fluid  in  the  pleural  cavity.  Air  and  fluid  under  these  circum- 
stances do  not  act  as  good  conductors,  and  will  hinder  the  vibration 
of  the  chest  wall ;  or,  as  another  explanation  has  it,  the  collapsed 
lung,  having  lost  its  elasticity,  does  not  cany  the  vocal  vibrations  to 
the  air  or  fluid.  Moreover,  a  thickened  pleura  damps  the  vibrations. 
If  a  main  bronchus  is  obstructed  by  a  foreign  body,  a  plug  of  mu- 
cus, or  the  pressure  of  a  tumour,  the  vocal  vibrations  are  not  con- 
ducted to  the  corresponding  lung  and  the  fremitus  is  lacking.  If  a 
large  bronchus  leading  to  a  consolidated  area — e.  g.,  in  pneumonia — is 
obstructed,  the  solidified  lung  will  not  offer  the  customary  increased 
fremitus. 

Friction  Fremitus. — If  a  fine  creaking  or  rubbing  vibration  is 
felt,  which  is  synchronous  with  the  heart  beat  or  the  respiration,  it 
is  significant  respectively  of  pericarditis  or  pleurisy. 


396  THE    EVIDENCES   OP   DISEASE 

BroncMal  Fremitus. — A  somewhat  coarse  fremitus,  synchro- 
nous with  the  respiration,  and  often  heard  some  inches  away  from 
the  chest,  is  a  palpable,  large,  moist  or  bubbling  rale,  due  to  the  pas- 
sage of  air  through  a  bronchus  partly  plugged  with  viscid  mucus,. 
or  constricted  by  swelling  of  the  mucosa;  or  the  bubbling  of  air 
through  fluid  in  a  cavity.  Bronchial  (or  rhonchal)  fremitus  is  com- 
mon in  infants  and  children  suffering  from  an  ordinary  bronchitis, 
and  in  asthma,  as  well  as  in  the  chronic  bronchitis  with  bronchiec- 
tases of  older  persons. 

IV.    PERCUSSION    OF   THE    LUNGS 

With  reference  to  the  lungs,  percussion  is  employed  for  four  pur- 
poses :  (1)  To  determine  the  boundaries  of  the  lungs  ;  (2)  to  ascertain 
whether  they  contain  more  or  less  than  the  normal  amount  of  air ; 

(3)  to  aid  in  determining  the  presence  of  cavities  in  the  lungs,  or 

(4)  of  air  or  fluid  in  the  pleural  cavities,  or  thickening  of  the  pleura.. 

(A)  Technic  of  Percussion  of  the  Lungs 

The  standing  or  sitting  position  is  preferable,  unless,  as  frequently 
happens,  the  patient  is  ill  in  bed  and  greatly  prostrated.  "With  the 
patient  facing  the  examiner,  arms  hanging  easily  at  the  side,  face 
looking  straight  forward,  head  turned  neither  to  the  right  nor  the 
left,  in  order  to  avoid  unequal  tension  of  the  muscles  and  fascia  on 
either  side,  the  front  of  the  chest  may  be  gone  over.  To  percuss  the 
sides  of  the  chest,  the  arms  should  be  raised  and  the  hands  clasped 
over  the  head.  To  examine  the  back,  let  the  arms  be  folded  and  the 
patient  lean  somewhat  forward.  Before  leaving  the  back,  it  is  well 
to  have  the  hands  again  placed  upon  the  head,  as  this  action  swings 
the  angles  of  the  scapulge  outward,  and,  by  uncovering,  renders  acces- 
sible a  portion  of  lung  in  which  there  is  not  infrequently  found  the 
earliest  evidence  of  tuberculous  disease.  In  percussing  the  lungs  it 
should  be  made  an  invariable  rule  to  compare  symmetrical  points  on 
each  side ;  moreover,  to  compare  interspace  with  interspace  and  rib 
with  rib,  never  letting  the  pleximeter  finger  rest  upon  two  ribs  or  a 
rib  and  an  interspace  at  the  same  moment. 

Beginning  above  the  clavicle  (Fig.  113),  with  a  rather  strong 
stroke,  note  how  high  above  this  bone  the  pulmonary  resonance  can 
be  elicited — i.  e.,  the  height  of  the  apices — and  compare  the  various 
qualities  of  the  sounds  upon  each  side.  Xext  percuss  and  contrast 
successively,  with  a  stroke  of  moderate  strength,  the  1st,  2d,  and  3d 
interspaces  upon  each  side,  along  their  length  from  sternal  edge  out- 
ward. Passing  down  the  right  mammillary  line,  the  covered  (deep) 
dulness  of  the  liver  becomes  manifest  by  strong  percussion  at  the  4th 


PERCUSSION   OP   LUNGS 


397 


Fig.  113. — Showing  the  two  triangular  areas — one  ante- 
rior, between  clavicle  and  line  of  trapezius;  the  other 
pohiterior,  between  trapezius  and  line  of  spine  of 
scapula— over  which  percussion  and  auscultation  are 
to  be  performed  in  order  to  determine  the  condition 
of  the  apices  of  the  lungs. 


interspace  or  5th  rib,  and  continuing,  with  gentle  percussion,  the  ex- 
posed (absolute  or  superficial)  dulness  of  the  same  organ  becomes 
evident  at  the  6th  rib  or  interspace,  thus  indicating  the  usual  loca- 
tion of  the  anterior  portion  of  the  lower  margin  of  the  lung  in  this 
line.     In  the  left  mam- 
millary  line  the   normal 
lung    resonance    is    im- 
paired at  the  4th  or  5th 
interspace  by  the  exposed 
(superficial)  cardiac  dul- 
ness ;  and  a  little  outside 
of  this  line  and  at  about 
the  same  level  strong  per- 
cussion elicits  a  tympan- 
itic quality  from  the  un- 
derlying left  end  of  the 
stomach,  which   mingles 
with  the  lung  resonance. 
From   this    point   down- 
ward very  gentle  percus- 
sion finally  offers,  at   or 
just  below  the  6th  rib,  a 
pure  tympanitic  sound,  indicating  the  usual  position  of  the  lower 
anterior  border  of  the  left  lung.     Any  areas  of  dulness  or  hyper- 
resonance  which  have  been  found  on  the  front  of  the  thorax  may 
now  be  more  carefully  mapped  out. 

The  lateral  (axillary)  regions  of  the  thorax  may  now  be  examined, 
percussing  from  the  axilla  downward  in  the  midaxillary  line,  finding, 
by  gentle  percussion,  the  last  trace  of  pulmonary  resonance — i.  e.,  the 
lower  lateral  border  of  the  lung — at  the  8th  rib,  if  it  is  in  its  normal 
position. 

Percuss  next  the  back  of  the  thorax  in  the  scapular  line,  from  the 
suprascapular  space  downward.  At  the  base,  the  liver  on  the  right,, 
and  the  kidney  and  spleen  on  the  left,  will  modify  the  lung  sound, 
but  it  may  be  traced  by  percussion  strokes  of  moderate  strength  as 
far  down  as  the  10th  rib  or  space  on  both  sides. 

By  implication  from  the  foregoing  suggestions  it  is  readily 
seen  that  during  the  examination  one  endeavours  to  ascertain  the 
boundaries  of  the  lungs  (topographical  percussion),  and  that  com- 
parison is  made,  not  only  between  the  sounds  from  corresponding 
portions  of  the  individual  chest,  but  that  each  sound  elicited  is 
assigned  to  its  proper  place  in  the  descriptive  list  of  percussion 
sounds. 


398 


THE  EVIDENCES   OF  DISEASE 


(B)  The  Results  of  Percussion  in  Normal  Lungs 

In  the  normal  chest  the  pulmonary  resonance  is  less  clear  (dulled 
or  muffled)  if  its  walls  are  thick  (obesity),  and  is  clearer  and  more 
resonant  if  the  chest  walls  are  thin  or  especially  resilient,  as  in  chil- 
dren.    If  the  lungs  are  healthy,  the  thorax  well  formed,  and  the  in- 

__    dividual  neither  obese 

nor  emaciated,  the  re- 
sults of  percussion  in 
the  various  topograph- 
ical areas  are  as  fol- 
lows (Fig.  114) : 

Supraclavicular 
Spaces. — There  is  pul- 
monary resonance  of 
a  moderate  character, 
becoming  somewhat 
tympanitic  if  percus- 
sion is  carried  toward 
and  over  the  trachea. 
Infraclavicular 
Spaces.  —  Below  the 
middle  of  the  clavicle 
(in  the  mammillary 
line)  there  is  typical 
well-marked  pulmon- 
ary resonance.  Per- 
cussing toward  the 
median  line,  osteal 
and  tympanitic  reso- 
nance tends  to  be 
heard,  owing  to  the 
presence  of  the  ster- 
num and  the  tracheobronchial  air  columns,  and  pulmonary  resonance 
diminishes.  From  the  mammillary  line  outward  there  is  a  slight 
diminution  in  the  pulmonary  quality.  The  pulmonary  quality  is 
slightly  less  marked  in  the  right  than  in  the  left  supraclavicular 
and  infraclavicular  areas. 

Mammary  Spaces. — In  both  mammary  spaces  the  pectoral  muscles 
and,  in  women,  the  mammary  glands  tend  to  muffle  the  sound  of 
pulmonary  resonance.  In  the  lower  portion  of  the  right  mammary 
region  the  presence  of  the  liver  causes  partial  dulness.  In  that  por- 
tion of  the  left  mammary  region  internal  to  the  mammillary  line,  and 


Fig.  114. — Showing  the  relative  resouaace  of  various  portions 
of  the  anterior  surface  of  the  thorax.  Horizontal  lines 
=  pulmonary  resonance.  Vertical  lines  =  tympanitic 
resonance  of  trachea  and  stomach.  Oblique  lines  =  im- 
paired resonance  or  moderate  dulness  due  to  mammary 
glands,  liver,  heart,  and  spleen.  Solid  shading  =  abso- 
lute dulness  due  to  liver  and  heart. 


PERCUSSION  OF  LUNGS  399 

at  and  below  the  fourth  space,  the  heart  dulness  modifies,  and,  over 
the  area  of  exposed  cardiac  dulness,  replaces  pulmonary  resonance. 
At  the  lower  portion  of  the  left  mammary  space  in  the  anterior  axil- 
lary line  the  percussion  sound  becomes  hyperresonant  and,  finally, 
purely  tympanitic  from  the  presence  of  the  stomach. 

Axillary  Space. — The  upper  axillary  spaces,  down  to  the  6th  rib 
on  both  sides,  afford  typical  pulmonary  resonance.  The  right  infe- 
rior axillary  space  is  less  resonant  because  of  the  liver ;  the  left  in- 
ferior space  is  partly  tympanitic  from  the  stomach,  partly  dull  from 
the  spleen. 

Suprascapular  and  Interscapular  Spaces. — These  give  a  moderate 
pulmonary  resonance. 

Scapular  Space. — The  overlying  scapula  and  its  muscles,  by  muf- 
fling the  sound,  cause  these  spaces  to  be  the  least  resonant  of  the  pul- 
monary areas. 

Infrascapular  Space. — Compared  to  the  upper  anterior  portions 
of  the  chest,  the  infrascapular  regions  have  only  a  fair  degree  of  pul- 
monary resonance,  but  they  are  the  least  muffled  and  most  resonant 
of  the  posterior  areas. 

(C)   The  Results  of  Percussion  in  Disease  of  the  Lungs 
and  Pleurae,  or  of  Neighbouring  Organs 

As  a  consequence  of  some  morbid  condition  of  the  respiratory 
apparatus,  or  of  some  contiguous  part  or  organ,  one  may  find  the 
boundaries  of  the  lungs  displaced,  or  an  abnormal  alteration  of  the 
percussion  sounds  in  a  given  point  or  area. 

(«)  Changes  in  the  Position  of  the  Borders  of  the  Lungs. — (1) 
Apices. — Xormally  the  pulmonary  resonance  extends  1^  to  2  inches 
above  the  clavicles,  the  right  apex  being  sometimes  slightly  higher 
than  the  left.  If  one  apex  is  found  to  be  distinctly  lower  than  the 
other — i.  e.,  shrunken — it  is  suggestive  of  past  or  present  tuberculous 
disease  of  the  lung,  a  contracting  adhesive  pleurisy  or  collapse  of  the 
lung.  If  both  apices  stand  unusually  high,  and  especially  if  the 
supraclavicular  spaces  bulge  during  inspiration,  the  lungs  are  em- 
physematous. Temporary  expansion  is  present  during  attacks  of 
bronchial  asthma. 

(2)  Anterior  Borders. — As  the  right  anterior  border  lies  for  its 
whole  length  behind  the  sternum,  its  position  can  not  be  determined, 
the  osteal  resonance  of  the  firm  bone  preventing.  The  same  state- 
ment applies  to  that  portion  of  the  left  anterior  border  extending 
from  the  apex  down  to  the  4th  costal  cartilage.  At  this  point  it 
curves  outward  from  under  cover  of  the  sternum  and  downward  to 
the  6th  rib,  becoming  accessible  to  percussion  and  forming  the  left 


400  THE  EVIDENCES  OP   DISEASE 

border  of  the  exposed  (superficial)  cardiac  dulness.  While  a  consid- 
erable increase  in  the  exposed  cardiac  dulness  may  indicate  an  en- 
larged heart  or  a  pericardial  effusion  displacing  the  left  anterior 
border  outward,  it  is  in  the  majority  of  cases  due  to  retraction  of  the 
lung  from  tuberculous  or  fibroid  disease,  the  whole  length  of  the 
anterior  border  sometimes  withdrawing  to  the  left  of  the  sternum,  or 
to  a  pleural  effusion  with  resulting  collapse  of  the  lung.  On  the 
other  hand,  if  the  lower  part  of  the  anterior  border  covers  the  usu- 
ally exposed  portion  of  the  heart,  it  is  indicative  of  emphysema  or,, 
temporarily,  of  bronchial  asthma. 

(3)  Lower  Borders. — In  drawing  inferences  from  the  position  of 
the  lower  borders  of  the  lung,  allowance  must  be  made  for  age  and 
respiratory  and  postural  displacement  as  follows : 

In  old  age  these  borders  lie  1  rib  below,  in  infancy  1  rib  above,  the 
position  which  is  normal  for  a  healthy  person  of  intermediate  age.  In 
quiet  respiration  the  edges  of  the  lung  advance  into  the  anterior  and 
inferior  complementary  pleura  about  |  inch.  If  percussion  is  made 
in  the  mammillary  line  at  the  end  of  inspiration  and  again  at  the 
end  of  full  expiration  {forced  respiration),  the  excursion  of  the  lower 
border  will  be  found  to  be  1:^  to  1^  inch.  In  a  person  lying  upon 
the  back,  the  lung  borders  in  the  mammillary  line  are  f  inch  lower 
than  when  erect.  If  lying  upon  the  side,  the  border  of  the  lung  upon 
the  uppermost  side  may  advance  downward  as  much  as  4  inches  in 
the  midaxillary  line. 

If  the  lower  borders  of  the  lung,  front,  side,  and  back,  are  found 
to  be  lower  than  normal,  it  is  significant  of  emphysema,  in  which 
case  it  may  be  that  pulmonary  resonance  is  elicited  as  far  down  as 
the  9th  rib  in  the  right  mammillary  line,  or,  temporarily,  bronchial 
asthma.  If  the  lower  borders  are  higher  than  normal,  it  may  be  due 
to  phthisical  shrinking,  collapse,  a  distended  abdomen  pushing  the 
diaphragm  and  lungs  upward,  or  to  paralysis  of  the  diaphragm. 
The  lung  may,  of  course,  be  pushed  up  by  air  or  fluid  in  the  pleural 
cavities,  but  in  such  cases  pulmonary  resonance  is  absent,  being  re- 
placed respectively  either  by  a  tympanitic  or  a  dull  percussion  sound. 

If  the  normal  respiratory  displacement  is  sought  for  and  not 
found,  its  absence  may  be  due  to  extensive  pleuritic  adhesions.  The 
movement  of  the  lung  borders  during  respiration  in  emphysema  is 
slight,  as  the  lungs  are  already  permanently  expanded  beyond  their 
natural  limits. 

(b)  Decreased  Resonance. — The  percussion  sound  over  the  lung 
becomes  less  resonant  in  proportion  to  the  diminution  in  the  amount 
of  air  underlying  the  part  of  the  chest  percussed.  Consequently,  ex- 
udation into  the  air  cells,  collapse  or  consolidation  of  the  lung,  the 


PERCUSSION  OP  THE   LUNGS 


401 


Heightened  pitch  or 
impaired  resonance 


Slight  dulness 


Moderate  dulness 


presence  of  fluid  in  the  pleural  cavities,  or  the  existence  of  a  solid 
tumour  renders  the  percussion  sound  over  such  areas  more  or  less 
dull  (Fig.  115). 

Consolidations  of  the  lung  are  found  in  pneumonia,  phthisis, 
hemorrhagic  infarcts,  gangrene,  abscess,  and  tumours.  In  order  to 
cause  appreciable  dulness  the  consolidation  must  be  at  least  1|  inch 
in  diameter,  and  lie  just  beneath  the  chest  wall.  More  remote  air- 
less portions  must  be  larger  and  lie  not  deeper  than  2|  to  3  inches, 
the  distance  to  which  the  percussion  stroke  penetrates  below  the 
under  surface  of  the  pleximeter  finger,  and  require  strong  percus- 
sion to  elicit  their  modifying  effect,  which,  indeed,  may  be  simply 
a  heightening  of 
pitch.  Fluid  in  the 
pleura  (serum,  pus, 
blood),  in  order  to 
cause  flatness,  must 
amount  at  least  to 
13^  oz. 

Variations  in  the 
degree  of  dulness 
are  recognised  by 
appropriate  terms 
(page  289).  The 
sense  of  increased 
resistance,  which  is 
very  obvious  to 
the  skilled  finger, 
should  not  be  for- 
gotten. It  is  most 
marked  over  con- 
solidations, fluid, 
thickened  pleura, 
high  grades  of  em- 
physema, and  pneumothorax  when  the  air  is  under  great  tension. 

(1)  Dulness  or  heightened  pitch  over  otie  apex  (sometimes  both), 
with  normal  resonance  elsewhere,  is  usually  suggestive  of  tubercu- 
losis, but  may  in  somewhat  rare  cases  be  due  to  pneumonia,  gangrene, 
or  new  growth.  Slight  impairment  at  both  apices,  disappearing  after 
a  few  forced  inspirations,  is  found  not  infrequently  in  persons  of 
sedentary  habits  who  are  not  accustomed  to  deep  breathing. 

(2)  Dulness  over  the  loiver  lobes  posteriorly  may  be  significant  of 
pneumonia,  pleurisy  with  effusion,  cedema,  atelectasis,  or  the  hypo- 
static congestion  which  is  found  in  patients  with  weak  heart,  as  in 


Fig.  115. — Showing  the  variations  of  lessened  resonance  due  to 
the  presence  of  consolidations  in  the  lung  or  fluid  in  the 
pleural  cavity. 


402 


THE  EVIDENCES  OF   DISEASE 


exhausting  fevers,  who  lie  persistently  in  the  dorsal  posture.  Much 
less  often  it  is  due  to  infarcts,  abscess,  gangrene,  tumour,  or  basic 
tuberculosis,  the  latter  usually  sequent  to  disease  of  the  upper  lobes. 
(3)  A  band  of  dulness  or  flatness  in  the  left  anterior  axillary  line 
from  the  6th  to  the  8th  rib  (Fig.  116),  where  normally  tympanitic 
resonance  is  found,  is  due  to  left  pleural  effusion,  the  fluid  gravitat- 


LlNE   OF    LUNG 


Line  of  pleura 
over    outline 

OF    LIVER 


Dulness  OF  FLUID 
replacing  nor- 
mal tympanitic 
resonance  of 
stomach  in 
Traube's  area 


Fig.  116. — Showing  the  dulness  due  tx)  fluid  in  the  left  comple 


reflected)  pleura. 


ing  into  the  complementary  (or  reflected)  pleural  sulcus,  which  at 
this  point  extends  3  to  4  inches  below  the  edge  of  the  lung.  This 
region  normally  offers  a  tympanitic  sound  (Fig.  114)  because  of  the 
presence  of  the  cardiac  end  of  the  stomach,  and  is  the  so-called 
Traube's  area  or  "  half-moon-shaped  space  "  (Fig.  142).  It  is  bounded 
above  and  laterally  by  the  contiguous  borders  of  the  liver,  lungs, 
and  spleen. 

(4)  A  "  wooden  "  percussion  sound,  with  an  unusual  sense  of  re- 
sistance, points  toward  a  marked  fibroid  change  in  the  lungs,  such  as 
occurs  in  chronic  fibroid  phthisis  or  chronic  interstitial  pneumonia. 
It  is  also  said  to  be  present  over  solid  lung  which  is  overlaid  by  a 
thin  layer  of  relaxed  pulmonary  tissue. 

(5)  Dulness  in  the  left  suprascapular,  and  especially  in  the  left 
interscapular,  space  may  be  due  to  an  aneurism  of  the  descending 
aorta — a  fact  to  be  remembered.  Over  one  or  both  interscapular 
spaces  lack  of  resonance  may  indicate  enlargement  of  the  bronchial 
glands  (so  also  with  dulness  instead  of  tympanicity  over  the  lower 
cervical  vertebrae)  or  collapse  of  the  lung. 

(6)  Dulness  at  either  base,  the  upper  line  of  which  shifts  with  a 
change  in  the  position  of  the  patient,  may  occur  in  pleurisy  with 


PERCUSSION  OF   THE  LUNGS 


403 


effusion,  but  is  most  characteristic  of  pneumohydrothorax,  the  fluid 
gravitating  more  readily  in  the  latter  condition. 

(c)  Increased  Resonance. — Taking  again  pulmonary  resonance  as 
the  standard,  the  percussion  note  may  depart  from  it  in  the  direction 
of  greater  resonance.  The  presence  of  a  tympanitic  sound  usually 
but  by  no  means  always  implies  a  greater  amount  of  air  under  the 
point  at  which  percussion  is  made.  The  general  conditions  which 
are  responsible  for  this  sound  and  its  modifications  are  (Fig.  117)  : 

(1)  Distention  of  the  air  cells  (increased  amount  of  air),  as  in 
emphysema  (C). 

{2)  The  presence  of  air-containing  cavities  in  the  lung,  as  in 
phthisis  {B  and  D).  If  the  cavity  becomes  filled  with  fluid  the  tym- 
panitic quality  disappears. 

(3)  The  presence  of  air  in  the  pleural  cavity  (E),  as  in  pneumo- 
thorax, if  not  under  too  great  tension. 


Tympanitic  (trachea 
A        and  bronchi  per- 
cussed      through 
consolidated  lung) 


7j      Tympanitic  or 
■^  amphoric 


Hyperresonant  (distended     /y 
air  cells) 


Tympanitic  (cavity 
percussed  through 
consolidated  lung) 


Tympanitic  or  am- 
phoric 


B 


E 


Fig.  117.- 


-Diagram  showing  the  physical  conditions  which  cause  hyperresonacce  and  tym- 
panitic or  amphoric  percussion  sounds. 


(4)  The  presence  of  a  shaft  of  consolidated  lung  leading  from  the 
trachea  and  main  and  larger  bronchi  to  the  surface,  through  which 
the  percussion  stroke  is  conducted  directly  to  the  column  of  air  in 
these  large  tubes,  practically  normal  cavities  {A ),  or  when  percussion 
is  made  immediately  over  the  trachea  and  main  bronchi. 

(5)  The  presence  of  a  large  pleural  effusion  or  pulmonary  consoli- 


404 


THE  EVIDENCES  OF   DISEASE 


Tympanitic  (skooaic)  resonance 
Crackeo-pot  resonance 

WlNTRlCH'S    PHENOMENON    (aT   TIMcs) 

Pectoriloquy  (rarely) 


dation  not  infrequently  causes  a  tympanitic  percussion  sound  in  that 
portion  of  the  lung  which  lies  above  the  fluid  or  solid  exudate  (Fig. 
118).  The  explanation  of  this  fact,  which  is  not  altogether  satisfac- 
tory, infers  that  the  part  of  the  lung  from  which  tympanitic  resonance 

may  be  elicited  is  in  a 
state  of  relaxation  or 
atony,  the  walls  of  the 
alveoli — as  their  tonus 
or  tension  is  in  abey- 
ance— permitting  the 
contained  air  to  vi- 
brate as  if  in  a  loose 
sac,  the  numerous 
cells  in  which  the  air 
lies  having  lost  their 
ordinary  power  of  im- 
parting a  characteris- 
tic pulmonary  quality 
to  the  percussion 
sound. 

The  pitch  of  the 
tympanitic  sound  va- 
ries. If  the  air  in  a 
cavity  is  under  con- 
siderable tension  the 
pitch  becomes  higher, 
and  the  volume  and  intensity  decrease  to  an  extent  (dull  tympan- 
icity)  which  may  suggest  dulness.  This  fact  may  be  demonstrated 
by  percussing  the  cheeks  while  inflated  under  varying  pressure  by 
buccal  contraction.  If  it  is  a  cavity  communicating  with  the  air 
which  furnishes  the  tympanitic  sound,  the  wider  the  channel  of  com- 
munication the  higher  the  pitch. 

For  the  termmology  of  the  variations  of  increased  resonance  see 
page  289.  There  are  certain  peculiar  percussion  sounds  which,  as 
their  resonance  exceeds  that  of  the  normal  lung,  are  classed  as  varie- 
ties of  tympanitic  sound — namely,  amphoric,  cracked-pot,  and  coin 
percussion.  There  are  other  minor  alterations  in  the  extraresonant 
percussion  sounds  which  will  be  noted. 

The  diagnostic  significance  of  increased  resonance  may  now  be 
pointed  out  as  follows  : 

(1)  A  hyperresonant,  almost  tympanitic,  note  on  both  sides  of  the 
chest  is  indicative  of  emphysema,  which,  if  extreme,  may  afford  a  dull 
tympany  on  account  of  the  tension  of  the  chest  walls. 


Fio.   118. — Showing    cortaiu    percussion    aud   auscultatory 
findings  above  consolidations  or  effusions. 


PERCUSSION  OP  THE  LUNGS  405 

(2)  Tympanicity  over  the  greater  part  of  one  side  of  the  chest 
may  be  due  to  compensatory  emphysema  of  one  lung,  the  other  hav- 
ing been  disabled  by  disease,  or  to  pneumothorax.  If  the  air  tension 
in  the  latter  disease  is  very  great,  the  tympany  may  be  so  raised  in 
pitch  as  to  be  mistaken  for  dulness. 

(3)  If  there  is  great  increase  of  cardiac  dulness  and  a  tympanitic 
quality  of  sound  is  discovered  above  and  to  the  left  in  front,  and  pos- 
teriorly on  the  left  side  as  well,  it  is  probably  due  to  an  unusually 
large  pericardial  effusion  displacing  the  lung.  In  a  case  under  my 
care,  which  presented  this  combination  of  signs,  the  pericardium  con- 
tained 90  oz.  of  serum. 

(4)  Dulness  at  one  or  both  bases,  with  hyperresonance  ("  skodaic  ") 
over  the  upper  portion  of  the  chest,  usually  most  marked  in  the  in- 
fraclavicular space  (Fig.  118),  may  be  caused  by  pleurisy  with  effu- 
sion, basic  pneumonia  (1st  and  3d  stages  of  lobar  pneumonia  particu- 
larly), large  pulmonary  infarctions,  and  pulmonary  oedema. 

(5)  If  dulness  is  discovered  over  one  or  both  apices,  and  a  tympa- 
nitic note  is  found  in  the  1st  and  2d  interspaces  close  to  the  edge  of 
the  sternum,  it  is  probably  due  to  the  conduction  of  the  tracheo- 
bronchial percussion  sound  by  consolidated  lung  {A,  Fig.  117)  in 
apical  or  upper  lobe  pneumonia  or  tuberculosis,  rarely  tumour. 

(6)  A  localized  tympanitic  sound  may  be  due  to  a  cavity  (phthisis, 
bronchiectasis,  pulmonary  actinomycosis,  gangrene,  abscess).  In  or- 
der to  produce  a  hyperresonant  sound  the  cavity  must  be  at  least  the 
size  of  a  walnut  (1x1^  inch),  and  either  lie  just  beneath  the  chest 
wall  or  be  put  in  touch  with  the  pleximeter  by  intervening  solid 
lung  {B  and  A  Fig.  117). 

(7)  It  must  be  reiterated  that,  owing  to  the  presence  of  the  stom- 
ach, tympanitic  resonance  of  varying  perfection,  in  the  anterior  axil- 
lary line,  from  the  6th  rib  downward,  is  a  normal  finding.  If  the 
stomach  is  greatly  distended  with  gas  the  tympanicity  may  begin  as 
high  as  the  ith  or  even  the  3d  interspace. 

(8)  Tympany  over  the  usual  area  of  exposed  liver  dulness,  from 
the  6th  rib  downward  in  the  axillary  line,  may  occur  in  great  gaseous 
distention  of  the  intestines  as  well  as  from  the  presence  of  air  in  the 
peritoneal  cavity,  so  that  the  transition  in  this  case  is  from  pulmo- 
nary resonance  to  tympanitic  resonance,  instead  of  the  normal  dull 
sound. 

(9)  Amphoric  resonance  is  a  tympanitic  sound  with  an  added 
metallic  clanging  or  echoing  quality.  It  is  rather  higher  in  pitch 
but  of  longer  duration  than  ordinary  tympany.  It  may  be  imitated 
by  percussing  an  empty  vessel.  "With  reference  to  its  diagnostic 
significance,  it  should  be  remembered  that  it  is  due  either  to  pneu- 

28 


406  THE  EVIDENCES  OP  DISEASE 

mothorax,  provided  that  the  air  is  under  a  certain  degree  of  tension 
(not  too  great),  or  to  a  cavity  {B  and  E,  Fig.  117).  If  present  over 
a  cavity,  it  may  be  inferred  that  the  latter  is  at  least  2^  inches  in 
diameter,  close  under  the  parietes,  and  with  smooth,  firm  walls.  If 
amphoric  resonance  is  suspected,  a  pleximeter  and  percussion  ham- 
mer may  be  used,  these  instruments  tending  to  develop  this  peculiar 
quality  of  sound  better  than  finger  percussion  alone,  especially  if 
simultaneous  auscultation  is  made.  If  due  to  pneumothorax  and 
not  to  a  cavity,  the  discrimination  may  be  made  by  noting  the  much 
greater  extent  over  which  it  is  heard  in  the  former. 

(10)  The  c7'acked-pot  sound  is  tympanitic,  but  has  a  superadded 
peculiar  hissing,  chinking  quality.  The  hissing  component  of  the 
sound  resembles  and,  indeed,  is  sometimes  due  to  an  outrush  of  air 
from  under  the  percussed  surface  through  the  upper  air  passages. 
The  chinking  element  resembles  the  sound  heard  on  tapping  a 
cracked  metal  vessel.  The  sound  as  a  whole  may  be  roughly  imi- 
tated by  clasping  the  hands  loosely  together  and  striking  them  over 
the  knee.  If  the  presence  of  this  sound  is  suspected  the  percussion 
stroke  should  be  sharp  and  rather  strong,  and  the  plexor  finger, 
after  its  descent,  allowed  to  rest  upon  the  pleximeter  finger,  thus 
adding  a  species  of  push  to  the  stroke.  The  patient's  mouth  should 
be  open  and  percussion  made  during  expiration. 

The  diagnostic  value  of  this  sign  is  somewhat  varied.  It  may  be 
obtained  from  the  chest  of  a  healthy  infant  (es2)ecially  while  crying) 
and  in  some  normal  adults.  If  occurring  (Fi^.  119)  over  one  apex  in 
a  thin  chest  wall,  it  may  be  due  to  a  cavity  having  a  communication 
with  a  bronchus ;  if  over  the  lower  half  of  one  side  of  the  chest,  to 
pneumothorax  opening  by  a  fistula  into  a  bronchus,  or  communicat- 
ing with  the  external  air  by  an  opening  through  the  chest  wall.  It 
may  also  be  elicited  from  the  lung  above  pleural  effusions,  and  in  the 
congestive  stage  of  pneumonia  (Fig.  118). 

(11)  There  are  certain  alterations  of  pitch — sound  mutation  or 
change  —  found  in  hyperresonant  percussion  notes  over  cavities, 
which  are  detected  by  and  partly  dependent  upon  special  postural  or 
other  disposition  of  the  patient.     These  changes  are : 

Wintricli's  Phenomenon. — If  a  tympanitic  note  becomes  louder 
and  raised  in  pitch  when  the  patient  opens  his  moutli.  protrudes  his 
tongue,  and  breathes  quietly,  it  is  suggestive  of  a  cavity  having  free 
communication  with  a  bronchus.  It  can  be  simulated  by  percussing 
over  the  trachea  while  opening  and  closing  the  mouth.  It  may  be 
obtained  in  cases  of  pneumothorax  with  a  large  fistulous  opening 
into  a  brondhus.  In  both  of  these  instances  (Fig.  119)  the  percus- 
sion vibrations  over  the  cavity  are  directly  transmitted  to  the  col- 


PERCUSSION  OP  THE  LUNGS 


407 


umn  of  air  in  the  bronchi  and  trachea,  and  the  opening  of  the  mouth 
allows  the  pharynx  to  act  as  a  resonator,  thus  causing  the  change  of 
sound.  It  may  occur  over  the  upper  lobes,  if  the  latter  are  consoli- 
dated' by  inflammation  or  compressed  by  pleural  effusion  (Fig.  118). 


Cracked-pot  percussion 
winthich's  phenomenon 
Pectoriloquy 
Amphoric  respiration 


Crackeo-pot  percussion 
Wintrich's  phenomenon 

FRIEDREICH'S    phenomenon 

Bronchial  respiration 
Pectoriloquy 


Tig.  119. — Showing  certain  percussion  and  ausrultatniy  lindimrs  over  cavity  or  jouuiuo- 
thorax,  provided  each  eoinnmnicates  lix-tly  with  a  bronchus. 

A  similar  change  of  sound,  normally  absent,  will  occur  when  per- 
cussing over  the  vpper  sternnm,  provided  that  the  tissues  lying  be- 
tween the  manubrium  and  the  trachea  are  of  sufficiently  increased 
consistence  to  conduct  the  percussion  vibrations  to  the  tracheal  air 
column  (Hoover).  Thus,  in  lymphosarcoma  of  the  mediastinum, 
aneurism  of  the  ascending  arch  of  the  aorta,  and  in  some  cases  of 
pericardial  effusion,  this  sign,  when  elicited  by  percussion  over  the 
manubrium,  has  been  of  much  value  in  diagnosis,  as  it  is  not  pres- 
ent in  cavity  or  consolidation  of  the  upper  lobes,  or  in  pleural  effu- 
sion. Certain  precautions  are  necessary.  The  chin  should  be  ele- 
Tated,  the  mouth  opened,  and  the  tongue  protruded.  As  this  sign 
may  be  found  at  the  end  of  inspiration  only,  the  patient  should  be 


408 


THE  EVIDENCES  OF  DISEASE 


CRECT 


instructed  to  inspire  deeply,  and  continue  the  effort  so  as  to  prevent 
the  instinctive  closure  of  the  glottis,  which  usually  takes  place  when 
the  breath  is  held  at  the  close  of  inspiration.  The  manubrium 
should  be  gently  percussed,  and  the  examiner's  ear  placed  close  to 

the  patient's  mouth.  The  metallic 
sound  when  present  is  readily  recog- 
nised. 

Interrupted  Wintrich^s  Plienoine- 
non. — If  the  change  just  described 
is  present  while  the  patient  is  in 
one  position — e.  g.,  recumbent — and 
disappears  in  another  posture — e.  g., 
erect — it  is  rare  but  reliable  evi- 
dence of  a  fluid-containing  cavity, 
the  secretion  in  one  position  occlu- 
ding, in  another  leaving  open,  the 
communicating  bronchus  (Fig.  120). 
Friedreich's  Plienomenon. — The 
resonance  over  a  cavity  opening  into 
a  bronchus  is  higher  in  pitch  dur- 
ing and  at  the  end  of  inspiration 
than  in  expiration.  This  respira- 
tory change  is  probably  due  to  the 
inspiratory  widening  of  the  glottis 
(channel  of  communication),  per- 
haps also  to  the  increased  tension, 
of  the  walls  of  the  cavity. 
Gerhardfs  Phenomenon. — If  the  pitch  of  the  percussion  sound 
over  a  cavity  varies  with  change  of  position,  it  is  indicative  of  a 
partly  filled  vomica,  one  diameter  of  which  is  considerably  longer 
than  the  others.  It  is  a  very  infrequent  finding,  but  is  good  proof 
of  a  cavity.  The  change  in  pitch  is  due  to  the  alteration  in  the 
shape  of  the  air-con^taining  part  of  the  cavity  caused  by  the  mobility 
of  the  fluid.  When  the  long  diameter  of  the  cavity  is  horizontal  the 
pitch  is  lowest  (Fig.  120). 

Biermer^s  Phenomenon. — In  pneumohydro thorax  the  percussion 
note  is  lower  when  the  patient  is  recumbent,  as  in  the  horizontal 
position  the  fluid  gravitates  upon  the  posterior  chest  walls,  thus  in- 
creasing the  long  diameter  of  the  air-filled  portion  of  the  pleural 
cavity.  The  explanation  of  the  change  in  pitch  is  similar  to  that  of 
the  preceding  (Gerhardt's)  phenomenon. 

(d)  Coin  Percussion — This  is  employed  where  pneumothorax  is 
suspected.     The  mouthpiece  of  the  stethoscope  is  placed  upon  the 


RECUHBCNT. 

Fig.  120. 


AUSCULTATION  OP  LUNGS 


409 


Absent  coin  (or  anvil) 

SOUND 


back  of  the  chest  and  an  assistant  percusses  the  front  of  the 
chest,  using  two  coins  (25  or  50  cent  pieces  preferably),  one  as  a 
pleximeter,  the  edge  of  the  other  as  a  plessor  (Fig.  121).  If  there 
is  air  in  the  pleural  cavity,  a  sound  {bruit  d'airain)  variously 
described  as  metallic  and 
echoing,  a  distant  soft  mu- 
sical chiming,  as  of  a  bell 
(bell  tympany)  or  a  far-off 
ring  of  a  hammer  on  anvil, 
is  heard — a  most  charac- 
teristic sign  of  this  condi- 
tion. Comparison  should 
be  made  with  the  opposite 
side.  By  noting  the  cessa- 
tion of  the  characteristic 
sound,  which  ceases  over 
lung  tissue,  the  outlines  of 

,,  .  +    •    ■  Fig.  121. — Showing  the  utility  of  coin  percussion,  also 

o       "  amphoric   respiration  and  pectoriloquy  over  an 

can  be  delimited.  open  pneumothorax. 


Amphoric  respiration 

Pectoriloquy      with 

amphoric  quauty 


Present  coin  (or  anvil) 

sound 


V.    AUSCULTATION    OF    LUNGS 

Auscultation  of  the  lungs  has  for  its  objects  the  determination 
of  the  character  of  the  breath  sounds,  the  presence  or  absence  of  ad- 
ventitious sounds,  and  the  amount  and  character  of  vocal  resonance. 

(A)   Teclinic  of  Auscultation 

Certain  points  with  reference  to  auscultation  of  the  lungs  in  par- 
ticular may  be  stated  here. 

The  patient  should,  if  practicable,  be  examined  in  the  sitting 
posture.  If  too  ill  for  this,  he  may  be  gently  turned  from  one  side 
to  the  other ;  or  a  flattened,  disklike  chest  piece  (Smith)  may  be 
used  for  the  back.  In  diseases  of  the  lung  which  confine  the  pa- 
tient to  bed  and  require  more  or  less  frequent  examinations  of  the 
back  (e.  g.,  pneumonia),  it  is  a  great  convenience  to  have  the  night- 
dress put  on  wrong  side  forward,  or  slit  down  the  back. 

In  the  majority  of  cases  it  is  necessary  to  direct  the  patient  how 
to  breathe,  as  it  is  of  great  importance  that  the  respirations  should 
be  deep,  regular,  quiet,  and  not  too  rapid,  so  far  as  such  qualities 
can  be  voluntarily  secured.  If  the  respirations  are  shallow,  valuable 
evidence,  such  as  distant  bronchial  breathing,  fine  rales,  etc.,  may  be 
overlooked.  If  irregular,  noisy,  and  rapid,  it  is  difficult  to  make 
certain  fine  discriminations  which  are  desirable.  The  desired  end  is 
most  conveniently  accomplished  by  a  personal  demonstration  on  the 


410  THE  EVIDENCES  OP  DISEASE 

part  of  the  examiner.  It  is  also  desirable,  when  possible,  to  cause  a 
temporary  cessation  of  moaning,  grunting,  or  noises  in  the  pharynx 
or  nares ;  or,  if  this  be  impracticable,  to  guard  against  mistaking  such 
sounds  for  those  of  intrathoracic  origin. 

(B)  Varieties  and  Characteristics  of  the  Normal 
Breath  Sounds 

There  are  three  kinds  of  breath  sounds  which  are  heard  normally 
in  certain  parts  of  the  chest,  but  if  found  over  other  portions  are  in- 
dicative of  disease.  Two  of  these  are  types,  the  third  is  a  combina- 
tion of  the  other  two — hroncliial^  vesicular,  and  broncho-vesicular. 

(1)  Bronchial  Breathing. — If  the  stethoscope  is  placed  over  the 
trachea,  just  above  the  suprasternal  notch,  two  sounds  are  heard,  one 
during  inspiration,  the  other  during  expiration,  separated  by  a  dis- 
tinct pause  or  silence,  just  previous  to  the  end  of  inspiration.  They 
are  of  practically  equal  length,  and  if  any  difference  exists  it  is  usu- 
ally that  the  expiratory  element  is  the  longer.  The  quality  of  both 
sounds  is  that  which  is  descriptively  termed  blowing,  tubular,  hollow, 
or  bronchial ;  the  pitch  of  both  is  higher  than  that  of  vesicular  res- 
piration. The  expiratory  element  is  more  intense  and  frequently  of 
higher  pitch  than  the  inspiratory  sound. 

This  breath  sound  is  caused  by  the  air,  which,  when  passing 
through  the  chink  of  the  glottis,  is  thrown  into  rotary  eddies,  and 
imparts  its  motion  to  the  air  columns  in  the  trachea  and  bronchi. 
It  may  be  imitated  by  placing  the  mouth  and  tongue  in  position  to 
sound  the  soft  German  cJi,  and  expiring  slowly. 

(2)  Vesicular  Breathing. — If  one  listens  to  the  breathing  over  a 
portion  of  the  lung  which  lies  some  distance  away  from  the  trachea 
and  larger  bronchi — e.  g.,  in  the  axillary  or  infrascapular  spaces — a 
sound  will  be  heard,  the  character  of  which  is  variously  described  as 
soft,  breezy,  sighing,  or  resembling  the  rustling  of  leaves  in  a  gentle 
wind — vesicular  respiration.  This  sound  is  audible  during  the  wliole 
of  inspiration,  and  is  immediately  followed,  without  an  interval  of 
silence  unless  the  breath  is  held,  by  a  short  expiratory  sound.  The 
inspiratory  element  is  moderately  intense,  low  in  pitch,  possesses  the 
true  breezy,  vesicular  quality,  and  is  3  times  the  length  of  the  ex- 
piratory element ;  while  the  expiration,  which  may  be  inaudible,  is 
less  intense,  somewhat  lower  in  pitch,  has  a  slight  blowing  as  well  as 
rustling  quality,  and  is  only  one  third  as  long  as  the  sound  of  inspi- 
ration. To  avoid  confusion  it  may  be  recalled  that  the  movements  of 
inspiration  and  expiration  are  to  each  other  in  point  of  duration  as  5 
to  6  respectively,  while  the  sounds  of  (vesicular)  respiration  stand  in 
the  ratio  of  3  to  1.     Vesicular  breathing  may  be  imitated  by  placing 


AUSCULTATION   OF  LUNGS 


411 


the  lips  and  teeth  in  position  to  articulate  the  letter/,  and  then  in- 
spiring slowly  and  steadily. 

The  exact  mode  of  origin  of  the  vesicular  sound  is  still  somewhat 
uncertain.  By  one  hypothesis  it  is  conceived  to  arise  from  the  pass- 
age of  air  into  and  out  of  the  infundibuli  and  alveoli ;  by  the  other  it 
is  considered  to  be  the  sound  of  bronchial  breathing  originating  in 
the  trachea  and  larger  bronchi,  transmitted  to  the  surface  and  modi- 
fied by  passing  through  the  spongy  vesicular  lung  tissue,  certain 
acoustic  elements  of  the  sound  having  been  absorbed  or  dissipated  in 
transit.  "Without  question  the  latter  hypothesis  best  explains  the 
modifications  of  the  breath  sounds  Avhich  are  heard  in  disease.  Thus 
bronchial  breathing  is  heard  over  a  consolidated  portion  of  the  lung, 
because  the  mitigating  effect  of  the  spongy  lung  tissue  is  abolished, 
and  the  tracheo-bronchial  breath  sounds  are  transmitted  with  little 
or  HO  restraint  through  the  well- 
conducting  solid  lung.  While 
the  major  portion  of  vesicular 
breathing  is  unquestionably  a 
modification  of  the  tracheo- 
bronchial sound,  it  is  possible 
that  a  minor  portion  may  be  con- 
ceded to  arise  from  the  entrance 
and  exit  of  air  into  and  from  the 
terminal  bronchioles  and  alveoli. 

(3)  Broncho-vesicular  Breath- 
ing.— This  is  a  form  of  breath- 
ing which  is  neither  distinctly 
bronchial  nor  distinctly  vesicular 
in  its  characteristics,  and  is 
therefore  sometimes  spoken  of 
as  "  indeterminate."  It  may  be 
heard  in  the  healthy  chest  over 
the  lower  portion  of  the  manu- 
brium, and  over  the  interscapu- 
lar regions  at  the  level  of  the  3d 
dorsal  vertebra  —  i.  e.,  over  por- 
tions of  the  chest  where  the  lar- 
ger bronchi  are  within  auscul- 
tating distance,  but  a  certain, 
not  great,  thickness  of  spongy 
lung  intervenes  between  the  ear 

and  the  main  bronchi,  thus  affording  a  breath   sound  with  com- 
mingled bronchial  and  vesicular  characters. 


Fio.  122.— Dotted  area  shows  where  bron- 
chial  (larger  dots)  and  broncho-vesicu- 
lar (smaller  dots)  breathing  normally 
exist.  Note  higher  origin  of  bronchus 
to  right  upper  lobe  compared  with  that 
to  left  upper  lobe.  Shows  also  line  of 
demarcation  between  upper  and  lower 
lobes  of  left  lung  anteriorly  (see  page 


412 


THE  EVIDENCES  OF  DISEASE 


It  is  necessary  not  only  to  become  thoroughly  familiar  with  these 
three  varieties  of  breathing,  and  the  special  characters  which  serve 
to  differentiate  one  from  the  other,  but  to  know  as  well  in  what  parts 
of  the  chest  they  may  normally  be  heard.  In  many  cases  of  pulmo- 
nary disease  the  principal  and  important  physical  sign  consists  in 
finding  one  kind  of  breath  sound  in  a  place  where  another  variety 
should  normally  exist — e.  g.,  bronchial,  instead  of  vesicular,  respira- 
tion over  an  infraclavicular  space.  It  sliould  be  remembered,  there- 
fore, that  in  the  normal  individual  vesicular  respiration  should  be 
found  in  all  parts  of  the  chest,  except  over  and  in  the  close  neigh- 
bourhood of  the  trachea  and  the  main  and  larger  bronchial  tubes. 

Consequently  (see  Fig.  122),  anteriorly^  bronchial  breathing  is 
found  in  the  anterior  (and  antero-lateral)  portions  of  the  neck,  from 

larynx  down  to  the  supra- 
sternal notch  and  over 
the  upper  portion  of  the 
manubrium.  Broncho- 
vesicular  respiration  is 
normal  over  the  lower 
portion  of  the  manubri- 
um, and  over  the  right 
and  left  sternal  edges 
at  the  same  level.  The 
breathing  in  the  right  in- 
fraclavicular space  is  nor- 
mally somewhat  harsher 
and  the  expiration  more 
prolonged  than  in  the 
corresponding  left  space, 
because  of  the  greater 
size  and  higher  origin  of 
the  large  bronchus  going 
to  the  right  upper  lobe. 
Posteriorly  (Fig.  123), 
bronchial  respiration  ex- 
ists over  the  lower  two 
or  three  cervical  verte- 
brae; broncho-vesicular  breathing  below  the  vertebra  prominens  as 
far  down  as  the  3d  or  4th  dorsal,  and  for  a  short  distance  to  right 
and  left  of  the  spine  at  this  level,  more  marked  on  the  right 
side. 

The  vesicular  breathing  over  the  remainder  of  the  chest  does  not 
vary  in  quality,  but  does  vary  in  intensity^  according  to  the  thickness 


Fio.  123.— Showin<r  tlie  site  of  iioriual  bronchial  (large 
dots)  and  broncho-vesicular  (small  dots)  respira- 
tion posteriorly. 


AUSCULTATION  OF  LUNGS 


413 


of  the  chest  wall  (pectoral  muscles,  mammary  gland,  scapula) ;  and  the 
amount  of  lung  substance  underlying  the  point  of  auscultation  (small 
amount  at  apices  and  over  the  thin  lower,  especially  anterior,  borders). 

(C)  The  Breath  Sounds  in  Disease 

In  all  cases  the  examiner  should  carefully  note  at  each  point  the 
relative  length  of  inspiration  and  expiration  after  having  distin- 
guished them ;  and  the  character^  whether  soft  and  vesicular,  harsh, 
blowing,  or  uncertain,  both  of  inspiration  and  expiration  (Fig.  124). 

{a)  Bronchial  Breathing. — In  the  majority  of  cases  bronchial 
breathing  signifies  consolidation  (exudate,  compression)  of  the  lung, 
the  solidified  tissue  acting  as  an  excellent  transmitter  of  the  breath 
sounds  ( G^  Fig.  124) ;  in  other  cases  a  large  cavity  having  free  com- 
munication with  a  bronchus  is  responsible  {A  and  J5,  Fig.  124). 


CAVITY   WITH 

SMOOTH,  FIRM 

WALLS 


Amphoric  breathing 
Pectoriloquy 

OFTEN 

Bronchial  breathing 


Bronchial  or 
Cavernous    respira- 
tion 


c 

PLUGGED     BRON- 
CHUS, WITHOUT 
CONSOLIDATION 

/ 

/ 

Absent    vesicular 
breathing 

Lessened  vocal  res- 
onance 

D 

PLUGGED    BRON- 
CHUS, WITH 
CONSOLIDATION 

\ 

Absent      bronchial 
respiration 

Absent  vocal  reso- 
nance 

\ 

E 

DEEP 
CONSOLIDATION 

Broncho  -  vesicular 
breathing 

Increased  vocal  res- 
onance 

i 

PARTIAL 
CONSOLIDATION 

F 

Broncho  -  vesicular 
breathing 

Increased  vocal  res- 
onance 

COMPLETE 
CONSOLIDATION 

G 

Bronchial    respira- 
tion 
Bronchophony  or 
Pectoriloquy 

H 

CONSOLIDATION 
WITH    EFFUSION 

Distant     bronchial 
breathing 

Fig.  124. — Schematic  diagram  of  the  varieties  of  breathing  and  vocal  resonance  in  disease. 

Bronchial  respiration  in  diseased  conditions  varies  in  pitch  and 
to  some  extent  in  quality.  If  the  sound  is  transmitted  directly  from 
the  larger  bronchi  by  consolidation  or  cavities  it  is  low  pitched,  and 
may  have  the  qualities  knoAvn  as  cavernous  or  amphoric.  On  the 
other  hand,  if  it  arises  from  consolidation  around  the  medium  and 
smaller  tubes,  it  is  high  pitched  and  whiffing,  as  in  pneumonia  involv- 


414 


THE  EVIDENCES  OF  DISEASE 


ing  the  bases  of  the  lungs.  A  practical  point  to  be  remembered  is 
that  bronchial  breathing  may  be  present  and  yet  not  heard,  unless 
the  patient  takes  a  full  and  deep  breath,  a  precaution  which  should 
never  be  omitted.  The  clinical  varieties  and  significance  of  this 
form  of  breathing  are  as  follows  : 

(1)  If  heard  at  the  base  of  the  lung,  it  signifies  most  commonly 
pneumonia,  exceptionally  tuberculosis ;  at  the  apex,  tuberculosis,  or 
(above  the  level  of  the  fluid)  compression  of  the  lung  by  pleural  effu- 
sion, less  frequently  pneumonia.  Much  more  rarely  it  results  from 
gangrene,  beginning  abscess,  a  septic  or  non-septic  infarction,  or 
compression  of  the  lung  by  aneurism  or  tumour. 

(2)  In  certain  cases  distant  bronchial  breathing  is  heard — i.  e., 
the  sound  does  not  appear  to  emanate  from  the  surface  of  the  chest. 
In  such  a  case  one  must  endeavour  further  to  determine  whether  it 

is  a  pure  but  far-away  bronchial  respiration, 
or  whether  it  is  mixed  with  a  vesicular  ele- 
ment (broncho-vesicular  respiration).  If  dis- 
tant but  pure  bronchial  breathing  is  heard 
(especially  at  the  base),  there  is  probably  a 
large  pleural  effusion  present  (Fig.  125),  and 
corroborative      evidence 

1     (displacement     of     the 

apex  beat,  characteristic 
history)  must  be  sought. 
Such  cases  are  not  un- 
common, and  exploratory 
puncture,  especially  in 
children,  maybe  required 
to  make  the  discrimina- 
tion between  fluid  and  consolidation.  Similar  breathing  may  be 
heard  if  effusion  and  consolidation  coexist  {H,  Fig.  124).  If  the 
breathing  is  vesicular  as  well  as  bronchial,  there  is  probably  a  deep- 
lying  consolidated  area — e.  g.,  a  central  pneumonia,  with  spongy  lung 
tissue  intervening  between  it  and  the  chest  wall  {E,  Fig.  124). 

(3)  Low-pitched  bronchial  respiration,  with  a  notably  hollow 
quality,  constitutes  amphoric  breathing.  It  may  be  imitated  by 
blowing  partly  into,  partly  across,  the  mouth  of  an  empty  bottle. 
Not  infrequently  cavernous  is  mistaken  for  amphoric  breathing. 
The  latter  can  be  said  to  exist  only  when  the  peculiar  musical,  hol- 
low intonation  is  present. 

Amphoric  respiration  is  never  found  in  the  normal  chest,  and 
when  discovered  indicates  one  of  two  things :  a  superficial  cavity 
with  smooth,  firm  walls,  communicating  with  a  bronchus  (J,  Fig. 


Absent  respiration 
Absent  vocal  resonance 

sometimes 
Distant  bronchial  breathing 


Fig.  125. — Showing  the  results  of  auscultation  over  a 
pleural  effusion. 


AUSCULTATION  OP  LUNGS  415 

124) ;  or  an  open  pneumothorax — i.  e.,  one  in  which  there  is  a  large 
patent  bronchial  fistula  (Fig.  119,  also  A^  Fig.  121).  The  pitch  of 
this  variety  of  breathing  varies  with  the  size  of  the  cavity, 

(5)  The  absence  of  bronchial  breathing,  when  it  might  reason- 
ably be  expected,  or  its  rather  abrupt  disappearance  when  previously 
found,  may  be  due  to  the  plugging  of  a  large  bronchus  leading  to 
the  consolidated  area,  thus  preventing  the  transmission  of  the  sound 
from  the  trachea,  and  coughing  may  make  it  manifest  (Z>,  Fig.  124). 
The  filling  up  of  a  cavity  with  secretion  may  abolish  cavernous  or 
amphoric  breathing,  which  will  return  when  the  fluid  is  raised  and 
expectorated. 

(b)  Bronclio-vesicular  Breathing. — One  of  the  common  mistakes 
of  the  physical  diagnostician  in  his  days  of  pupilage  is  to  call  bron- 
cho-vesicular "  bronchial "  breathing.  There  are,  indeed,  so  many 
variations  between  pure  bronchial  and  pure  vesicular  respiration  in 
diseased  conditions  that  such  an  error  is  excusable,  and  the  alternative 
names,  "  indeterminate  "  or  "  transition  "  breathing,  are  well  deserved. 
The  term  is  applied  to  a  breath  sound  of  which  either  inspiration  or 
expiration  has  more  or  less  of  the  harsh,  blowing  bronchial  quality, 
with  an  expiration  usually  as  long,  rarely  longer,  often  shorter,  than 
the  inspiration ;  or,  as  nearly  as  can  be  judged,  midway  between 
bronchial  and  vesicular. 

Broncho-vesicular  respiration  is  in  general  indicative  of  the  same 
pathological  conditions,  but  of  lesser  amount  and  degree,  as  bronchial 
breathing — i.  e.,  partial  consolidations,  small  patches  of  solid  or  col- 
lapsed lung,  or  consolidations  overlaid  by  unaffected  lung  (see  (2) 
under  (a)  preceding,  also  B  and  F,  Fig.  ]24).  If  harsh  broncho- 
vesicular  respiration,  with  prolonged  expiration,  is  heard  perma- 
nently at  one  apex,  especially  the  left,  it  is  very  significant  of 
tuberculosis.  With  reference  to  this  form  of  breathing  it  must 
be  confessed  that  at  times  one  may  remain  doubtful  as  to  its 
exact  meaning. 

(c)  Vesicular  Breathing.— While  retaining  its  characteristic  quali- 
ties, vesicular  respiration  presents  certain  variations  of  diagnostic  im- 
portance.    It  may  be — 

(1)  Weak  or  Absent.— In  old  persons  the  vesicular  breathing  is 
normally  of  slight  intensity  (senile  respiration),  so  also  in  some 
younger  individuals  when  breathing  quietly.  The  respiratory  mur- 
mur is  weak  in  emphysema,  as  the  air  cells  are  permanently  much 
distended,  comparatively  little  air  enters,  and  conduction  of  the 
tracheal  sound  is  impaired.  Weakness  may  be  due  also  to  fat  chest 
walls,  thickened  or  adherent  pleura,  and  a  moderate  pleural  effusion. 
Absence  or  weakness  of  vesicular  breathing  may  be  found  over  the 


416  THE   EVIDENCES  OF  DISEASE 

area  of  lung  supplied  by  an  obstructed  bronchus  (foreign  body,  pres- 
sure, or  secretion,  (7,  Fig.  124) ;  over  a  closed  pneumothorax  (one 
not  communicating  with  a  bronchus) ;  over  large  pleural  effusions 
(Fig.  125),  in  which  case  either  the  relaxed  lung  fails  to  vibrate,  or 
the  fluid  acts  under  such  circumstances  as  a  poor  transmitter  of 
sound;  over  portions  of  a  fibroid  lung;  and  sometimes  over  the 
earliest  state  of  a  tuberculous  apex. 

(2)  Increased  or  Puerile. — Loud  vesicular  breathing  is  normal  in 
infants  and  children,  diminishing  in  intensity  up  to  the  age  of  12 
years.  It  is  sometimes  confounded  with  bronchial  respiration  by  the 
inexperienced  auscultator,  and  closely  resembles  broncho-vesicular 
breathing ;  but  no  matter  how  intense  and  apparently  harsh  it  may 
be,  the  normal  ratio  between  the  length  of  inspiration  and  expira- 
tion is  retained.  In  the  adult  the  respiration  over  the  right  infra- 
clavicular space  and  apex  normally  approaches  this  type.  It  is  heard 
in  many  cases  of  dyspnoea,  especially  from  cardiac  causes,  because  of 
the  increased  vigour  of  the  respiratory  movements.  Puerile  breathing 
over  one  lung  is  usually  compensatory  for  disease  of  the  other  lung 
(extensive  consolidation,  effusion,  or  congestion),  or  in  a  portion  of 
one  lung  for  disease  in  the  remainder  of  the  same  lung. 

(3)  Harsh  or  Prolonged  Expiration. — Under  this  name  are  in- 
cluded certain  forms  of  vesicular  respiration  which  differ  from  the 
type  by  having  an  unusually  harsh  or  prolonged  expiration.  When 
it  is  heard  over  both  sides  of  the  chest,  and  is  rather  soft  and  low- 
pitched,  it  is  usually  due  to  asthma  or  emphysema  with  bronchitis. 
The  most  important  diagnostic  occurrence  of  prolonged  expiration, 
especially  if  high  pitched,  is  its  discovery  over  an  apex  of  the  lung 
as  an  early  sign  of  tuberculosis.  When  found  over  the  left  apex  it  is 
very  significant  of  disease ;  but  at  the  right  apex,  in  the  absence  of 
other  signs  (rales,  elevated  temperature,  etc.),  its  diagnostic  value  is 
by  comparison  slight,  because  of  the  normal  existence  at  that  point 
of  puerile  or  moderately  broncho-vesicular  breathing. 

(4)  Cog-wheel  Breathing. — Jerky,  wavy,  or  interrupted  breathing — 
vesicular  respiration,  with  short,  irregular  intermissions,  especially  dur- 
ing inspiration — is  by  itself  of  little  diagnostic  value.  It  is  observed 
in  healthy  but  nervous  individuals,  and  is  due  in  this  case  to  the  lack 
of  smooth  muscular  respiratory  action.  In  disease  it  is  caused  either 
by  the  air  forcing  its  way  by  a  series  of  efforts  through  the  small 
bronchioles,  the  air  column  being  broken  and  delayed  by  tenacious 
mucus,  or  by  the  expansion  of  different  lobules  at  different  times — 
for  the  same  reasons — or  by  both.  It  may  be  confused  with  the  car- 
dio-pulmonary  whiff  due  to  rapid  and  excited  action  of  the  heart. 
The  conditions  for  its  production  are  present  in  early  and  late  phthisis. 


AUSCULTATION  OF  LUNGS  417 

(D)  The  Voice  Sounds  in  Health  and  Disease 

Having  applied  the  stethoscope,  if  the  patient  is  asked  to  speak 
aloud  with  his  face  turned  away  from  the  examiner,  a  buzzing  noise 
without  any  semblance  of  articulate  sounds  is  perceived.  It  varies  in 
intensity  according  to  the  loudness  and  depth  of  the  subject's  voice, 
and,  following  a  suggestion  by  Rainy,  seems  to  originate  at  the  sur- 
face of  the  chest.  The  nearer  the  stethoscope  is  placed  over  the 
main  bronchi,  the  more  decided  is  the  buzzing  sound — the  vocal 
resonance.  Consequently,  it  is  well  marked  over  the  right  upper 
chest.  Just  as  the  vocal  fremitus  consists  of  the  vocal  vibrations 
transmitted  from  the  larynx  through  the  tracheo-bronchial  air  col- 
umns and  the  substance  of  the  lung  to  the  chest  wall,  so  the  vocal 
resonance  consists  of  the  same  vibrations  appreciated  by  the  sense  of 
hearing,  and  it  varies  in  intensity  under  similar  conditions.  The 
variations  in  vocal  resonance  and  their  significance  are  as  follows : 

(1)  Lessened  or  Absent  Vocal  Resonance. — If  the  sound  is  indis- 
tinct, and  seems  to  come  from  a  point  more  or  less  below  the  surface 
of  the  chest,  or  no  vibration  whatever  is  perceived,  one  may  infer 
that  there  is  a  pleural  effusion  (Fig.  125),  thickening  of  the  pleura, 
or  obstruction  of  a  large  bronchus  by  pressure  or  a  mucous  plug 
(Cand  Z),  Fig.  124).     It  is  also  weakened  in  emphysema. 

(2)  Increased  Vocal  Resonance. — If  the  sound  is  insistent,  and 
appears  to  be  produced  not  far  from  the  examiner's  ear,  the  vocal 
resonance  is  increased.  If  the  increase  is  very  well  marked  it  is 
bronchophony.  Its  most  common  cause  is  consolidation  of  the  lung 
in  the  neighbourhood  of  the  larger  or  medium  bronchi  {E,  i^,  and  G, 
Fig.  124).  The  causes  of  increased  vocal  fremitus  (page  395)  are  also 
the  causes  of  bronchophony. 

(3)  Pectoriloquy. — If  the  sounds  become  articulate,  the  uttered 
words  being  apparently  spoken  directly  into  one's  ear,  it  is  pectoril- 
oquy^ and  denotes  either  a  consolidation  connecting  a  large  bronchus 
with  the  chest  wall,  and  acting  as  an  unusually  perfect  conductor 
((?,  Fig.  124) ;  the  presence  of  a  cavity  having  a  free  communication 
with  a  bronchus  (Fig.  119,  also  J,  Fig.  124) ;  an  open  pneumothorax, 
one  having  free  communication  with  a  bronchus  (Fig.  119) ;  or,  more 
rarely,  is  observed  over  the  compressed  lung  above  a  large  pleural 
effusion  (Fig.  118).  When  pectoriloquy  is  extremely  distinct  it  is 
fairly  reliable  evidence  of  a  cavity. 

(4)  Whispering  Pectoriloquy. — If,  instead  of  speaking  aloud,  the 
patient  is  required  to  wliisper,  nothing  but  a  slight  distant  expira^ 
tory  whiff  is  heard  in  the  normal  lung  with  each  syllable  of  the  whis- 
pered words.     But  when  the  conditions  which  cause  bronchophony 


418  THE  EVIDENCES  OF  DISEASE 

and  pectoriloquy  are  present,  the  whiffing  sound  is  nearer  and  more 
distinct,  according  to  the  increase  in  the  conductivity  of  the  lung ; 
and  if  the  conductivity  is  perfect,  or  a  cavity  exists,  the  words  them- 
selves are  heard  with  curious  distinctness  and  Lilliputian  dimen- 
sions. The  use  of  the  whispered  voice  is  a  much  more  accurate  and 
discriminating  method  of  estimating  the  state  of  the  vocal  reso- 
nance, than  to  have  the  patient  speak  aloud.  Its  employment  should 
be  routine. 

Here  may  be  mentioned  "  BacelWs  sign  " — i.  e.,  that  the  whispered 
voice  is  transmitted  readily  and  distinctly  through  a  pleural  effusion, 
provided  the  fluid  is  serous ;  while  if  the  efi'usion  is  purulent  and 
therefore  denser,  the  whispered  voice  is  not  transmitted,  thereby 
permitting  a  differential  diagnosis  between  a  simple  serous  pleurisy 
and  an  empyema.  It  is  a  sign  which  is  unquestionably  of  some 
service,  but  if  the  serous  effusion  is  large  the  whisper  may  fail  of 
transmission. 

(5)  Egophony. — When  the  voice  has  a  peculiar  nasal,  tremulous, 
or  quavering  intonation,  resembling  somewhat  the  bleating  of  a  goat, 
it  is  termed  egophony.  It  is  heard  at  and  Just  below  the  upper  limit 
of  moderate  pleural  effusions,  and  is  usually  best  perceived  at  the 
angle  of  the  scapula,  or  the  space  between  the  angle  and  the  poste- 
rior axillary  line.  No  very  satisfactory  explanation  of  the  mechan- 
ism of  its  causation  has  as  yet  been  offered.  It  is  variously  attributed 
to  collapse  of  the  bronchial  tubes  or  to  the  interception  by  the  effu- 
sion of  the  fundamental  tones  of  the  voice,  the  overtones  remaining. 

(6)  Amplioric  Vocal  Resonance. — The  voice  has  a  metallic  echoing 
quality  in  pneumothorax,  similar  in  all  respects  to  the  breath  sounds 
under  the  same  circumstances. 

(E)  Adventitious   Sounds   or  Accompaniments 

In  normal  lungs  nothing  is  heard  but  the  breath  sounds,  but  in 
diseased  conditions  various  additional  sounds  may  be  perceived, 
which  originate  either  in  the  lungs  or  the  pleura — as  follows : 

{a)  Relies. — This  is  the  generic  name  given  to  adventitious  sounds 
produced  either  in  the  bronchial  tubes  or  the  air  cells.  Rales  are 
divided,  according  to  the  impression  made  upon  the  mind  of  the  ob- 
server, into  dry  and  moist  (Fig.  126). 

(1)  Dry  Relies  (Rhonchi). — These  are  whistling,  squeaking  sounds 
caused  by  the  passage  of  air  through  bronchial  tubes  Avhich  are  partly 
occluded  by  swelling  of  the  mucosa,  or  by  spasm,  or  a  lining  of  tough, 
viscid  mucus.  If  high  pitched,  whistling,  and  heard  in  greatest 
abundance  toward  the  end  of  inspiration,  they  are  called  small  or 
sibilant  rales,  and  originate  in  the  smaller  tubes.    If  low  pitched  and 


AUSCULTATION  OF  LUNGS 


419 


of  greater  volume,  purring,  almost  snoring,  in  quality,  beginning 
early  and  continuing  during  inspiration,  and  perhaps  during  expira- 
tion also,  they  are  large  or  sonorous  rales,  having  their  seat  in  the 
larger  tubes.     Tubes  of  medium  size  afford  rales  of  medium  pitch. 


SONOROUS    / jn 

RALES      ^  ^ 


^METALL 
[tin  KLIN 
;OUCHI 

OR 
>UCCUSSI 
[SPLASHI 
SOUND 


GURGLING 
BUBBLING    Ri 
COARSE   OR 
MUCOUS  RALES, 
(ALSO  GURGLES) 
\nNEORSUBCREP. 
ITAIlifl-  RALES. 

EPITANT 
RALES. 


Fig.  126. — Adventitious  respiratory  sounds  or  accompaniments. 

In  many  cases,  especially  in  children,  sonorous  rales  may  be  heard  at 
a  distance,  and  are  readily  palpable  by  the  hand  upon  the  chest. 
These  riiles  are  significant  of  bronchitis  in  the  early  stage  when 


420  THE  EVIDENCES  OF  DISEASE 

the  bronchial  mucosa  is  congested  and  swollen,  with  perhaps  a  small 
amount  of  thick  secretion ;  are  heard  abundantly  and  typically  in 
bronchial  asthma  ("  nest  of  kittens  ") ;  and  isolated  sonorous  rales 
are  frequently  found  in  pulmonary  phthisis,  due  to  the  partial  block- 
ing of  a  bronchus  by  a  plug  of  tenacious  muco-pus. 

(2)  Moist  Rales. — Crepitations  or  moist  rales  are  produced  either 
by  the  expansion  of  previously  closed  alveoli,  or  the  passage  of  air 
through  fluid  in  the  bronchi  or  in  a  cavity.  Some  crepitations  origi- 
nate in  the  pleural  sacs.  Moist  rales  vary  in  size  and  character,  ac- 
cording to  the  calibre  of  the  tube  or  the  dimensions  and  nature  of 
the  cavity  in  which  they  are  created.  The  absence  of  rales  can  not 
be  affirmed  until  after  deep  inspiration  or  the  act  of  coughing. 

The  crepitant  rdle  is  the  finest  of  all  rales,  and,  although  classified 
as  moist,  possesses  a  dry  quality.  It  may  be  imitated  by  rubbing  a 
lock  of  the  hair  just  above  the  ear  between  the  thumb  and  fore- 
finger. It  is  caused  in  many  instances  by  the  separation  of  the  walls 
of  the  alveoli  and  terminal  bronchioles  previously  collapsed  or  ad- 
herent from  the  presence  of  exudate  or  fluid.  It  is  heard  typically 
as  a  shower  of  fine  crepitations  toward  the  end  of  inspiration.  This 
rale  was  formerly  considered  to  be  pathognomonic  of  pneumonia; 
but,  while  it  is  a  very  characteristic  finding  in  the  first  stage  of  this 
disease,  it  is  heard  also  in  pulmonary  oedema,  hemorrhagic  infarction, 
and  localized  atelectasis.  Mixed  with  larger  crepitations  it  may  be 
heard,  during  a  deep  inspiration,  over  the  apices,  in  those  who  habit- 
ually underinflate  the  lungs ;  over  the  bases,  in  those  who  have  been 
lying  for  some  time  in  the  dorsal  position,  especially  during  the 
course  of  an  exhausting  disease. 

It  is  further  to  be  noted  that  a  fine  pleural  friction  may  simulate 
the  crepitant  rale  so  closely  that  the  two  are  indistinguishable  by  the 
ear,  and  the  discrimination  must  be  made  by  the  preponderance  of 
the  associated  symptoms  and  signs.  Indeed,  it  is  a  question  whether 
the  crepitant  rale  should  not  be  defined  as  a  fine  crepitation  of  a  dry 
quality  produced  either  in  the  air  cells  or  the  pleura. 

Tlhefine  moist  or  siibcrepitant  rale  is  next  in  size  to  the  crepitant, 
and  originates  in  the  small  bronchi.  It  is  heard  both  during  inspira- 
tion and  expiration.  Rdles  of  this  character  indicate  the  presence  of 
fluid,  and  are  therefore  suggestive  of  bronchitis  in  the  stage  of  secre- 
tion (moist  replacing  dry  rales),  pulmonary  oedema,  or  hemorrhage 
into  the  tubes.  They  are  heard  temporarily  during  deep  inspiration 
in  disused  or  atelectatic  portions  of  the  lung,  disappearing  after  a  half 
dozen  respirations ;  in  the  later  stages  of  pneumonia  {rale  redux) ; 
and  around  the  borders  of  patches  or  areas  of  consolidation  from  any 
cause.     A  number  of  small,  moist  "  crackling  "  rales  at  one  apex  is 


AUSCULTATION  OF  LUNGS  421 

yery  significant  of  beginning  phthisis.  A  few  moist  rdles  at  the  base 
of  the  lungs  usually  indicate  slight  oedema,  hypostatic  congestion,  or 
disuse  of  the  lungs. 

Coarse,  large,  or  "  mucous  "  rdles,  existing  during  inspiration,  ex- 
piration, or  both,  originate  in  the  larger  bronchi,  and  arise  from  the 
same  causes  as  do  fine  or  subcrepitant  rales.  Large  rales  of  a  gur- 
gling or  bubbling  character  may  be  due  to  the  interrupted  passage  of 
air  through  a  considerable  amount  of  fluid  in  a  cavity  or  a  large 
bronchus,  and  are  best  developed  by  coughing  or  forced  breathing. 
They  are  most  commonly  heard  in  the  softening  stage  of  phthisis, 
more  rarely  in  bronchitis  with  profuse  secretion  and  bronchiectases. 

Hinging  or  metallic  rales  derive  their  peculiar  character  from  the 
acoustic  properties  (due  to  size,  shape,  character  of  walls,  contents) 
of  the  cavities  or  tubes  in  which  they  originate.  Such  rales  are  usu- 
ally found  over  the  upper  half  of  the  lungs  in  conjunction  with  am- 
phoric respiration  and  percussion  note,  and  accordingly  denote  cavi- 
ties, consolidation  around  large  bronchi,  or  compressed  lung. 

A  single  metallic  rale  {metallic  tinkling),  occurring  perhaps  in  a 
series  of  3  or  4,  after  coughing  or  deep  respiration,  is  due  to  pneu- 
mohydrothorax,  rarely  to  a  large,  partly  filled  cavity.  It  sounds  like 
and,  indeed,  is  the  falling  of  a  drop  of  fluid  from  the  surface  of 
the  lung  upon  the  surface  of  fluid  in  the  pleural  cavity  (Fig.  126). 
It  has  been  compared  to  the  dropping  of  water  into  a  cistern,  and 
derives  its  peculiar  characteristics  from  the  resonating  qualities  of 
the  air-containing  space. 

It  is  sometimes  difficult  to  decide  whether  a  given  sound  is  a  fine 
moist  rale  or  a  fine  friction  sound.  It  Avill  aid  in  the  discrimination 
to  remember  that  rales  may  be  caused  to  disappear  by  coughing  (re- 
moval of  fluid  from  the  tube) ;  that  they  are  less  superficial ;  not 
strictly  localized ;  are  heard  mainly  during  inspiration ;  and  have  a 
moist  quality. 

Two  other  clinical  points  may  here  be  noted.  First,  that  when 
bronchitis,  asthma,  and  pleural  effusion  coexist,  the  rales  may  be  so 
numerous  and  plainly  heard  that  the  presence  of  the  effusion  may 
readily  be  overlooked.  In  a  personal  case  of  this  kind  the  lessened 
resonance  and  the  displaced  heart  led  to  a  correct  diagnosis,  and 
aspiration  took  away  80  oz.  of  fluid.  Second,  that  if  the  temperature 
is  elevated  and  the  patient  evidently  quite  ill,  while  the  whole  chest 
is  filled  with  numerous  fine  and  coarse,  dry  and  moist  rales,  so  abun- 
dant as  utterly  to  obscure  the  breath  sounds,  a  diagnosis  of  broncho- 
pneumonia may  safely  be  made. 

(b)  Succiission  Sounds.— If,  when  the  upper  part  of  the  body  is 
somewhat  vigorously  shaken  from  side  to  side,  a  metallic  splashing 
29  " 


422  THE  EVIDENCES  OF  DISEASE 

sound  is  heard,  audible  at  a  distance,  it  is  almost  certain  evidence  of 
the  presence  of  air  and  fluid  in  the  pleural  cavity  (Fig.  126).  A 
similar  sound  originating  in  the  stomach  or  colon  may  be  a  source 
of  error.  Very  exceptionally  it  is  due  to  a  large,  partly  filled  lung 
cavity, 

(c)  Friction  Sounds.  —  Sounds  variously  described  as  rubbing, 
creaking,  grating,  rasping,  crepitating,  or  leathery  are  due  to  the 
friction  of  apposed  inflamed  and  fibrin-coated  pleural  surfaces.  If 
the  pleural  surfaces  are  subsequently  separated  by  effusion  the  sounds 
disappear,  and  may  return  when  the  fluid  is  absorbed.  Friction 
sounds  are  superficial — i.  e.,  give  an  impression  of  nearness  to  the 
ear ;  are  quite  strictly  localized  and  do  not  tend  to  shift  their  posi- 
tion; are  not  removed  or  perceptibly  modified  by  cough  or  forced 
respiration ;  can  sometimes  be  intensified  by  pressure  with  the  steth- 
oscope, which  is  painful ;  are  heard  especially  during  inspiration ; 
may  continue  during  expiration ;  and  at  times  become  palpable  (fric- 
tion fremitus).  Friction  sounds,  according  to  the  impression  made 
upon  the  observer,  may  also  be  classified  as  fine,  medium,  and  coarse. 
The  finer  frictions  may  very  closely  simulate  the  small  or  crepitant 
rale,  but  the  points  noted  in  the  preceding  sentence  will  in  most 
cases  serve  for  differentiation. 

Friction  sounds  over  the  thorax  signify  pleurisy  or  pericarditis, 
more  rarely  (over  lower  thorax)  peritonitis.  They  are  absent  in  be- 
ginning hydrothorax,  as  the  pleura  is  not  inflamed.  If  found  at  the 
base  of  the  right  lung  posteriorly,  or  over  the  7th,  8th,  or  9th  right 
interspace  anteriorly,  it  may  indicate  hepatic  abscess,  or  cancer,  or 
subphrenic  abscess  (subdiaphragmatic  peritonitis),  because  of  the  in- 
volvement either  of  the  peritoneal  covering  of  the  liver  (perihepati- 
tis) or  of  the  complementary  pleura  from  its  contiguity  to  the  in- 
flamed peritoneum  (Fig.  151). 

Subpleural  friction  (Riesmax)  is  a  soft  rubbing  or  fine,  soft  crepi- 
tation, without  pain  or  evidence  of  consolidation,  which  has  been 
observed  in  cases  of  miliary  tuberculosis,  the  tubercles  not  causing 
inflammatory  roughening  of  the  pleura  but  lying  just  beneath  and 
projecting  sufficiently  to  produce  the  sounds  observed. 


EXAMINATION  OP  THE  ABDOMEN 


423 


SECTION  XXXIU 

THE  ABDOMEN.     METHODS  AND  EESULTS  OF  ITS 
GENERAL  EXAMINATION 

It  is  desired  to  consider  here  the  topographical  anatomy  of  the  ab- 
domen, and  the  methods  and  results  of  its  general  physical  examinar 
Hon  by  inspection,  palpation,  percussion,  and  auscultation. 


I.  TOPOGRAPHICAL  MARKS,  AREAS,  AND  ANATOMY 
OF  THE  ABDOMEN 

Anatomical  Landmarks  of  the  Abdomen. — At  the  upper  portion  of 
the  abdomen,  the  ensiform  appendix  and  down-curving  arches  of  the 
ribs  are  important  landmarks  which  are  readily  identified.  At  the 
lower  part  of  the  abdomen,  the  iliac  crests  and  especially  the  anterior 


Linese  transversa? 
Linea  semilunaris 


Situation  of  fat 
grooves  in  the 
obese 


Beginning   of   ab- 
dominal aorta 

Coeliae  axis 
Renal  artery- 
Superior  mesen- 
teric artery 

Inferior    mesen- 
teric artery- 
Bifurcation  of 
aorta 


Fig.  127.— Showing  the  surface  and  bony  lamiinarks  of  the  al)domen  and  the  location  of 
the  abdominal  aorta  and  its  more  important  branches. 

superior  spines  of  the  ilium  are  easily  found,  even  in  the  obese.  The 
symphysis  pubis  marks  the  lower  anterior  limit  of  the  abdomen  in 
the  median  line.     These  constitute  the  hony  landmarks. 

There  are  certain  more  or  less  distinct  surface  markings  which  it 
is  useful  to  bear  in  mind  (Fig.  127).     The  linea  alba,  lying  between 


424  THE  EVIDENCES  OF  DISEASE 

the  recti  muscles,  and  running  from  ensiform  appendix  to  pubic 
symphysis,  is  visible  as  a  groove  only  above  the  umbilicus.  The  um- 
hilictis  itself  is  a  most  important  point  of  departure,  although  its 
position  is  somewhat  variable.  It  lies  usually  about  2  inches  above 
the  bispinal  line  (drawn  between  anterior  upper  spines  of  ilium),  and 
corresponds  to  the  tip  of  the  spinous  process  of  the  od  lumbar  verte- 
bra, on  a  level  with  the  disk  between  the  3d  and  4tli  lumbar  verte- 
bras. On  either  side  of  the  linea  alba  lie  the  recti  muscles,  bounded 
externally  by  the  linece  semilnnares,  which  run  with  an  outward  curve 
from  the  lowest  part  of  the  7th  rib  down  to  the  pubic  spines.  The 
semilunar  lines  lie  on  either  side  about  3  inches  from  the  umbilicus, 
farther  away  if  the  abdomen  is  distended.  The  muscular  segments 
of  the  recti  are  separated  by  the  Unem  transversce,  one  of  which  is 
at  the  ensiform  appendix,  one  at  the  umbilicus,  and  one  midway 
between  the  other  two  on  a  level  with  the  costal  cartilages  of  the 
10th  ribs.  Earely  there  is  an  additional  line  below  the  umbilicus. 
If  the  abdominal  walls  are  thick  with  fat,  two  deep  wrinkles  or 
grooves  cross  the  abdomen,  varying  in  depth  according  to  the  de- 
gree of  obesity.  One  is  at  the  umbilicus,  the  other  just  above  the 
pubes. 

Topographical  Areas  of  the  Abdomen. — The  surface  of  the  abdo- 
men is  divided  arbitrarily  into  certain  regions  in  order  to  describe 
intelligibly  the  situation  of  organs  or  lesions.  Two  sets  of  areas,  one 
more  elaborate  than  the  other,  are  in  use,  according  to  the  personal 
preference  of  the  examiner. 

The  first  set  divides  the  abdomen  into  9  regions,  by  the  use  of  4 
lines,  2  horizontal  and  2  vertical.  The  liorizontal  lines  are  :  the  in- 
fracostal or  subcostal,  drawn  across  at  the  level  of  the  lowest  part  of 
the  10th  ribs ;  and  the  iisjnnal,  a  line  connecting  the  anterior  supe- 
rior spines  of  the  ilia.  The  vertical  lines  are  drawn  through  the  cen- 
tre of  Poupart's  ligament,  and  are  practically  downward  prolonga- 
tions of  the  mammillary  lines  of  the  thorax.  Fig.  128  shows  these 
regions  (after  Joessel.  somewhat  modified),  and  the  names  by  which 
they  are  known.  It  may  be  noted  here  that  as  the  lumbar  region  ex- 
tends from  the  vertical  line  in  front  to  the  median  line  posteriorly, 
it  may  be  further  subdivided,  by  prolonging  the  anterior  and  posterior 
axillary  lines  downward,  into  anterior,  lateral,  and  posterior  portions 
(Fig.  72).  The  boundary  lines  between  the  epigastric  region  and 
the  hypochondriac  regions  on  either  side  are  made  (as  they  should 
be)  to  correspond  with  the  costal  margin.  The  iliac  spaces  are  fre- 
quently referred  to  as  right  and  left  inguinal. 

The  second  set  of  areas  requires  2  lines,  1  vertical,  1  horizontal, 
drawn  through  the  umbilicus.     The  abdomen  is  thus  subdivided  into 


TOPOGRAPHY  OP  THE  ABDOMEN 


425 


quadrants,  right  upper  and  lower,  left  upper  and  lower  (Fig.  129). 
This  arrangement  has  the  desirable  merit  of  simplicity. 

Topographical  Anatomy  of  the  Abdomen. — The  ahdominal  aorta 
(Fig.  127)  begins  just  above  a  point  midway  between  the  upper  bor- 
der of  the  sternum  and  the  umbilicus,  lying  to  the  left  of  the  spinal 
column.  It  commonly  bifurcates  about  f  inch  to  the  left  of  and 
the  same  distance  below  the  umbilicus,  corresponding  to  the  body  of 
the  4th  lumbar  vertebra.     One  inch  above  the  umbilicus  arises  the 


Fio.  128. — Showing  nine  topo^rrai'liical  areas  of  abdomen,     i  Alter  .Kie.ssel.    Redrawn  and 
modified.)     See  also  Fig.  72,  page  307. 

inferior  mesenteric  artery ;  3^  to  4  inches,  the  renal  artery ;  4  to  4^ 
inches,  the  superior  mesenteric  artery ;  4^  to  5  inches,  the  cceliac  axis, 
corresponding  to  the  body  of  the  12th  dorsal  vertebra. 

The  exact  surface  relations  of  the  different  abdominal  viscera  are 
stated  in  connection  with  the  detailed  examination  of  each  organ. 
The  contents  of  the  various  regions  are  indicated  in  Fig.  130.  See 
also  Plates  I  and  II. 


426 


THE   EVIDENCES  OF  DISEASE 


Practically  there  are  various  methods  of  indicating  the  location 
of  abdominal  lesions  and  physical  signs. 

(1)  The  findings  may  be  roughly  stated  to  lie  in  one  or  more  of  the 
9  areas  or  regions  marked  out  by  the  older  system ;  or  in  one  of  the 
quadrants  of  the  simpler  method. 

(2)  To  localize  more  minutely  (Fig.  129) :  Suppose  a  vertical  and 
a  horizontal  line,  intersecting  the  umbilicus,  to  be  already  drawn. 


Two  FINGERBREADTHS 
BELOW  COSTAL  MAR- 
GIN 


One  inch  and  a 
half  internal  to 
anterior  superior 
spinous  process 


Three  inches  to  the 

LEFT    of,    and    two 

inches  above,   um- 
bilicus 


Three  and  a  half 
inches  above  sym- 
physis, one  inch  to 

LEFT  of  median  LINE 


Fig.  129.— Showing  the  quadrants  (right  and  kil  upj^ci'  and  right  and  left  lower)  of  the 
abdomen :  also  different  method*  of  describing  with  accuracy  the  location  of  abdom- 
inal signs  or  lesions. 


Then  measure  the  distance  of  the  point  (centre  of  tumour,  tender 
spot)  above  (or  below)  the  umbilical  horizontal  line,  and  to  right  (or 
left)  of  the  median  line.  These  measurements  will  accurately  orient 
the  desired  spot,  according  to  the  position  of  the  lesion  or  physical 
sign. 

Measure  its  distance  above  the  symphysis  pubis  in,  and,  if  to  one 
side,  to  the  right  (or  left)  of,  the  median  line. 

Measure  its  distance  above,  and  also  inward  from,  the  right  (or 
left)  anterior  superior  iliac  spine. 

It  is  sometimes  convenient  to  state  that  the  lower  border  of  an 
enlarged  liver  or  spleen  lies  so  many  fingerbreadths  or  a  hand- 
breadth  below  the  costal  margin.     One  fingerbreadth  is  f  inch  ;  two, 


INSPECTION  OF  THE  ABDOMEN 


427 


1^  inch  ;  three,  2:^  inches,  and  the  width  of  the  broadest  part  of  the 
flat  hand  is  from  3i^  to  4  inches. 

The  Normal  Abdomen. — In  irrfants  and  young  children  the  abdo- 
men is  normally  large  and  prominent  relatively  to  the  size  of  the 
chest.  It  is  larger  in  women  (especially  multipara)  than  in  men, 
and  in  the  former  frequently  presents  a  bulging  of  its  lower  half  as 
a  result  of  corset  wearing.  The  upper  abdomen  may  be  temporarily 
distended  by  a  hearty  meal. 

The  normal  abdomen  on  inspection  is  seen  to  be  moderately 
arched.  Its  upper  portion  moves  easily  and  quietly  with  the  move- 
ments of  respiration.  By  palpation^  it  is  found  to  be  soft,  its  walls 
are  readily  depressed,  without  causing  pain,  and  the  abdominal  mus- 


FiG.  130. — Showing  roughly  the  contents  of  the  nine  topognipliioal  aR-as  of  the  abdomen. 

cles  are  not  contracted  unless  the  patient  is  "ticklish"  or  nervous. 
Xo  swellings  or  hard  masses  can  be  perceived  unless  there  happen  to 
be  large  portions  of  faecal  matter  in  the  colon.  On  percussion,  it  is 
everywhere  tympanitic  except  over  the  liver  and  spleen.  Ausculta- 
tio7i  is  negative  except  for  occasional  gurgling  or  sonorous  sounds. 


II.    METHODS    AND    GENERAL    RESULTS    OF 
ABDOMINAL    INSPECTION 

Teclmic. — With  the  patient  in  bed  the  abdomen  should  be  ex- 
posed by  turning  well  down  all  the  bed  clothing,  thick  quilts  or 
blankets  particularly,  except  the  sheet;  then,  under  cover  of  the 
sheet,  drawing  the  nightdress  as  far  up  as  the  lower  sternum,  and 


428  THE  EVIDENCES  OF  DISEASE 

afterward  folding  the  sheet  down  from  a  point  a  short  distance  above 
the  pubes.  The  position  of  the  patient  should  be  as  symmetrical  as. 
possible,  the  trunk  being  turned  neither  to  right  nor  left  (i.  e.,  the 
bispinal  line  horizontal),  and  a  good  illumination  secured.  While 
the  recumbent  position  is  necessary  for  an  examination  of  the  abdo- 
men, it  is  sometimes  of  service,  when  practicable,  to  make  an  observa- 
tion in  the  standing  or  sitting  posture,  as  pendulosity  or  prolapse  of 
the  abdominal  walls  or  viscera  may  thus  be  more  clearly  manifested. 
Inspection  of  the  abdomen  should  be  made  from  various  directions — 
front,  side,  and  back,  and  obliquely  as  well — in  order  to  detect  pulsa- 
tions or  vermicular  movements.  Owing  to  the  very  intimate  correla- 
tion of  inspection,  palpation,  and  percussion,  as  applied  to  the  abdo- 
men, some  of  the  results  of  inspection  Avill  be  rehearsed  in  connection 
with  palpation  and  percussion. 

Results  of  Abdominal  Inspection  in  Disease. — The  abdomen  should 
be  inspected  with  reference  to  its  cutaneous  surface,  nutrition  of 
walls,  shape,  size,  bulging  (local  or  general),  retraction,  and  move- 
ments. 

(1)  Skin  of  Abdomen. — The  skin  is  smooth,  shining,  and  stretched 
in  excessive  abdominal  distention.  "Whitish  streaks  or  striae  {Unem 
alMcantes)  are  significant  of  previous  long-continued  distention,  as  in 
ascites,  fat,  or  pregnancy,  and  may  be  seen  on  the  buttocks  and  up- 
per portions  of  the  thigh,  as  well  as  upon  the  abdomen.  A  deposit 
of  pigment,  especially  in  the  middle  line  (the  Ihiea  alba  becoming 
the  linea  nigra),  is  observed  in  pregnancy  and  in  chronic  abdominal 
enlargements.  Copper-coloured,  scaly,  somewhat  circular  spots  upon 
the  abdomen  are  significant  of  secondary  syphilis.  The  brownisli  or 
yellowish  macular  areas  of  chloasma  may  also  be  found  here.  En- 
larged glands  in  the  groins  or  retracted  cicatrices  may  be  indices  of" 
present  or  past  specific  or  other  venereal  infection. 

(2)  Enlarged  Superficial  Abdominal  Veins. — A  number  of  en- 
larged veins  radiating  from  the  umbilicus  constitutes  the  capiit  Me- 
dusm.  This  is  significant  of  portal  obstruction  (hepatic  cirrhosis  or 
tumour),  and  represents  an  effort  to  establish  a  freer  communication 
between  the  portal  veins  and  those  of  the  abdominal  parietes  by  way 
of  the  round  and  falciform  ligaments,  the  small  veins  of  the  latter 
becoming  enlarged. 

General  enlargement  of  the  superficial  abdominal  veins  occurs 
from  similar  conditions — e.  g.,  cirrhosis  or  tumour  of  liver;  ascites 
of  long  duration  and  greatly  dilated  stomach ;  or  pressure  upon  the 
inferior  or  superior  cavse  by  abdominal  or  mediastinal  tumours.  If 
there  is  obstruction  to  the  inferior  cava,  a  dilated  lateral  vein  may 
be  present,  running  up  the  right  midaxillary  line,  connecting  the^ 


IXSPECTIOX  OP  THE  ABDOMEN  429 

tributaries  of  the  superior  cava  with  the  enlarged  inferior  epigastric 
veins.  An  effort  should  be  made,  by  emptying  the  vein  and  watch- 
ing it  refill,  to  determine  the  direction  of  the  blood  flow.  In  obstruc- 
tion of  the  portal  vein  and  inferior  cava  the  current  is  upward,  the 
most  usual  finding ;  but  if  the  superior  cava  is  pressed  upon,  the 
direction  is  downward,  the  blood  from  the  superior  cava  endeavour- 
ing to  enter  the  inferior  cava  through  the  medium  of  the  azygos 
veins,  which  communicate  with  many  of  the  tributaries  of  the  in- 
ferior cava.  If  the  veins  in  the  pubic  region  alone  are  distended 
there  is  probably  some  obstruction  (pressure  or  thrombosis)  below 
the  liver. 

(3)  Enlarged  and  visible  epigastric  arteries  in  the  abdominal  walls 
constitute  a  sign  of  the  rare  condition  of  obstructed  aorta  or  iliac 
arteries. 

(4)  Umbilicus. — The  navel  is  deeply  retracted  in  stout  people ; 
if  projecting,  it  may  be  due  to  portal  obstruction,  pregnancy,  or  her- 
nia ;  it  is  flattened,  or  protruding  and  stretched,  in  excessive  ascites 
or  other  abdominal  distentions ;  or  it  may  be  eczematous  or  inflamed. 

(5)  Absent  respiratory  movement  of  the  abdomen  is  a  somewhat 
significant  sign  of  peritonitis,  the  great  pain  inducing  tonic  contrac- 
tion and  rigidity  of  the  abdominal  muscles.  This  symptom,  together 
with  inspiratory  retraction  and  excessive  abdominal  breathing,  has 
been  elsewhere  considered. 

(6)  Visible  Peristalsis. — The  vermicular  movements  of  the  intes- 
tines are  sometimes  visible  if  the  abdominal  walls  are  not  too  thick. 
The  peristalsis  may  be  made  more  active  by  manipulation ;  by  sharply 
tapping  the  surface  with  the  finger ;  flicking  with  a  wet  towel ;  the 
laying  on  of  a  cold  hand ;  or  the  application  of  faradism.  It  pre- 
sents itself  as  a  series  of  rolling,  rounding  elevations,  which  increase 
and  subside,  accompanied  or  not  by  borborygmi.  At  their  height 
the  protuberances  are  noticeably  resistant  and  tympanitic.  It  is 
sometimes  possible  to  differentiate  peristalsis  of  the  transverse  colon 
from  peristalsis  of  the  stomach  by  the  fact  that  the  waves  of  mo- 
tion run  in  the  former  from  right  to  left,  in  the  latter  from  left  to 
right. 

While  visible  peristalsis  may  occur  as  a  normal  event  in  persons 
with  extremely  thin  and  relaxed  abdominal  walls,  especially  mul- 
tiparae,  its  principal  diagnostic  association  is  with  intestinal  obstruc- 
tion and  stenosis.  At  times  an  inference  may  be  drawn  as  to  the 
site  of  the  obstruction  by  the  location  and  character  of  the  moving 
distention.  If  the  obstacle  is  at,  or  a  short  distance  proximal  to, 
the  ileo-csecal  valve,  the  swollen  and  mobile  coils  of  intestine  lie  one 
above  the  other  (ladder  pattern)  in  the  central  portion  of  the  abdo- 


430  THE   EVIDENCES  OP   DISEASE 

men;  but  if  the  constriction  is  low  down  in  the  large  intestine,  in 
the  neighbourhood  of  the  sigmoid  flexure,  the  distention  is  observed 
mainly  in  the  circumferential  portion  of  the  abdomen — i.  e.,  the 
course  of  the  colon.  If  there  is  a  persistently  recurring  excessive 
protuberance  at  one  point,  which  disappears  with  a  loud  sound,  it 
may  be  conjectured  to  be  at  the  point  of  stenosis. 

Visible  peristalsis  in  the  upper  left  quadrant  with  the  waves  of 
motion  running  from  left  to  right  may  be  due  to  a  much-dilated 
stomach. 

III.    METHODS    AND    RESULTS    OF    GENERAL 
ABDOMINAL    PALPATION    AND    PERCUSSION 

Technic  of  Abdominal  Palpation. — The  abdomen  being 
exposed  as  for  inspection,  the  warm  hand  is  laid  flat  upon  the  sur- 
face, letting  it  remain  quiet  until  the  skin  has  become  somewhat 
accustomed  to  its  presence.  Palpation  should  then  be  made  mainly 
by  somewhat  circular  pressing  movements,  sliding  the  skin  over 
subjacent  parts,  and  passing  smoothly  and  steadily  from  one  portion 
of  the  surface  to  another.  A  sudden  poke  with  the  finger  tips  will 
often  defeat  the  examiner's  object  by  causing  immediate  contraction 
of  the  abdominal  muscles.  After  tolerance  is  established,  deeper 
and  localized  palpation  may  be  made  with  the  pulps  of  the  fingers  to 
determine  more  exactly  the  existence  of  tender  spots,  or  the  size, 
shape,  and  mobility  of  existing  masses  or  swellings.  As  in  all  exam- 
inations to  detect  pain  on  pressure,  one  should  pay  attention  to  the 
face  of  the  patient  rather  than  to  verbal  expressions  of  suffering. 
If  it  requires  firm  pressure  to  elicit  tenderness  the  latter  is  apt  to  be 
real  and  deep  seated  rather  than  a  superficial  hyperaesthesia  or  sur- 
face lesion.  If  malingering  or  hysterical  exaggeration  is  suspected, 
it  is  helpful  to  divert  the  attention  of  the  patient  by  pressure  with 
one  hand  upon  a  widely  different  portion  of  the  surface,  conjoined 
with  suggestion,  while  the  other  explores  the  original  point  of  com- 
plaint— a  procedure  which  not  infrequently  reveals  a  significant  ab- 
sence of  tenderness  with  greater  pressure  than  that  of  which  bitter 
complaint  was  originally  made. 

If  the  abdominal  muscles  are  contracted  to  an  extent  which  inter- 
feres with  proper  palpation,  the  patient  may  be  encouraged  to  relax 
them  voluntarily ;  or  the  knees  may  be  flexed,  and  a  pillow  placed 
under  the  head  and  shoulders  to  diminish  the  tension ;  or  he  may  be 
directed  to  take  several  deep  respirations  ;  or  to  breathe  as  rapidly  as 
possible.  Toward  the  end  of  expiration  the  muscles  are  usually  in  a 
momentarily  relaxed  condition.  Deep  breathing,  moreover,  deter- 
mines, by  the  occurrence  of  relaxation,  whether  a  mass  felt  is  a  con- 


PALPATION  AND  PERCUSSION  OP  THE  ABDOMEN  43I 

tracted  belly  of  the  rectus  or  ridge  of  the  lateral  and  posterior 
abdominal  muscles,  and  whether  a  tumour  found  is  movable  with 
respiration.  If  it  is  desired  to  get  deep  down  into  the  abdomen,  one 
hand,  re-enforced  by  the  other  laid  upon  it,  should  exercise  increas- 
ing pressure  during  a  series  of  forced  respirations,  following  the  sink- 
ing abdominal  walls  with  each  expiration,  and  maintaining  during 
each  inspiration  the  ground  which  has  been  gained.  The  re-enforce- 
ment of  the  palpating  hand  by  the  other  preserves  the  perceptive 
delicacy  which  the  former  would  otherwise  lose  on  account  of  the 
very  considerable  muscular  power  required  to  be  exerted.  If  there  is 
fluid  in  the  peritoneal  cavity  and  one  wishes  to  palpate  an  organ  ob- 
scured by  its  presence,  a  sudden  deep  pressure  with  the  finger  tips 
("dipping")  may  successfully  displace  the  fluid  and  allow  the  desired 
end  to  be  attained.  Finally,  if  the  diagnosis  is  of  suflScient  impor- 
tance, a  general  anaesthetic  may  be  given  in  order  to  eliminate  the 
difficulties  due  to  pain  or  contraction  of  the  muscles. 

The  various  regions  of  the  abdomen  should  be  systematically  ex- 
plored, never  forgetting  to  examine  the  umbilical,  inguinal,  and  femo- 
ral sites  of  hernia.  To  examine  the  lateral  portions  of  the  abdomen, 
both  hands  should  be  employed,  one  being  slipped  under  the  body  so 
as  to  make  forward  pressure  in  the  space  between  the  last  rib  and  the 
iliac  crest,  thus  pushing  the  deeper  structures  up  against  the  other 
hand  placed  over  the  abdomen  in  front,  which  can  then  appreciate 
the  consistence  and  character  of  the  intervening  tissues.  It  is  some- 
times serviceable  to  examine  in  the  knee-elbow  position,  or  with  the 
patient  standing  and  leaning  forward,  supporting  the  body  by  the 
hands  upon  a  table  or  chair.  If  the  patient  has  a  large,  fat  abdomen, 
it  is  advantageous  to  have  him  turn  partly  over  to  one  side  or  the 
other,  thus  "  spilling  "  the  intestines  and  thick  abdominal  walls  away 
from  the  area  under  investigation.  The  utility  of  a  digital  rectal 
and  vaginal  examination  in  tracing  the  origin  of  abdominal  lesions, 
especially  those  which  are  situated  in  the  lower  third  of  the  abdo- 
men, should  not  be  forgotten.  Mensuration  of  the  abdominal  cir- 
cumference at  the  level  of  the  umbilicus,  and  the  length  of  its 
anterior  wall  from  ensiform  to  symphysis,  are  useful  in  keeping 
track  of  the  increase  of  ascitic  fluid  or  the  rate  of  growth  of  a  large 
tumour. 

Technic  of  Abdominal  Percussion. — Pulmonary  resonance, 
except  in  defining  the  upper  limits  of  the  liver  and  stomach,  can  be  « 
eliminated,  and  the  distinctions  to  be  made  are  between  degrees  of 
dulness  and  tympanicity. 

Barring  hepatic  and  splenic  dulness,  the  abdomen  normally  is 
tympanitic,  the  pitch  of  the  resonant  note  varying  with  the  size  of 


432  THE  EVIDENCES  OF  DISEASE 

the  air  space  and  the  degree  of  tension  of  the  containing  cavity.  The 
smaller  the  air  space  and  the  greater  the  tension  the  higher  is  the 
pitch.  Consequently  the  stomach  and  colon  afford  a  lower  pitched 
note  than  the  small  intestines,  although  the  great  variations  in  size 
and  tension  which  take  place  from  time  to  time  greatly  minimize 
the  value  of  this  sign. 

Auscultatory  percussion  finds  perhaps  its  greatest  usefulness  in 
outlining  the  contiguous  air-containing  abdominal  viscera.  "  Flick- 
ing "  percussion  has  many  advocates,  and  is  claimed  to  be  very  use- 
ful in  detecting  slight  degrees  of  dulness.  In  this  method  the  left 
forefinger  is  placed  nail  downward  upon  the  surface,  and  the  nail  of 
the  middle  finger  of  the  right  hand  having  been  pressed  against  the 
palmar  surface  of  the  end  of  the  thumb,  is  suddenly  allowed  to 
escape,  so  as  to  strike  sharply  against  the  palmar  surface  of  the  left 
forefinger.  If  the  percussion  note  of  a  deep-lying  mass  in  the  abdo- 
men is  to  be  elicited,  the  pleximeter  finger  must  be  pressed  slowly 
and  firmly  down  in  order  to  push  away  or  compress  air-containing 
coils  of  intestine,  which  would  otherwise  afford  a  masking  tympanitic 
sound.  If  dulness  is  found  in  any  part  of  the  abdomen  where  it 
should  not  exist,  it  is  of  great  importance  to  ascertain  whether  it 
disappears  or  shifts  with  changes  in  the  position  of  the  patient  (fluid, 
sometimes  air). 

Results  of  General  Abdominal  Palpation  and  Percus- 
sion.— Observation  should  be  directed  to  ascertain  the  condition 
and  resistance  to  pressure  of  the  abdominal  walls,  general  or  local 
retraction  or  distention,  the  shape  and  consistence  of  palpable  organs, 
the  presence  of  tumours,  thrill,  fluctuation,  abnormal  dulness  or  tym- 
panicity  and  other  points,  as  follows  : 

(1)  Abdominal  Walls. — The  thickness  of  the  abdominal  wall  may 
be  estimated  by  endeavouring  to  grasp  it  in  the  hand,  or  better  by 
placing  one  hand  on  either  side  and  approximating  them.  Increased 
thickness  is  due  to  fat  or  cedema.  If  the  latter,  there  is  pitting  on 
steady  pressure,  and  the  swelling  is  more  marked  in  the  lower  and 
lateral  portions  of  the  abdomen.  Thickening  may  also  be  due  to  ex- 
tensive suppuration  in  the  abdominal  walls,  in  which  case  the  signs 
of  inflammation  will  be  present.  Lax  and  thin  walls,  with  wrinkled 
skin,  are  due  to  long-standing  distention  from  ascites,  tumour,  re- 
peated pregnancies,  old  age,  or  wasting  disease.  Induration  and  in- 
filtration around  the  umbilicus  are  caused  by  periomphalitis,  said  to 
be  a  significant  sign  of  tuberculous  peritonitis.  Fixation  of  the 
umbilicus  may  be  present  as  an  evidence  of  malignant  disease  of  the 
liver,  a  sign  comparable  to  the  similar  condition  of  the  nipple  in 
mammary  cancer. 


PALPATION  AND   PERCUSSION  OP  THE  ABDOMEN  433 

(2)  Rigid  Recti  Muscles. — A  persistent  tonic  contraction  of  one 
or  both  recti,  amounting  perhaps  to  extreme  rigidity,  if  not  due  to 
nervousness  or  "  ticklish  "  sensitiveness,  is  very  significant  of  perito- 
neal inflammation ;  of  the  right  rectus  alone,  of  appendicitis  in  par- 
ticular; of  both  recti  and  all  the  abdominal  muscles,  of  general  peri- 
tonitis. In  the  slighter  degrees  there  is  merely  a  sense  of  resistance, 
the  muscles  contracting  only  when  pressure  is  made. 

(3)  General  Retraction  of  the  Abdomen. — The  abdomen  as  a  whole 
may  be  sunken  in  Avasting  diseases.  It  is  very  marked  in  inanition 
from  stricture  of  the  esophagus  or  pyloric  stenosis  and  gastric 
dilatation ;  in  the  violent  vomiting  an©  purging  of  cholera  and  severe 
gastro-enteritis ;  and  in  the  pernicious  vomiting  of  pregnancy.  If 
tenderness  and  muscular  rigidity  is  associated  with  the  retraction, 
one  may  suspect  the  early  stage  of  peritonitis.  The  scaphoid  (boat- 
shaped)  abdomen  is  also  seen  as  a  symptom  of  meningitis  (basal 
especially),  tumour  of  the  brain,  and  lead  colic,  because  of  the  irrita- 
tive tonic  spasm  of  the  abdominal  muscles. 

(4)  General  Distention  of  the  Abdomen. — As  a  rule  general  enlarge- 
ment of  the  abdomen  is  due  to  one  of  four  things  :  fat  in  the  abdomi- 
nal walls,  fluid  in  the  peritoneal  cavity,  an  excessive  amount  of  gas 
in  the  stomach  and  intestines,  rarely  in  the  peritoneal  cavity,  or  the 
presence  of  a  large  abdominal  tumour. 

Fat. — Enlargement  due  to  adipose  tissue  is  usually  easy  to  deter- 
mine, as  it  is  associated  with  general  obesity  and  the  bulk  of  the 
extremities  is  proportionate  to  the  dimensions  of  the  abdomen.  In 
some  cases  fat  abdominal  walls  constitute  a  very  serious  obstacle  to 
the  discovery  of  small  neoplasms.  A  possible  source  of  error  arises 
from  the  occasional  accumulation  of  fat  in  the  great  omentum  in  the 
middle-aged,  which  at  first  glance  simulates  a  pregnant  uterus  or 
median  tumour,  but  careful  palpation  will  reveal  its  nature. 

Fluid.— li  the  distention  is  due  to  ascites— an  accumulation  of 
fluid  in  the  peritoneal  cavity — the  centre  of  the  abdomen,  in  the  dor- 
sal decubitus  and  provided  the  amount  of  fluid  is  not  excessive,  is 
flattened,  and  the  lateral  and  dependent  portions  bulge  outward  from 
the  weight  of  the  fluid.  If  the  amount  is  very  great  the  entire  abdo- 
men is  arched  and  prominent,  the  umbilicus  is  stretched  or  bulging, 
and  the  shape  of  the  abdomen  does  not  change  when  the  posture  is 
altered.  If  ascites  occurs  in  a  previously  lax  and  pendulous  abdo- 
men, the  latter  may  protrude  in  an  oddly  conical  form.  On  percus- 
sion the  flanks  are  dull  and  the  centre  of  the  abdomen  resonant,  the 
air-containing  intestines  floating  upward  toward  the  highest  point 
(Fig.  131).  Unless  the  fluid  is  encapsulated  or  its  amount  excessive, 
the  line  of  dulness  changes  position  as  the  patient  is  turned  to  one 


434 


THE  EVIDENCES  OF  DISEASE 


side  or  the  other,  the  fluid  gravitating  to  the  lowest  point  and  being 
replaced  by  the  tympanitic  intestine.     The  uppermost  flank,  previous- 


FiG.  131. — Showing  the  central  tympanicity  and  lateral  dulness  of  an  abdomen  containing 
free  fluid.     Compare  with  Fig.  132. 


Central  part  of  abdomen 
Tympanitic 


Fig.  132. — Sliowing  both  flanks  dull  in  ascites,  dorsal  posture. 


Formerly  dull 
now  tympanitic  \ 


Fig.  133. — Showing  uppermost  flank  tympanitic,  with  change  in  line  of  flatness  in  opposite 
flank  in  ascites,  after  assuming  the  latero-dorsal  posture.    Compare  Fig.  132. 


PALPATION  AND  PERCUSSION  OP  THE  ABDOMEN 


435 


ly  dull,  is  now  resonant  (Figs.  132  and  133).  If  the  presence  of  a  small 
amount  of  fluid  is  suspected,  the  patient  may  be  put  into  the  knee- 
hand  position,  when,  if  the  suspicion  is  correct,  an  area  of  dulness 
may  be  made  out  in  the  umbilical  region,  due  to  the  subsidence  of 
the  fluid  to  that  point.     If  the  amount  of  fluid  is  considerable,  fluctu- 


Fio.  134. — Showing  cent 


I'.ulncss  and  lateral  tympaiiicity  of  abdominal  cystic  or  solid 
tuiuours.    Compare  with  Fig.  135. 


ation  may  be  elicited.  To  obtain  fluctuation,  the  ulnar  edge  of  an 
assistant's  hand  should  first  be  pressed  firmly  upon  the  linea  alba  in 
order  to  cut  off  the  vibrations  of  the  abdominal  wall  which  may 
closely  simulate  fluctuation.     One  hand  of  the  examiner  is  then  laid 


Dull 


Tympanitic 


-Tympanitic 


Fig.  1- 


■tion  f.xphmatory  of  Fig.  134. 


upon  one  lateral  wall  of  the  abdomen,  while  the  fingers  of  the  other 
hand  tap  rather  smartly  upon  the  opposite  side.  If  fluid  is  present, 
a  transmitted  wave,  which  may  also  be  visible,  is  distinctly  felt  by 


4-36  THE  EVIDENCES  OF  DISEASE 

the  palpating  hand.  Very  light  percussion  is  often  sufficient  to 
cause  it.  This  sign  may  fail  in  very  large  effusions  under  high  pres- 
sure. 

It  is  necessary  to  discriminate  ascites  from  pregnancy,  ovarian 
cystoma,  distended  bladder,  and  rarely  hydatid  cyst  of  the  liver  or 
cyst  of  the  pancreas.  Aside  from  the  history,  vaginal  examination, 
catheterization  and  aspiration,  these  sources  of  error  can  be  ruled 
out  if  there  is  dulness  on  percussion  of  the  flanks.  The  first  three 
conditions  mentioned  give  rise  to  dulness  in  the  centre  of  the 
abdomen  and  tympanitic  resonance  in  the  lateral  regions,  signs 
directly  contrary  to  those  of  ascites,  as  the  fluid  (amniotic,  ovarian, 
urine)  is  not  free  in  the  peritoneal  cavity  and  can  not  seek  the  low- 
est points  of  the  latter  (Figs.  134  and  135). 

Uncomplicated  ascites — i.  e.,  without  general  oedema — is  most 
commonly  due  to  cirrhosis  of  the  liver ;  less  frequently  to  chronic 
peritonitis.  Other  causes  of  the  accumulation  of  fluid  in  the  peri- 
toneal cavity  are  obstruction  of  the  thoracic  duct,  compression  of 
the  portal  vein  by  abdominal  tumours,  portal  thrombosis,  or  oblit- 
erating pericarditis.  Hemorrhage  into  the  abdominal  cavity,  due  to 
ruptured  tubal  pregnancy,  may,  if  sufficiently  large,  give  rise  to  the 
physical  signs  of  free  fluid.  In  any  case  of  ascites  there  may  be 
a  secondary  oedema  of  the  lower  extremities,  but  the  history  will 
show  that  the  abdominal  distention  antedated  the  swelling  of  the 
legs. 

Ascites  plus  general  oedema  constitutes  a  part  of  the  latter,  and 
is  due  to  renal,  more  rarely  to  cardiac,  disease.  A  large  accumula- 
tion is  not  often  found  as  a  result  of  a  diseased  heart.  Very  rarely 
it  is  due  to  the  rupture  of  a  cyst  of  the  ovary  or  broad  ligament,  in 
which  case  there  may  be  a  history  of  a  slow-growing  localized  (pel- 
vic, right  or  left)  tumour. 

Some  evidence  of  the  causative  disease  may  be  obtained  by  an 
examination  of  the  ascitic  fluid  withdrawn  by  puncture  {q.  v.). 

Gas. — If  the  distention  is  due  to  gas  in  the  intestines  (meteorism, 
tympanites),  the  abdomen  is  arched  and  tense,  universally  tympanitic 
upon  percussion  (Fig.  136),  and  fluctuation  can  not  be  obtained— 
physical  signs  which  render  it  an  easily  determined  condition.  If 
the  distention  is  extreme,  the  diaphragm  is  pressed  upward,  and  the 
action  of  the  heart  may  be  seriously  impeded. 

With  reference  to  the  causes  of  meteorism,  it  may  be  noted  that, 
in  moderate  degree,  it  is  often  due  to  acute  or  chronic  gastro-intes- 
tinal  disorders,  and  is  a  frequent  source  of  complaint  in  such  cases 
when  occurring  in  neurotic  women.  It  is  almost  always  present  in 
typhoid  fever,  sometimes  to  an  extreme  degree,  and  in  the  typhoid 


PALPATION  AND  PERCUSSION  OF  THE  ABDOMEN    437 


Fio.  136. — Showing  abdominal  meteorism,  percus- 
sion note  Universally  tympanitic.  Frozen  sec- 
tion from  PirigoflF,  redrawn. 


state  in  general.  A  high  grade  of  tympanites  conjoined  with  great 
abdominal  tenderness  is  significant  of  acute  general  peritonitis. 
Great  and  rapid  gaseous  distention  of  the  stomach  and  intestines 
{pnemnatosu)  is  an  occasional  symptom  of  hysteria.  In  all  cases  of 
excessive  meteorism  the  possibility  of  intestinal  obstruction  should 
be  borne  in  mind.  Intestinal 
paresis,  due  to  sepsis,  to  quick 
removal  of  pressure  from 
intestines  previously  con- 
stricted —  e.  g.,  strangulated 
hernia — or  compressed — e.  g., 
hy  tumour  or  fluid — or  to 
deranged  or  defective  inner- 
vation, may  also  be  a  cause 
of  meteorism  and  obstinate 
constipation  (Wood). 

In  comparatively  rare  in- 
stances there  is  free  gas  in 
the  peritoneal  cavity,  due  to 
perforating  ulcer  of  the  stom- 
ach or  intestine,  a  perforated 
appendix,  or  the  presence  of 

a  gas-forming  micro-organism  in  the  cavity  of  the  peritoneum.  If, 
from  the  sudden  onset  of  collapse,  meteorism,  and  severe  abdominal 
pain,  a  perforation  peritonitis  is  suspected,  one  may  endeavour  to 
determine  that  the  distention  is  extra-intestinal  by  finding  whether 
lateral  liver  dulness  is  present  in  the  dorsal  position,  and  if  so, 
whether  it  disappears  when  the  patient  is  turned  well  over  on  the 
left  side ;  and  similarly  with  the  splenic  dulness.  If  this  change 
takes  place,  one  may  infer  that  the  air  is  in  the  peritoneal  cavity, 
and  that,  being  free,  it  has  in  each  case  risen  to  the  highest  point, 
thus  interposing  itself  between  the  liver  (or  spleen)  and  the  abdom- 
inal walls.  The  alteration  with  change  of  position  is  the  significant 
sign,  as  liver  dulness  may  nearly  disappear  as  a  result  of  ordinary 
meteorism,  marked  emphysema,  hepatic  cirrhosis,  and  a  disease  of 
rare  occurrence — acute  yellow  atrophy  of  the  liver. 

Tumour. — Abdominal  distention  from  tumours  may,  if  the  latter 
are  very  large,  closely  simulate  enlargement  due  to  the  previously 
mentioned  causes.  It  may  be  said  that  in  general  a  large  neoplasm 
gives  a  greater  increase  in  the  antero-posterior  than  in  the  transverse 
diameter  as  compared  to  the  manner  of  increase  caused  by  fat,  fluid, 
or  gas.  Moreover,  in  the  majority  of  large  tumours  the  enlargement 
of  the  abdomen  is  not  quite  symmetrical ;  percussion  does  not  show 
30 


438  THE   EVIDENCES  OF   DISEASE 

the  uniform  resonance  of  gas  nor  the  lateral  dulness  and  central 
tympanicity  of  free  fluid ;  and  palpation  may  declare  the  solidity  of 
the  mass.  The  tumours  or  organs  which  may  grow  to  such  a  size  as 
to  cause  general  abdominal  tumidity  or  distention  are :  of  the  livery 
hydatid  cyst,  cancer,  syphilitic  and  amyloid  disease ;  of  the  spleen, 
malarial,  leucaemic,  and  amyloid  enlargement ;  of  the  kidney,  sar- 
coma and  cysts ;  cancer  of  the  peritoneum  and  intestine ;  dilated 
stomach ;  ovarian  cystoma  and  uterine  fibroids ;  finally,  as  a  source 
of  error,  the  pregnant  uterus. 

The  abdomen  may  be  generally  protuberant  because  of  the  pres- 
ence of  a  considerable  number  of  enlarged  mesenteric  glands,  either 
tuberculous  or  a  part  of  the  glandular  hyperplasia  of  Ilodgkin's 
disease ;  so  also  in  the  chronic  gastro-intestinal  catarrh  or  greatly 
dilated  colon  of  children;  and  in  cretinism,  rachitis,  and  pseudo- 
hypertrophic paralysis. 

(5)  Local  Bulgings,  Swellings  or  Tumours. — One  can  not  exercise 
too  much  care  in  searching,  first  by  inspection  and  then  by  pains- 
taking palpation,  for  the  presence  of  local  swellings  or  small  tumours 
in  all  cases  presenting  symptoms  referable  to  the  abdominal  viscera. 
The  following  remarks  apply  equally  to  inflammatory  swellings  or 
new  growths : 

(a)  Sources  of  Error. — There  are  certain  difficulties  or  sources  of 
error  in  the  search  which  are  worthy  of  mention.  The  occasional 
and  sometimes  almost  insuperable  obstacle  presented  by  excessive 
thickness  of  the  abdominal  wall  may  be  partly  overcome  by  strong 
palpation,  one  hand  being  re-enforced  by  pressure  with  the  other,  and 
by  spilling  the  fat,  thick  walls  to  one  side  or  the  other  by  position ; 
ascites  by  "  dipping  "  (page  431) ;  and  "  ticklishness  "  by  slow,  equa- 
ble movement  and  moderately  firm  pressure.  The  segments  of  the 
recti  muscles  when  contracted  may  very  exactly  simulate  a  small 
tumour,  and  one  may  endeavour  to  eliminate  this  not  uncommon 
element  of  doubt  by  insinuating  the  tips  of  the  fingers  under  the 
edge  of  the  apparent  tumour,  and  then  asking  the  patient  to  raise 
his  head,  upon  which  the  muscle,  if  it  be  such,  is  felt  to  contract 
and  thicken. 

A  localized  spasmodic  contraction  of  the  abdominal  muscles  or 
persistent  gaseous  distention  of  a  knuckle  of  intestine  ("phantom 
tumour ")  may  be  extremely  deceptive.  An  ostensible  tumour  of 
this  kind  occurs  as  a  rule  in  an  hysterical  woman,  is  dull  or  dull  tym- 
panitic, may  disappear  during  rapid  and  forced  respiration,  and — a 
crucial  test — vanishes  during  full  anaesthesia.  It  should,  however,  be 
stated  that  some  "  phantom "  tumours  are  probably  congenital  or 
acquired  dilatations  of  the  colon  (Fitz). 


PALPATION  AND  PERCUSSION   OF  THE  ABDOMEN 


439 


WITHOUT   DEFINITE   LOCATION 


FjCcal  masses  (in  course  of  colon) 

Large  gallstones  or  f/ecal  concretions  (in  intestine) 

Floating  kidney  (usually  remains  on  its  own  side,  but  may 

BE    FOUND   anywhere    BETWEEN    RIBS   AND    PELVIs) 

Floating  spleen  (left  side,  but  may  descend  into  pelvis) 

Tumour  of  intussusception 

Pyloric  tumour,  usually  cancer  (very  movable) 

Phantom  tumour 

Masses  of  tuberculous  or  carcinomatous  peritonitis 

Enlarged  glands  (tubercle,  cancer,  Hodgkin's  disease) 


(b)  Points  to  he  Observed. — If  one  is  satisfied  of  the  presence  of  a 
tumour,  the  following  points  remain  for  determination  : 

Is  it  intra-abdominal  or  extra-abdominal ;  is  it  freely  movable,  and 
does  it  move  with  respiration ;  what  is  its  size,  shape,  consistence, 
the  nature  of  its  surface ;  does  it  fluctuate ;  in  what  region  of  the 
abdomen  does  it  lie ;  and  from  what  organ,  if  any,  does  it  spring  ? 

(1)  If  situated  in  the  abdominal  wall,  it  is  usually  possible  to 
gather  up,  either  in  one  hand  or  between  both,  that  portion  of  the 
abdominal  wall  overlying  the  tumour,  when  the  latter  can  be  dis- 
tinctly felt  to  lie  in  the  grasp  of  the  hand.  An  intra-abdominal 
growth,  on  the  contrary, 

can  not  thus  be  elevated 
and  seized,  the  abdomi- 
nal wall  slipping  easily 
over  it  unless  it  has  con- 
tracted firm  parietal  ad- 
hesions. 

(2)  The  mobility  of 
the  tumour  should  be 
tested  by  moving  it  in 
various  directions,  observ- 
ing the  extent  of  move- 
ment and  the  line  in 
which  it  is  most  readily 
pushed  —  e.  g.,  floating 
kidney,  which  is  most 
easily  carried  upward  and 
backward. 

If,  when  the  hand  is 
laid  upon  the  tumour, 
the  latter  is  found  to 
move  up  and  down  with 
each  respiration,  it  may 
be  inferred  that  it  springs 
from  organs  in  close  rela- 
tion with  the  diaphragm 
— i.  e.,  liver,  spleen,  and, 
to  a  less  extent,  the  kid- 
ney. This  is  a  sign  which  possesses  considerable  diagnostic  value, 
but  it  must  be  remembered  that  the  tumour  may  have  contracted  ad- 
hesions in  such  a  manner  as  to  produce  the  same  effect.  On  the 
other  hand,  tumours  which  would  ordinarily  move  with  respiration 
may  be  hindered  from  so  doing  by  interference  with  the  contraction 


Fig.  137. — Showing  the  clinical  areas  of  the  abdomen 
with  reference  to  the  diagnostic  value  of  the  situ- 
ation of  circumscribed  swellings  or  tumours ;  also 
lesions  without  definite  location. 


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440 


PALPATION  OF  THE  ABDOMEN 


441 


of  the  diaphragm  consequent  upon  pleurisy,  emphysema,  or  a  greatly 
enlarged  liver  or  spleen. 

The  tumours  which  are  readily  movable  by  palpation,  and  which 
descend  when  the  patient  is  in  the  erect  position,  are  floating  liver, 
spleen  and  kidney ;  tumour  of  the  stomach  (especially  pyloric)  or 
intestine ;  faecal  masses  or  concretions,  and  gallstones.  Slightly 
movable  are  tumours  of  the  gall  bladder  and  omentum  above ;  uterus 
and  ovaries  below.  Immovable  are  tumours  of  the  pancreas,  aneurism 
of  the  abdominal  aorta,  abscess  or  inflammation  due  to  disease  of  the 
appendix,  tumour  of  bone  or  abscess  resulting  from  caries,  and  en- 


r        ' ' 

SIGMOID  AREA 

Cancer  of  sigmoid  flex- 

!        URE       OR       descending 

colon 

F/ECAL  accumulation 

Enteroliths 
Gallstones 
Psoas  abscess 
F/€c«L  abscess 
Enlarged  glands 
Tuberculous     perito- 
nitis 

SPLENIC   AREA 

Enlarged,   or   movable 
and  prolapsed  spleen 

Enlarged,   or   movable 
and  prolapsed  kidney 

Perinephhitic  abscess 

Dilated  stomach 

f/ecal  accumulation 

Enteroliths 
Gallstones 
Effusion  in  lesser  peri- 

Cancerous peritonitis 

Intussusception 

Hernia 

toneal  CAVITY 
Subphrenic  abscess 

(rarely  palpable) 
Abscess  due  to  spinal 

caries 

Movable  spleen 
Movable  kidney 
Ovarian  tumour 
Ovarian  abscess 
Cyst    of    broad    liga- 
ment 

H/EMATOMA  or  H/€MAT0- 

cele 

^^Hk   - 

Fibboid  tumours 

^^^^Httiiv^ 

Fig.  139. — Showing  possible  findings  in  the  splenic  and  sigmoid  areas. 


larged  retroperitoneal  glands  or  abscess.     Tumours  of  the  stomach 
or  intestine  may  change  position  with  the  peristaltic  movements. 

(3)  Note  also  its  size,  approximately  or  by  measurement ;  its 
phape — round,  ovoid,  or  irregular ;  its  surface,  whether  smooth  or 
nodular ;  and  its  consistence — soft,  doughy,  and  indentable  (faecal 
mass),  moderately  hard  or  stony.  Can  fluctuation  be  obtained — i.  e., 
is  it  of  a  cystic  nature,  with  fluid  or  semifluid  contents  (hydrone- 
phrosis or  pyonephrosis,  ovarian  cystoma,  distended  bladder,  hydatid 
cyst,  pregnant  uterus,  ectopic  gestation,  or  encysted  abscess)  ?    If 


442 


THE   EVIDENCES  OP  DISEASE 


fluctuation  is  present,  test  for  the  "  hydatid  thrill,"  by  placing  three 
fingers  over  the  fluctuating  mass  and  percussing  strongly  upon  the 
middle  one  of  the  three,  letting  the  plessor  or  striking  finger  rest  at 


GASTRIC    AREA 


Fatty  tumour  or  abscess  of  abdominal  wall 
Distended  stomach  (gas,  fluid,  food) 
Dilated  stomach  (rarely) 

Tumour  of  pylorus  or  anterior  wall  of  stom- 
ach (usually  cancer) 
Induration  of  chronic  gastric  ulcer  (rare) 
Cyst,    cancer,    or   sclerosis   of   pancreas,    or 

ACUTE    hemorrhagic    PANCREATITIS 

Tumour  (cancer,  hydatid  cyst)  or  enlargement 
(part  of  general  increase)  of  left  lobe  of 

LIVER 

Distended  (bile,  pus,  concretions)  or  cancer- 
ous gall  bladder  (right  side  of  area) 

Cancer  of  transverse  colon 

Tumour  of  intussusception 

Tuberculous  or  cancerous  omentum  (trans- 
verse, cordlike  tumour) 

Enlarged  posterior  mediastinal,  mesenteric  or 
retroperitoneal  glands  (tuberculous,  can- 
cerous,   HODGKIN'S    disease) 

Tuberculous  abscess 
Subphrenic  abscess  (rarely  palpable) 
Aneurism  of  abdominal  aorta  (middle  line) 
Effusion  into  lesser  peritoneal  cavity  (to  left) 


Fig.  140. — Showing  po-ssible  lindings  in  the 
gastric  and  pelvic  areas. 


PELVIC   (PUBIC)   AREA 


In  median  line  :  Distended  bladder  ;  uterus, 
pregnant,  distended  (imperforate  hymen); 
OR  fibroid  tumour 

Laterally  :  Ovarian  tumour,  abscess  of  ovary, 
masses  due  to  pyosalpinx,  ruptured  ectopic 
gestation  (h/cmatoma),  tuberculous  peri- 
tonitis,   OR     AN     unusually     LONG     INFLAMED 

appendix  lying  in  the  pelvis 


the  end  of  each  stroke,  when,  if  the  thrill  is  elicited,  it  will  be  per- 
ceived by  the  two  lateral  fingers. 

(4)  Observe  carefully  in  what  part  or  region  of  the  abdomen  the 
swelling  or  tumour  lies. 

(5)  Determine  as  accurately  as  possible  whether  it  is  entirely  of 
abdominal  origin,  or  whether  it  springs  from  the  pelvis.  Careful 
deep  palpation,  just  above  the  brim  of  the  pelvis,  together  with  a 
rectal  or  vaginal  examination,  will  usually  determine  this  point,  but 
cases  occur  in  which  errors  are  quite  possible — e.  g,,  an  abscess  of  the 
ovary  rising  out  of  the  pelvis  sufficiently  high  to  be  diagnosed  as  an 
appendical  abscess. 

A  decision  as  to  the  particular  organ  or  structure  from  which  a 
tumour  springs,  or  a  diagnosis  of  the  nature  and  seat  of  the  disease 
causing  local  swelling  or  bulging  in  various  parts  of  the  abdomen, 
depends  not  only  upon  the  location  and  characters  of  the  tumour  or 
swelling,  but  also,  and  often  to  a  large  extent,  upon  the  history  of 


PALPATION  OP  THE  ABDOMEN 


443 


the  case  and  the  results  of  chemical  and  microscopical  examinations 
of  the  sputum,  gastric  contents,  blood,  urine,  or  faeces. 

{c)  Indications  Derived  from  the  Situation  of  Abdominal  Swell- 
ings or  Tumours. — For  the  sake  of  clinical  convenience  in  describing 
the  significance  of  swellings  or  tumours  according  to  the  part  of 
the  abdomen  in  which  they  are  found,  one  may  recognise  7  areas  or 
regions,  each  named,  with  2  exceptions  (pelvic  and  umbilical),  after 
the  most  important  organ  or  part  underlying  it.  These  areas  (Fig. 
137),  the  boundaries  of  which  necessarily  overlap  to  some  extent,  are 
in  the  median  line  gastric,  umbilical,  and  pelvic ;  to  the  right,  the 
hepatic  and  appendical ;  to  the  left,  the  splenic  and  sigmoid.  Fur- 
thermore, as  certain  bulgings  or  tumours  may  occupy  almost  any 
point  in  the  abdominal  cavity,  it  is  practicable  to  form,  according 
to  their  distribution  but  with  some  necessary  repetition,  8  groups  of 
palpable  abdominal  lesions.  It  is  helpful  from  a  diagnostic  view- 
point to  have  in  mind  the  possible  findings  when  palpating  and  per- 
cussing special  regions  or  areas  of  the  abdomen.  It  is  to  be  remem- 
bered that  a  tumour  or  an  enlarged  organ  in  one  of  these  areas  may 


UMBILICAL   AREA 


Umbilical  hernia 

Dilated    and     distended    (gas,    fluid) 

STOMACH 

Large  cancer  of  stomach 

Movable  and    prolapsed  or   enlarged 

kidney,  spleen,  or  liver 
Enteroptosis  (bulging) 
Cancer    of     intestine     or     omentum 

(tumour) 
Prolapsed  colon  (transverse  cord  in 

LOWER    portion   OF   AREA) 

Enlarged    mesenteric   glands  (tuber- 
cle, cancer,  etc.) 
Tuberculous  or  cancerous  peritonitis 
Projecting    vertebr/e    (simulating    a 
tumour) 


Fig.  141. — Showing  possible  findings  in  umbilical  area. 


grow  to  such  dimensions  that  it  underlies  several  of  these  areas,  or 
indeed  may  occupy  nearly  the  entire  abdominal  cavity — e.  g.,  liver, 
spleen,  ovarian  tumour — but  careful  palpation,  aided  perhaps  by  the 
history,  enables  it  to  be  traced  to  its  origin  in  a  particular  region. 


444  THE   EVIDENCES  OF  DISEASE 

Figs.  137  to  141,  inclusive,  show  sufficiently  these  areas  and  pos- 
sible findings. 

Auscultation  of  the  Abdomen. — Auscultation  is  only  occa- 
sionally useful  in  the  examination  of  the  abdomen. 

Over  the  stomach  one  may  hear  the  sounds  of  swallowed  fluid 
entering  the  viscus,  and  splashing  or  bubbling  sounds  with  move- 
ment of  the  body  (succussion),  which  are  of  little  or  no  diagnostic 
value  ;  or  an  unusual  intensity  or  quality  of  heart  sounds,  the  hollow 
air-containing  organ  acting  as  a  resonator  to  re-enforce  or  alter  their 
normal  characters. 

Over  healthy  intestine  one  can  always,  at  least  with  patient  wait- 
ing, hear  bubbling,  gurgling,  ringing,  sonorous,  or  cooing  sounds, 
due  to  peristaltic  contraction  forcing  gas  through  fluid  or  through 
coiled  or  knuckled  intestine.  If  a  diagnosis  is  to  be  made  between 
mechanical  obstruction  and  intestinal  paresis  (sepsis,  defective  inner- 
vation, etc.),  both  having  tympanites  and  obstinate  constipation  as 
symptoms  in  common,  the  entire  absence  of  sound  during  prolonged 
auscultation  is  significant  of  paresis.  On  the  other  hand,  in  mechani- 
cal obstruction  the  sounds  are  usually  increased  in  intensity  and 
number  by  the  greater  vigour  of  the  peristaltic  movements  in  en- 
deavouring to  overcome  the  stenosis. 

Soft  rubbing  or  crepitating  friction  sounds  are  sometimes  heard 
in  peritonitis,  especially  over  the  right  hypochondrium  (perihepatitis) 
or  an  enlarged  spleen  (perisplenitis)  or  a  systolic  bruit  over  the  lat- 
ter. One  may  hear  at  times  a  venous  hum,  or  the  bruit  of  aneu- 
rism (or  pressure)  affecting  the  abdominal  aorta ;  and  if  pregnancy 
exists,  the  foetal  heart  sounds  (funic  souffle,  uterine  souffle,  clioc 
fetal).  Auscultatory  percussion  is  dealt  with  in  the  examination  of 
special  organs. 


SECTION   XXXIV 
EXAMINATION   OF   THE   DIGESTIVE   SYSTEM 

The  digestive  system  comprises  the  mouth,  salivary  glands, 
pharynx,  tonsils,  esophagus,  stomach,  intestines,  liver,  pancreas,  and, 
for  convenience,  the  peritoneum. 

The  subjective  symptoms  of  disease  of  these  organs  are  sum- 
marized elsewhere  (Synopsis  of  Examinations,  q.  v.),  with  page  refer- 
ences to  their  detailed  consideration.  The  objective  examination  of 
some  portions  {q.  v.)  of  the  digestive  apparatus  has  already  been  de- 
scribed— viz..  Mouth,  Salivary  Glands,  Pharynx,  and  Tonsils. 


EXAMINATION  OP  ESOPHAGUS  445 


I.    THE    ESOPHAGUS 

Anatomy  of  the  Esophagus. — The  esophagus  is  a  muscular  tube 
varying  from  f  of  an  inch  to  a  scant  inch  in  diameter.  It  is  about 
10  inches  (25.5  centimetres)  long,  beginning  at  the  upper  border  of 
the  cricoid  cartilage  opposite  the  disk  between  the"  5th  and  6th  cer- 
vical vertebrae,  and,  after  passing  through  the  diaphragm,  ends  at 
the  cardiac  orifice  of  the  stomach  opposite  the  10th  dorsal  vertebra. 

Of  its  relations  the  following  are  of  special  clinical  importance  : 
Li  the  neck,  in  front  and  at  the  sides  with  the  thyroid  gland ;  at  the 
sides  with  the  recurrent  laryngeal  nerves.  In  the  thorax,  in  front 
with  the  aorta,  the  left  bronchus  (between  4th  and  5th  dorsal  verte- 
brae), and  the  pericardium ;  laterally,  the  pleura  and,  except  at  its 
lower  portion,  the  pneumogastric  nerves. 

Examination  of  the  Esophagus. — The  cardinal  symptom  of 
esophageal  disease  is  dysphagia,  with  or  without  regurgitation. 
The  object  of  physical  examination  is  mainly  to  determine  the  pres- 
ence of  a  stricture  or  diverticulum. 

(1)  Palpation  of  the  esophagus  is  possible  only  in  the  neck,  usually 
on  the  left  side,  behind  the  trachea.  A  distinct  tumour  found  here 
may  be  a  diverticulum  distended  with  food  or  fluid.  A  brawny 
swelling,  perhaps  with  subcutaneous  emphysema,  is  indicative  of 
rupture  or  perforation  of  the  esophagus  with  resulting  inflammation 
of  the  periesophageal  tissues  which  may  proceed  to  suppuration. 
An  abscess  in  this  locality  may  be  due  to  caries  of  the  cervical  ver- 
tebrae. 

(2)  Auscultation  of  the  esophagus  is  occasionally  of  some  diagnos- 
tic value.  The  stethoscope  should  be  placed  posteriorly  just  to  the 
left  of  the  spine  about  the  level  of  the  6th  dorsal  vertebra  while  the 
patient,  at  signal,  swallows  a  mouthful  of  water.  At  the  instant  of 
swallowing  a  sound  (deglutitory)  is  heard,  followed  in  6  or  7  seconds 
by  the  esophageal  bruit,  a  sound  like  that  heard  in  one's  own  ears 
when  swallowing  saliva.  Three  to  5  seconds  later  ensues  a  second- 
ary sound  caused  either  by  the  fluid  entering  the  stomach  or  by 
regurgitation  of  air  bubbles.  If  the  primary  esophageal  bruit  is 
weak,  or  delayed  longer  than  7  seconds,  or  replaced  by  a  loud  splash- 
ing or  gurgling  noise ;  or  if  the  secondary  sound  is  delayed  longer 
than  from  5  to  12  seconds,  partial  stenosis  may  be  suspected.  If  the 
1st  or  2d  sound  is  absent  complete  stenosis  may  be  suspected.  If 
loud  gurgling  or  bubbling  sounds  lasting  for  some  minutes  are  heard 
at  any  point  along  the  left  side  of  the  spine  they  may  be  a  result  of 
contractions  of  the  esophagus  upon  fluid  contained  in  a  diverticulum 
or  in  the  dilated  portion  of  the  canal  immediately  above  a  stricture. 


446  THE  EVIDENCES  OF   DISEASE 

(3)  Instrumental  examination  of  the  esophagus  is  made  either  by 
the  passage  of  the  somewhat  flexible  but  solid  bougie  or  sound,  or 
by  the  perfectly  flexible  stomach  tube.  The  technic  of  introduction 
will  be  more  conveniently  described  in  connection  with  the  examina- 
tion of  the  stomach  (page  453).  Inspection  of  the  interior  of  the 
esophagus  has  been  practised,  but  at  present  this  method  is  mainly 
of  academic  interest. 

The  following  average  measurements  are  to  be  remembered  in 
connection  with  the  use  of  the  sound :  From  the  incisor  teeth  it  is 
6  inches  to  the  beginning  of  the  esophagus  (at  the  cricoid  cartilage); 
9  inches  to  the  crossing  of  the  left  bronchus ;  and  16  inches  to  the 
cardiac  orifice  of  the  stomach.  The  esophagus  is  normally  somewhat 
constricted  at  its  beginning,  at  the  crossing  of  the  bronchus,  and  at 
its  cardiac  end. 

Obstruction  to  the  passage  of  the  tube  may  be  due,  especially  in 
a  nervous  patient,  to  spasm  of  the  esophagus,  but  by  waiting  a 
moment  the  spasm  will  subside.  If  the  tube  passes  readily  at  one 
sitting  and  refuses  to  pass  at  another  it  is  significant  of  a  divertic- 
ulum, which  in  the  first  case  was  empty  and  allowed  the  tube  to 
slip  by  it,  and  in  the  second  sufficiently  distended  with  food  or  fluid 
to  engage  the  end  of  the  instrument  and  prevent  its  passage.  If  the 
obstruction  is  found  to  be  permanent,  it  is  necessary  to  decide  whether 
it  is  due  to  the  most  common  cause,  narrowing  (stricture)  of  the  tube, 
or  to  pressure  upon  it  from  the  outside  (aneurism,  mediastinal  tu- 
mour, enlarged  bronchial  glands). 

If  the  presence  of  a  stricture  has  been  ascertained,  one  must  de- 
termine its  locality,  calibre,  and  permeability.  The  locality  is  found 
by  passing  the  tube  to  the  strictured  point,  nipping  it  between  the 
fingers  close  to  the  incisor  teeth  and  measuring  the  distance  from 
the  fingers  to  the  end  after  withdrawal.  It  is  thus  possible  to  decide 
the  practicability  of  surgical  relief.  The  calibre  is  discovered  by 
using  sounds  or  tubes  of  varying  diameters,  finding  one  which  will 
pass  with  moderate  resistance.  Its  permealility  is  evidenced  by  hear- 
ing the  esophageal  bruit  as  previously  described,  and  by  the  passage 
of  a  somewhat  rigid  sound,  as  a  very  flexible  instrument  may  curve 
upon  itself  in  the  upper  dilated  portion  of  the  canal.  If  the  stric- 
ture is  cancerous,  which  is  usually  the  case  in  elderly  patients,  and 
the  tube  is  fenestrated,  small  particles  of  the  new  growth  may  be 
found  in  the  openings.  If  the  tube  is  bloody,  ulceration  or  erosion 
is  present. 

The  presence  of  aneurism  of  the  thoracic  aorta  is  an  absolute  bar 
to  the  use  of  the  sound  or  tube,  and  it  should  rarely,  if  ever,  be  em- 
ployed if  there  has  been  recent  vomiting  of  blood. 


EX^VMINATION  OP  THE  STOMACH 


447 


II.    STOMACH 

Anatomy  and  Surface  Relations  of  the  Stomach. — The 

stomach  lies  in  the  epigastric  and  left  hypochondriac  regions.     Five 

sixths  of  its  bulk  is  to  the  left  of  the  median  line,  one  sixth  to 

the  right.     The  larger  end, 

the    fundus,    fits    into    the     '  ' 

concave    left    vault    of    the 

diaphragm.     The  important 

points  to  be  remembered  are 

as  follows  (Plate  I  and  Fig. 

142): 

The  cardiac  orifice  (or 
cardia)  is  situated  directly 
behind  or  a  little  to  the  left 
of  the  sternal  junction  of 
the  left  7  th  cartilage,  on  a 
level  with  the  body  of  the 
11th  dorsal  vertebra.  It  lies 
4^  inches  distant  from  the 
anterior  surface  of  the  abdo- 
men. The  cardia  occupies  a 
relatively  fixed  position  be- 
cause of  its  attachment  to 
the  esophagus. 

The  pylorus  lies  between 
the  right  sternal  and  para- 
sternal lines  on  a  level  with 
or  slightly  below  the  tip  of 
the  ensiform  appendix,  and 
corresponds  to  the  body  of 

the  1st  lumbar  vertebra.  It  is  quite  freely  movable,  passing  down- 
ward and  somewhat  to  the  right,  as  the  stomach  becomes  distended 
by  air  or  food. 

The  lesser  curvature  descends  from  the  cardia,  passes  transversely 
to  the  right  and  then  ascends  to  the  pylorus.  The  two  orifices  lie 
closer  together,  and  the  lesser  curvature  is  shorter  and  sharper  than 
is  sometimes  realized. 

The  greater  curvature,  when  the  stomach  is  moderately  distended, 
lies  2  to  3  fingerbreadths  (1^  to  2^  inches)  above  the  umbilicus,  on 
a  level  with  the  infracostal  line  connecting  the  lowest  points  of  the 
costal  margins.     The  lower  border  of  a  normal  but  much- distended 


LIVER 


Fio.  142. — This  cut  shows  the  shape  and  the  topo- 
graphical relations  of  a  normal  stomach.  The 
portion  of  the  stomach  overlapped  by  the  lung 
is  indicated  by  the  dotted  area,  and  the  por- 
tion covered  by  the  liver  by  the  shaded  area. 
Traube's  area  is  that  portion  which  is  covered 
by  the  ribs  alone. 


448  THE  EVIDENCES  OF   DISEASE 

stomach  may  be  found  at  the  level  of  the  navel.  If  below  the  um- 
bilicus, the  condition  is  pathological. 

The  fundus  rises  as  high  as  the  lower  border  of  the  left  5th  rib  in 
the  mammillary  line — from  1  to  2  inches  higher  than  the  eardia — 
above  and  behind  the  apex  of  the  heart. 

The  anterior  surface  is  for  the  most  part  overlapped  by  the  liver, 
left  lung,  and  certain  of  the  left  ribs,  leaving  a  comparatively  small 
extent  of  its  surface  in  direct  contact  with  the  anterior  muscular 
wall  of  the  abdomen.  The  pyloric  end,  the  lesser  curvature,  and  the 
eardia  lie  behind  and  beneath  the  quadrate  and  left  lobes  of  the 
liver ;  the  fundus  and  a  portion  of  the  body  are  overlaid  by  the  lower 
anterior  portion  of  the  left  lung,  and  the  anterior  parts  of  the  7th, 
8th,  and  9th  left  ribs.  Traube's  space  is  the  area  over  which  the 
stomach  is  in  direct  contact  with  the  ribs  just  mentioned,  and  is 
bounded  above  by  the  liver  and  lung,  externally  by  the  spleen,  the 
remaining  boundary  being  formed  by  the  left  costal  margin.  Over 
this  space,  as  well  as  the  exposed  area  of  the  stomach  in  the  epigas- 
tric region,  pure  gastric  tympany  may  be  elicited. 

The  diameters  of  the  stomach  when  moderately  distended  (Sappey) 
are,  between  fundus  and  pylorus,  10  to  12  inches ;  between  lesser 
and  greater  curvature,  4  to  5  inches ;  and  between  the  anterior  and 
posterior  walls,  3^  inches.  The  distance  between  the  eardia  and 
pylorus  varies  from  3  to  6  inches.  The  long  diameter  lies  in  general 
transversely,  but  with  a  downward  inclination  from  left  to  right.  As 
the  stomach  distends  (food,  fluid,  gas)  it  rotates  in  such  a  manner 
that  the  lesser  curvature  is  directed  toward  the  spine,  the  greater 
curvature  moves  forward,  the  anterior  surface  looks  upward  and  for- 
ward, and  the  pylorus  moves  to  the  right. 

Physical  Examination  of  the  Stomach. — The  stomach 
and  its  diseases  (omitting  the  anamnesis)  are  investigated  by  direct 
physical  examination,  and  by  chemical  and  microscopical  analysis  of 
the  stomach  contents  (Index — Stomach,  Examination  of  contents  of). 

The  principal  object  of  physical  examination  of  the  stomach  is  to 
determine  its  size  and  position,  although  there  are  certain  other 
physical  signs  to  be  observed  which  do  not  bear  directly  upon  the 
dimensions  and  location  of  the  organ.     The  methods  are  as  follows  : 

(rt)  Inspection. — A  distinct  bulging  in  any  part  of  the  abdomen  ex- 
cept the  epigastric  region  may  be  due  to  a  dilated  stomach.  A  swell- 
ing due  to  this  cause  is  most  frequently  seen  in  the  hypogastric  or 
the  umbilical  region,  while  the  epigastrium  is  notably  hollow  and 
transversely  depressed.  As  the  eardia  is  the  comparatively  immobile 
point  of  attachment  of  the  stomach  to  the  diaphragm  through  the  me- 
dium of  the  esophagus,  the  descent  of  the  enlarged  or  prolapsed  organ 


EXAMINATION  OP  THE  STOMACH  449 

increases  toward  the  pylorus.  With  the  patient  in  the  recumbent  pos- 
ture, a  marked  concavity  between  the  costal  arches,  extending  from  the 
ensiform  appendix  to  or  below  the  umbilicus,  with  perhaps  a  vertical 
median  sulcus  wider  above  than  below,  the  abdomen  being  as  a  whole 
flattened  in  the  central  portions  and  bulging  in  the  lateral  regions, 
is  significant  of  prolapse  of  the  stomach  (gastroptosis).  In  the  erect 
position  the  epigastric  region  becomes  still  more  depressed,  while  the 
umbilical  and  in  particular  the  pubic  regions  bulge  outward.  In- 
spection may  also  show  peristaltic  waves  passing  from  left  to  right 
(rarely  reversed)  along  the  dilated  viscus. 

(b)  Palpation. — This  determines  the  existence  of  tenderness, 
swelling  or  tumour,  and  succussion  or  splashing. 

Tenderness  {q.  v.),  more  or  less  general,  is  common  in  acute  and 
chronic  inflammations  of  the  stomach.  It  is  a  sign  of  gastric  ulcer 
only  when  permanently  and  very  strictly  localized. 

Tumour  of  the  stomach,  if  found  in  an  elderly  person,  is  usually 
cancerous,  most  commonly  affecting  the  pyloric  extremity  and  gener- 
ally situated  a  little  to  the  right  of  the  median  line  between  the 
ensiform  appendix  and  the  umbilicus.  It  may  be  extremely  mobile 
and  capable  of  displacement  into  almost  any  one  of  the  abdominal 
regions.  But  if  it  has  contracted  adhesions  to  fixed  organs  or  tissues 
it  may  be  quite  firmly  moored ;  or,  if  adherent  to  the  liver  or  dia- 
phragm, may  move  with  respiration.  In  younger  persons  a  tumour 
here  may  be  the  result  of  hypertrophy  of  the  pylorus.  A  palpable 
diffuse  thickening  (perigastritis)  of  a  portion  of  the  stomach  wall 
may  be  found  as  a  consequence  of  chronic  gastric  ulcer.  If  the 
abdominal  walls  are  thin  and  relaxed  and  the  stomach  prolapsed,  it 
may  be  possible  but  not  likely  for  the  pancreas  to  be  felt  and  mis- 
taken for  a  tumour  of  the  stomach  (Ewald),  and  a  similar  mistake 
may  arise  from  the  finding  of  a  small  lymphatic  gland  in  the  gastro- 
colic ligament,  at  the  middle  of  the  greater  curvature.  If  the  stom- 
ach is  dilated  and  the  abdominal  walls  are  thin  and  relaxed,  it  may 
be  practicable  to  feel  the  lower  border  of  the  enlarged  viscus. 

If  fluid  and  air  are  present  in  the  stomach,  splashing  or  succus- 
sion sounds  or  sensations  may  be  elicited  by  placing  one  hand  over 
the  lower  ribs  posteriorly,  while  with  the  other  hand  a  series  of  sud- 
den, quick  pressures  are  made  over  various  points  of  the  abdomen. 
If  splashing  is  found  as  long  as  3  hours  after  a  meal,  particularly  if 
it  exists  below  the  umbilicus,  one  may  suspect  the  presence  of  a 
dilated  or  prolapsed  stomach.  There  is,  however,  one  source  of  error 
in  that  similar  sounds  may  be  elicited  from  the  transverse  colon  or 
other  portion  of  the  intestine.  If  this  question  arises  the  colon 
•should  be  emptied  by  a  high  enema  or  a  laxative. 


450  THE  EVIDENCES  OF  DISEASE 

(c)  Percussion. — In  attempting  to  ascertain  the  shape  and  posi- 
tion of  the  stomach  by  percussion  two  methods  may  be  employed, 
ordinary  and  auscultatory. 

(1)  Ordinary  Percussion. — As  a  rule,  this  is  not  trustworthy, 
mainly  because  of  the  fact  that  the  percussion  note  of  the  surround- 
ing intestines,  in  particular  the  colon,  so  closely  resembles  gastric 
tympany  as  to  be  indistinguishable  from  it.  Moreover,  the  colon,  if 
distended,  may  overlie  the  adjacent  edge  of  the  stomach  and  thus 
render  it  impracticable  to  determine  with  any  accuracy  the  position 
of  the  lower  border.  The  degree  of  distention  of  the  stomach,  whether 
the  distention  is  due  to  fluid  or  solid  material  (dulness)  or  gas  (tym- 
pany), and  the  fact  that  the  stomach  is  overlapped  by  the  liver 
(which  may  be  enlarged)  and  left  lung  are  additional  sources  of 
uncertainty.  If  the  stomach  is  considerably  distended  by  gas,  ordi- 
nary percussion  may  be  of  some  service. 

The  position  of  the  lower  border  of  the  organ  may  be  determined, 
using  simple  percussion,  by  causing  the  patient  to  drink  measured 
quantities  of  water  (Dehio),  7  or  8  ounces  at  a  time,  while  in  the  erect 
position,  and  then  percussing.  The  fluid  in  the  stomach  causes  a 
line  of  dulness,  indicating  the  position  of  the  lower  border,  and  each 
additional  quantity  of  water  ingested  broadens  the  line  of  dulness 
and  lowers  the  border  f  to  1\  inch,  formally  the  lower  border  is 
never  found  below  the  umbilicus.  If  it  is  discovered  below  the  navel, 
either  dilatation  or  prolapse,  or  both,  exist.  The  distinction  must 
be  made  by  ascertaining,  through  auscultatory  percussion  or  infla- 
tion, whether  the  pylorus  and  lesser  curvature  have  or  have  not 
shared  in  the  descent. 

Ordinary  percussion  enables  one  to  determine  the  upper  and  left 
borders  of  the  exposed  gastric  tympany,  less  perfectly  the  outline  of 
the  fundus  and  lesser  curvature,  which  are  overlapped  by  the  liver 
and  lung.  Practically  this  is  accomplished  by  the  delimitation  of 
the  lower  border  of  the  left  lung  {q.  v.),  the  lower  border  of  the  left 
lobe  of  the  liver  {q.  v.),  and  of  the  spleen  {q.  v). 

The  average  normal  area  of  gastric  tympany  is  shown  in  Fig. 
142.  An  increase  in  its  extent,  mainly  in  a  vertical  direction,  will 
be  found  if  the  stomach  is  distended  by  gas  (common  in  general 
meteorism),  and  if  the  left  lobe  of  the  liver  is  shrunken  or  the 
left  lung  retracted  by  pleurisy  or  fibroid  changes,  thus  allowing  the 
stomach  to  lie  in  contact  with  a  larger  surface  of  the  abdominal  or 
lower  left  thoracic  wall.  On  the  other  hand,  this  area  is  made 
smaller  by  enlargement  of  the  left  lobe  of  the  liver  or  of  the 
spleen,  and  the  tympanicity  of  Traube's  space  is  abolished  by  a  left 
pleural  effusion. 


EXAMINATION  OF  THE  STOMACH 


451 


(2)  Auscultatory  Percussion. — For  determining  the  outline  and 
position  of  the  stomach  this  method  {q.  v.)  is  by  far  better  than 
simple  percussion.  The  liver  and  lung  do  not  interfere  with  its  ac- 
curacy, as  the  tympanitic  sound  of  the  underlying  stomach  is  clearly 
transmissible  through  these  viscera.  Like  simple  percussion,  it  is 
perhaps  not  reliable  in  ascertaining  the  actual  size  of  the  organ,  be- 
cause of  the  varying  degree  of  distention  at  different  times  and  the 
possibility  that  an  inflated  colon  has  intruded  over  the  lower  border 
of  the  stomach.     The  technic  is  as  follows  : 

Place  the  chest  piece  of  the  stethoscope  at  the  usual  position  of 
the  fundus,  over  the  6th  or  7th  rib  in  the  left  mammillary  line,  or  in 
the  angle  between  the  ensiform  appendix  and  the  left  costal  mar- 
gin, and  percuss  near  the 
stethoscope  in  order  to 
fix  in  the  mind  the  char- 
acteristics of  the  sound 
(Fig.  143).  Then  percuss 
from  above  and  from 
each  side  toward  the 
stethoscope,  as  well  as 
from  below  upward,  in 
various  lines,  beginning 
in  each  instance  well  out- 
side of  the  usual  normal 
limits.  When  percuss- 
ing from  below,  com- 
mence at  a  point  not 
much  above  the  symphy- 
sis pubis,  as  the  greater 
curvature    may    be    far 

down.  A  characteristic  sound  of  greater  intensity  and  clearness  and 
of  higher  pitch  denotes  that  the  border  of  the  stomach  has  been 
reached,  and  at  each  point  a  mark  should  be  made.  The  strokes 
should  be  of  only  moderate  strength.  In  order  to  check  the  result 
percussion  should  be  repeated,  this  time  from  the  stethoscope  out- 
ward, or  the  instrument  may  be  placed  over  another  part  of  the 
stomach  during  the  repercussion.  It  is  to  be  remembered  that  the 
bulk  of  the  stomach  lies  to  the  left  of  the  median  line  even  when 
dilated  or  prolapsed.  By  this  method  the  position  of  the  lesser  and 
greater  curvatures,  the  fundus,  and  the  pylorus  can  be  quite  reliably 
determined. 

It  is  generally  possible   (Stengel),  in  the  case  of  a  tumour  in  the 
pyloric  region,  to  determine  by  auscultatory  percussion  whether  or 


tl^ 


Fig.  143. — To  determine  the  outline  of  the  stomach  by 
auscultatory  percussion.  The  stethoscope  may  be 
placed  at  either  of  the  points  indicated  by  the  cir- 
cles during  the  first  percussion.  During  the  reper- 
cussion it  should  be  shifted  to  the  other  point_ 
Arrows  show  lines  along  which  percussion  should  be 
conducted. 


462 


THE  EVIDENCES  OF  DISEASE 


not  it  belongs  to  the  stomach.  Place  the  stethoscope  over  the  body 
of  the  stomach  and  percuss  toward  the  tumour  from  all  directions. 
The  sound  heard  over  the  tumour  (Fig.  144,  C)  differs  in  character 
from  that  obtained  over  the  stomach,  D,  but  if  the  new  growth  in- 
volves the  stomach  wall,  C  resembles  D  much  more  nearly  than  A 

(liver)  and  B  (intestine)  re- 
semble D.  This  method  is  es- 
pecially useful  in  the  differen- 
tial diagnosis  between  tumours 
of  the  stomach  and  tumours  of 
the  gall  bladder. 

{d)  Auscultation  of  the 
Stomach. — There  is  little  of 
definite  diagnostic  value  to  be 
obtained  from  auscultation  of 
the  stomach.  The  sounds 
which  may  be  heard  and  the 
significance  which  they  may 
possess  are  as  follows : 

(1)  The  sounds  caused  by 
the  swallowing  of  fluid  have 
been  previously  described  as 
heard  upon  auscultation  of  the 
esophagus  {q.v.).  Upon  listen- 
ing over  the  notch  between  the  ensiform  appendix  and  the  left  costal 
margin  the  same  sounds  may  be  heard — viz.,  at  the  instant  of  swal- 
lowing, the  deglutitory  sound  (which  is  not  often  heard  over  the 
stomach) ;  the  esophageal  bruit,  6  or  7  seconds  after  the  act  of  deglu" 
tition ;  and  the  secondary  murmur,  3  to  5  seconds  later.  The  absence 
of  the  latter  two  sounds,  if  demonstrated,  may  be  of  some  signifi- 
cance as  indicating  esophageal  stenosis,  or  possibly  also  a  lack  of 
motor  power  in  the  deglutitory  muscles. 

(2)  Crackling  or  fizzing  sounds  may  be  heard  over  the  stomach,  and 
when  detected  constitute  positive  proof  of  active  fermentation  and 
stasis  of  food.     The  sounds  arise  from  the  bursting  of  bubbles  of  gas. 

(3)  Succussion  sounds  {q.  v.)  have  been  described  as  audible  at  a 
distance  from  the  patient.  The  same  variety  of  sounds  of  less  in- 
tensity may  be  heard  by  direct  auscultation  upon  shaking  the  trunk 
from  side  to  side,  or  upon  voluntary  change  of  position  of  the  pa- 
tient. While  these  are  often  audible  in  the  normal  stomach,  if  they 
are  present  at  times  when  the  organ  should  be  empty  it  is  presump- 
tive evidence  of  loss  of  motor  power  (atony)  or  dilatation  with  re- 
tention. 


Fig.  144. — Showing  the  method  of  determining, 
by  auscultatory  percussion,  that  a  tumour 
belongs  to  the  stomach  rather  than  to  the 
liver  or  intestine.  If  the  tumour  involves  the 
wall  of  the  stomach  the  percussion  notes  over 
points  A,  J?,  C  and  D  differ,  but  C  resembles 
D  much  more  nearly  than  A  or  ^resemble  D- 


EXAMINATION  OF  THE  STOMACH  453 

(4)  Loud  rumbling  or  gurgling  sounds  or  rasping  vibrations, 
which  are  often  synchronous  with  respiration,  are  not  infrequently 
heard,  even  at  some  distance  away.  They  are  caused  by  the  respira- 
tory rise  and  fall  of  fluid.  Such  sounds  are  especially  liable  to  occur 
in  gastric  dilatation  or  prolapse,  or  in  the  wearers  of  tight  corsets. 

(5)  The  sounds  of  the  heart  may  be  heard  over  a  gas-distended 
stomach  (acting  as  a  resonating  chamber),  and  are  encountered  par- 
ticularly in  gastric  dilatation.  In  such  cases  the  sounds  possess  a 
ringing,  reverberating  quality  quite  foreign  to  their  usual  character. 

{e)  Inflation  or  Ballooning  of  the  Stomach. — Probably  the  best 
method  of  determining  the  size,  shape,  and  position  of  the  stomach, 
including  an  accurate  outline  of  the  lesser  and  greater  curvatures 
and  pyloric  extremity,  is  that  of  inflation.  There  are  two  ways  of 
inflating  the  stomach,  of  which  the  second  is  by  far  the  better. 

(1)  The^rs^  is  to  administer  in  solution  1  drachm  of  sodium  bicar- 
bonate, followed  immediately  by  the  same  amount  of  tartaric  acid, 
also  in  solution.  The  carbon  dioxide  evolved  promptly  distends  the 
stomach.  This  procedure  is  open  to  the  very  serious  objection  that 
the  evolution  of  the  gas  is  not  under  control.  Thus  the  stomach 
may  be  dangerously  overdistended,  causing  hemorrhage  or  cardiac 
embarrassment,  or  there  may  not  be  sufficient  gas  to  fully  balloon 
the  organ,  and  its  full  size  and  shape  fail  to  be  shown. 

(3)  The  second  manner  of  inflation  is  to  introduce  the  stomach 
tube,  and  attach  to  its  external  end  by  a  bit  of  glass  tubing  the  bulb 
of  a  Davidson  syringe.  Air  should  then  be  pumped  into  the  stom- 
ach, at  first  vigorously,  in  order  by  somewhat  sudden  distention  to 
cause  the  pylorus  to  contract  and  thereby  prevent  the  passage  of  the 
air  into  the  intestines  (Pepper,  Stengel).  The  amount  of  air  injected 
is  under  control,  and  it  may  be  allowed  to  escape  immediately  if  un- 
pleasant symptoms  should  appear. 

iis  the  stomach  is  distended  its  outlines  become  apparent  through 
the  abdominal  walls  and  it  is  comparatively  easy  to  determine  its 
general  size,  shape,  and  position,  as  well  as  the  more  important  de- 
tails relating  to  the  position  of  the  upper  and  lower  borders  and  the 
pylorus.  If,  because  of  great  thickness  of  the  abdominal  walls,  the 
stomach  does  not  become  manifest  to  inspection  (a  rare  occurrence 
in  cases  requiring  this  method  of  examination),  inflation  greatly  facil- 
itates either  ordinary  or  auscultatory  percussion. 

Inflation  should  not  be  employed  in  very  feeble  patients,  or  after 
recent  haematemesis,  or  where  there  is  a  suspicion  of  gastric  ulcer,  or 
in  cases  of  organic  cardiac  disease. 

(/)  Obtaining  the  Stomach  Contents. — (1)  Technic.—T\xe  method 
is  as  follows  :  Provide  a  soft-rubber  stomach  tube  having  two  or  more 
31 


454  THE  EVIDENCES  OP  DISEASE 

openings  in  its  lower  end.  Into  the  upper  end  a  piece  of  glass  tubing, 
3  or  4  inches  long,  is  inserted.  Have  also  a  pitcher  or  basin  of  hot 
water,  a  wide-mouthed  6  or  8  ounce  glass  bottle,  a  large  towel  or 
sheet,  and  a  Politzer  bag  or  aspirating  bottle  (seldom  required). 
Place  the  tube  in  the  warm  water,  let  the  patient  sit  in  a  chair  or 
nearly  upright  in  bed,  pin  the  towel  or  sheet  around  the  neck  so  that 
it  covers  the  front  of  the  body,  and  let  him  hold  the  bottle  in  his 
left  hand.  Take  the  tube  from  the  water,  using  no  other  lubricant, 
as  the  mucus  in  the  pharynx  and  esophagus  is  sufficient  to  prevent 
friction  of  the  moistened  tube.  Eequest  the  patient  to  bend  the 
head  slightly  forward  and  open  the  mouth,  but  not  to  protrude  the 
tongue.  He  should  be  asked,  and  admonished  at  intervals,  to  breathe 
steadily  and  deeply.  Then,  loitliout  at  any  time  putting  a  finger  in 
the  mouth,  pass  the  tube  back  to  the  pharynx,  and  when  its  further 
progress  is  arrested,  ask  the  patient  to  swallow,  at  the  same  time 
pushing  the  tube  farther  in,  when  it  will  enter  the  esophagus.  It 
should  now  be  rapidly  fed  into  the  mouth.  Practically  there  need 
be  no  fear  of  entering  the  larynx.  If  the  progress  of  the  tube  is 
arrested,  it  is  probably  due  to  muscular  spasm  of  the  esophagus, 
which  will  relax  after  a  moment  of  waiting ;  or,  rarely,  to  a  diverticu- 
lum or  stenosis  of  the  esophagus.  The  passage  of  the  tube  should 
be  continued  until  at  least  17  or  18  inches  of  its  length,  measured 
from  the  incisor  teeth,  and  indicated  by  a  ring  imprinted  upon  the 
tube,  or  a  thread  tied  around  it,  has  been  introduced.  The  glass 
tube  should  then  be  placed  in  the  bottle  and  the  patient  asked  to 
hold  his  breath  and  strain  as  in  defecation,  or  make  an  attempt  to 
vomit.  Either  of  these  efforts  will,  as  a  rule,  result  in  successive  ex- 
pulsions of  the  contents  of  the  stomach  into  the  bottle.  It  may  be 
necessary  to  push  the  tube  farther  in  or  to  withdraw  it  somewhat, 
the  end  of  the  tube  either  not  reaching  to  the  fluid  in  the  stomach, 
or,  by  reason  of  too  great  a  length  having  been  introduced,  is  coiled 
upon  itself  above  the  level  of  the  fluid.  If,  as  seldom  happens,  these 
efforts  are  unsuccessful,  the  tube  of  the  Politzer  bag  may  be  slipped 
over  the  end  of  the  glass  tube  and  suction  exercised.  If  mucus  or 
saliva  collects  in  the  mouth  or  throat,  incline  the  head  forward  and 
let  it  trickle  out.  After  having  obtained  all  that  is  possible  of  the 
gastric  contents,  the  finger  should  be  placed  firmly  upon  the  end  of 
the  glass  tube  (as  in  using  a  catheter),  the  rubber  tube  withdrawn 
and  its  contained  fluid  allowed  to  run  into  the  bottle. 

Until  tolerance  has  been  established,  the  earlier  introductions  of 
the  tube  usually  cause  more  or  less  violent  efforts  to  vomit.  Steady, 
regular  deep  breathing  is  most  likely  to  diminish  such  attempts. 
Passing  cyanosis,  due  to  the  temporary  cessation  of  respiration,  is 


EXAMINATION  OP  TBE  STOMACH 


455 


sometimes  encountered,  but  very  rarely  persists  sufficiently  to  require 
withdrawal  of  the  tube. 

(2)  Contraindications. — Certain  contraindications  to  the  use  of 
the  tube,  largely  because  of  the  strain  and  effort  of  vomiting,  must 
be  recognised.     The  conditions  to  be  considered  as  an  absolute  bar 
to  its  employment,  subject 
in   part  to  the  exercise  of 
judgment  and  the  dictates 
of  experience,  are  as  follows : 

Marked  prostration,  con- 
tinued fevers,  or  cachectic 
states ;  broken  compensation 
of  heart  lesions,  advanced 
fibrous  or  fatty  degenera- 
tions of  the  heart,  and  angi- 
na pectoris ;  thoracic  aneu- 
rism and  advanced  general 
arteriosclerosis ;  last  stages 
of  pulmonary  tuberculosis, 
emphysema,  bronchitis,  and 
recent  haemoptysis ;  gastric 
ulcer  with  recent  haemateme- 
sis  or  tarry  stools ;  recent  in- 
tracranial, renal,  vesical,  or 
rectal  hemorrhages  ;  and 
pregnancy  and  old  age. 

Interpretation  of  the 
Results  of  the  Physi- 
cal Examination  of  the 
Stomach. — The  size  and 
position  of  the  stomach  hav- 
ing been  ascertained  and 
marked  upon  the  abdominal 
wall,  it  remains  to  decide 
from  the  findings  whether 
the  stomach  is  normal  in 
size  and  position,  whether  it 
is  nearly  normal  in  size  but 

is  prolapsed  (gastroptosifi),  or  whether   it   is  dilated  {gastr ectasia). 
Some  degree  of  prolapse  usually  accompanies  dilatation. 

(1)  The  Normal  Stomacli. — The  normal  positions  of  the  lesser  and 
greater  curvatures  and  the  pylorus  have  been  previously  described 
and  are  shown  in  Fig.  142. 


Fir,.  14"i.  — Krokoii  line  slmws  [.lohipse  of  the 
stomach  (gastroptosis).  Note  vertical  position 
of  stomach ;  also  the  situation  of  the  pyloric 
end  at  or  near  the  umbilicus  as  compared  to 
its  normal  location  (indicated  by  the  cross). 
Solid  line  shows  dilatation  of  the  stomach 
(gastrectasia).  Note  descent  of  lower  border 
to  or  below  the  umbilicus,  while  the  pyloric 
end  lies  a  relatively  short  distance  below  the 
normal  point.  Note  also  the  much  increased 
distance  between  pylorus  and  the  most  depend- 
ent portion  of  the  lower  border. 


456  THE  EVIDENCES  OP  DISEASE 

(2)  Gastroptosis. — If  the  pyloric  end  is  low  down  (Fig.  145),  so 
that  while  the  lower  border  is  below  the  umbilicus  the  lesser  curva- 
ture and  pylorus  are  correspondingly  depressed  (to  a  point  near  the 
umbilicus),  the  organ  as  a  whole  taking  a  decidedly  vertical  position, 
prolapse  of  the  stomach  may  be  assumed  to  be  present. 

(3)  Gastrectasia. — If,  on  the  other  hand,  the  pylorus  and  lesser 
curvature  are  found  to  have  descended  only  to  a  relatively  slight 
extent  below  their  normal  position,  while  the  lower  border  lies  below 
the  umbilicus  (Fig.  145),  dilatation  is  present.  It  will  be  noted  that 
the  descent  of  the  greater  curvature  affects  mainly  its  pyloric  (and 
most  dependent)  half,  and  that  in  consequence  the  distance  between 
this  part  of  the  lower  border  and  the  pylorus  is  greatly  increased. 

It  is  quite  evident  that  a  determination  of  the  site  of  the  lower 
border  alone  is  not  sufficient  to  discriminate  between  prolapse  and  dila- 
tation, but  that  a  knowledge  of  the  position  of  the  pylorus  and  lesser 
curvature  is  an  absolute  requisite.  It  must  also  be  borne  in  mind 
that  in  some  individuals  the  stomach  is  normally  much  larger  than 
the  average  (megastria,  megalogastria),  and  a  diagnosis  of  patho- 
logical  dilatation  can  not  be  made  unless  there  are  coexisting  evi- 
dences of  motor  weakness  and  stagnation  of  food  (Index — Stomach 
contents,  examination  of). 

III.    INTESTINES    AND    PERITONEUM 

Topographical  Anatomy  of  the  Intestines. — (1)  Small 
Intestines. — The  jejunum  and  ileum  occupy  in  general  the  central 
portion  of  the  abdomen.  The  coils  of  the  ileum  lie  in  the  left  lum- 
bar, left  iliac,  and  left  half  of  the  umbilical  regions.  The  coils  of 
the  jejunum  are  found  in  the  right  half  of  the  umbilical,  right 
lumbar,  right  iliac,  and  the  pubic  regions.  As  the  coils  are  ex- 
tremely movable  these  boundaries  are  ill-defined  and  of  little  value. 

(2)  Large  Intestine. — The  colon  occupies  the  periphery  of  the 
abdomen,  and  by  comparison  with  the  small  intestine  remains  in  a 
relatively  fixed  position  (Fig.  146). 

The  middle  of  the  lower  border  of  the  ccecum  (its  apex)  lies  at 
the  centre  of  a  line  drawn  from  the  anterior  spine  of  the  ilium  to 
the  symphysis  pubis.  The  ileum  joins  the  caecum  on  its  inner  and 
posterior  aspect,  about  3  inches  internal  to  the  anterior  spine. 

The  appendix  vermiformis  is  found  in  the  right  iliac  region.  Its 
base  lies  at  the  middle  of  a  line  drawn  from  the  anterior  spine  to  the 
umbilicus,  corresponding  to  the  right  edge  of  the  rectus  muscle 
(McBurney's  point).  It  is  attached  close  to  the  ileocaecal  valve  on 
the  inner  and  posterior  side  of  the  caecum,  and  the  upper  portion  of 
the  appendix  is  therefore  concealed  by  the  latter.     The  appendix 


EXAMINATION  OF  INTESTINES 


457 


may  lie  in  any  radius  of  a  circle  having  this  point  as  a  centre.  In 
the  majority  of  cases  it  passes  either  downward,  outward,  or  inward ; 
in  a  minority  upward.  It  averages  3^  to  4  inches  in  length,  with 
the  diameter  of  a  goose  quill. 

The  ascending  colon,  running  upward  on  the  right  side  from  the 
comparatively  superficial  caecum,  sinks  back  against  the  posterior 
abdominal  wall  and  may 
be  partly  overlaid  by  the 
small  intestines.  It  passes 
up  to  the  under  and  con- 
cave surface  of  the  liver, 
by  which  it  is  sheltered, 
and  then  turns  sharply  to 
the  left,  forming  the  he- 
patic flexure. 

The  t?-ansverse  colon 
passes  forward  and  down- 
ward to  the  left  until  its 
lower  border  lies  at  the 
level  of  the  umbilicus, 
then  curving  upward  and 
backward  it  disappears 
under  the  left  costal  arcli 
and  behind  the  fundus  of 
the  stomach  to  form  the 
splenic  flexure,  which  lies 
at  a  higher  point  than 
the  hepatic  flexure. 

The  descending  colon 
then  proceeds  downward 

on  the  left,  terminating  in  the  sigmoid  flexure  in  the  left  iliac  re- 
gion. It  may  be  noted  that  the  caecum,  the  transverse  colon,  and  the 
upper  part  of  the  sigmoid  flexure  are  quite  superficial,  while  the 
hepatic  and  splenic  flexures  lie  deeply  under  the  protecting  costal 
arches. 

Examination  of  the  Intestines  and  Peritoneum.— The 
principal  symptoms  and  signs  of  disease  of  the  intestines  and^  peri- 
toneum have  been  already  discussed  under  the  heads  {q.  v.)  of  Vomit- 
ing, Constipation,  Diarrhea,  Pain,  and  General  Examination  of  the 
Abdomen.     Certain  points,  however,  may  here  receive  consideration. 

(1)  Inspection  of  Intestines.— If  the  colon  is  distended  by  gas  its 
course,  with  the  exception  of  the  hepatic  and  splenic  flexures,  may 
be  well  defined.     In  such  a  case  the  ascending  and  descending  por- 


Fio.  146.— Showing  the  topographical  relations  of  the 
colon  and  vermiform  appendix  (semidiagrammatic). 
Note  (1)  the  line  from  the  anterior  superior  spinous 
process  to  the  symphysis  pubis  and  the  relation  of 
the  apex  of  the  caecum  thereto;  (2)  the  relation  of 
the  ileo-cfccal  junction  and  the  base  of  the  appendix 
to  the  line  running  from  anterior  superior  spine  to 
umbilicus ;  (3)  the  concealment  of  the  hepatic  and 
splenic  flexures  of  the  colon  by  the  costal  arches; 
and  (4)  the  relation  of  the  transverse  colon  to  the 
stomach  above  and  the  umbilicus  below. 


468 


THE  EVIDENCES  OF  DISEASE 


tions  are  seen  as  elongated  swellings  in  either  lateral  region  of  the 
abdomen,  while  its  transverse  portion  becomes  prominent  at  or  just 
above  the  umbilicus.  The  caecum  is  the  largest  in  diameter,  and 
therefore  the  most  distensible,  of  any  portion  of  the  large  intestine. 
Tlie  junction  of  the  sigmoid  flexure  and  the  rectum  is  the  narrowest 
and  the  most  liable  to  stricture.  The  visible  "  patterns  of  tumidity  " 
in  intestinal  obstruction  have  been  considered  (page  429). 

(2)  Palpation  of  Intestines. — By  touch  one  discovers  an  accumu- 
lation of  fsecal  matter  in  the  intestine,  known  by  its  doughy  feeling 
and  the  fact  that  the  mass  may  be  indented  by  pressure.  It  is  stated 
that  under  certain  circumstances  a  crepitating  or  "  sticky  "  sensation 
may  be  perceived  as  the  palpating  fingers  relax  their  pressure.  This 
is  due  to  the  separation  of  the  intestinal  wall  from  a  faecal  lump,  but, 
as  this  sign  requires  for  its  production  that  the  intestine  should  be 
sufficiently  distended  with  gas  to  effect  such  a  separation,  as  well  as 
the  proper  degree  of  adhesiveness  in  the  faecal  mass,  it  must  be  of 
limited  availability.  Fascal  accumulation  occurs  most  frequently,  per- 
haps, in  the  caecum  and  ascending  colon,  often  also  in  the  sigmoid  flex- 
ure. Gallstones  and  enteroliths  are  sometimes  encountered.  Their 
hardness  and  mobility  and  the  history  of  the  case  must  be  depended 

upon  for  differentiation. 
It  is  to  be  remembered 
that,  owing  to  the  close 
relation  of  the  hepatic 
flexure  to  the  liver  and 
gall  bladder,  a  gallstone 
may  ulcerate  through 
into  this  portion  of  the 
large  intestine. 

Gurgling  on  pres- 
sure in  the  right  iliac 
fossa  occurs  in  typhoid 
fever,  but  is  met  with 
too  often  in  healthy  in- 
dividuals to  be  of  much 
diagnostic  value.  Vol- 
vulus affects  most  com- 
monly the  sigmoid  flex- 
ure, because  of  the  very 
considerable  mobility  of 
the  latter. 

(3)  Percussion  of  Intestines.— Ordinary  percussion  is  of  little  or 
no  value  in  delimiting  the  large  from  the  small  intestine,  the  tym- 


Fio.  147.— Determining  the  limits  of  the  colon  by  aus- 
cultatory percussion.  Arrows  show  the  lines  along 
which  percussion  should  be  conducted;  the  circle, 
the  point  at  which  the  stethoscope  is  placed. 


EXAMINATION  OF  INTESTINES 


459 


panitic  quality  of  one  resembling  that  of  the  other  too  closely  for 
discrimination. 

If,  however,  the  colon  is  empty  of  solids,  and  distended  with  air 
or  gas,  it  is  occasionally  practicable  to  ascertain  its  size  and  course 
by  auscultatory  percussion. 
If  required,  the  colon  may 
be  emptied  by  irrigation  and 
inflated  by  pumping  air  into 
it.  It  is  requisite  that  the 
small  intestines  should  not 
be  excessively  ballooned,  as 
otherwise  their  percussion 
sound  is  too  much  like  that 
of  the  colon  to  be  clearly 
separated.  To  outline  the 
colon  by  this  method,  place 
the  stethoscope  over  the 
caecum  (Fig.  147).  Begin 
percussion  at  a  point  mid- 
way between  umbilicus  and 
symphysis,  and  carry  it  to 
right,  to  left,  and  upward, 
until  in  each  direction  the 
greater  intensity,  heightened  pitch,  and  altered  quality  of  the  sound 
announce  that  the  inner  limit  of  the  colon  has  been  encountered. 
Then  percuss  from  the  epigastrium  downward,  and  from  each  lateral 
lumbar  region  inward  toward  the  centre  of  the  abdomen,  to  deter- 
mine the  outer  limits  of  the  transverse,  ascending,  and  descending 
portions  of  the  colon. 

Aside  from  congenital  anomalies  in  the  position  of  the  colon  dis- 
covered by  operation  or  autopsy,  displacement  may  occur  as  a  part  of 
a  prolapse  of  one — e.  g.,  gastroptosis — or  several  of  the  abdominal  vis- 
cera (visceroptosis,  splanchnoptosis).  Such  a  displacement  largely 
affects  the  transverse  colon,  the  middle  of  which  descends  below  the 
navel  so  that  it  assumes  a  V  shape  (Fig.  148),  with  consequent  kink- 
ing at  the  hepatic  and  splenic  flexures,  and  perhaps  obstinate  consti- 
pation, meteorism,  and  other  symptoms  of  obstruction.  In  one  such 
case  of  my  own,  exploratory  cceliotomy  was  done,  by  the  advice  of  a 
most  competent  surgeon,  and  this  condition  of  affairs  was  found. 

It  is  claimed  (Stengel)  that  it  is  possible  by  auscultatory  percus- 
sion to  determine  that  a  tumour  found  to  lie  in  the  previously  ascer- 
tained course  of  the  intestine  originates  in  the  wall  of  the  colon. 
The  stethoscope  is  placed  over  the  colon  near  to  the  tumour,  and 


Fig.  148. — V-shaped  colon. 


460 


THE  EVIDENCES  OF  DISEASE 


percussion  made  over  the  tumour  and  toward  it  from  every  direction. 
The  note  over  the  tumour  (C,  Fig.  149),  if  the  latter  is  connected 
with  the  colon,  will  resemble  much  more  nearly  than  the  note  B 
(over  the  small  intestines)  the  note  A  over  the  colon, 

(4)  Auscultation. — Aside  from  auscultatory  percussion  the  only 
use  of  the  stethoscopic  examination  of  the  intestines  is  to  determine 
the  activity  of  peristalsis  (page  444). 

Here  may  be  mentioned  the  condition  of  flatulence  or  flatulency, 
a  tendency  toward  the  accumulation  of  gas  in  the  stomach  or  in- 
testines, not  sufficient  to  constitute  tympanites  [q.  v.),  and  usually 

associated  with  increased  peristalsis, 
borborygmi,  belching,  and  the  passage 
of  flatus  ^jer  anum.  The  gas  most  com- 
monly arises  from  fermentative  pro- 
cesses ;  sometimes  it  is  swallowed ;  and 
its  rapid  passage  into  the  intestine  from 
the  blood  must  be  admitted  in  the  cases 
of  sudden  flatulency  in  certain  neu- 
roses. Flatulency  is  a  symptom  of  gas- 
tritis and  of  gastric  neuroses.  It  is 
very  common  in  hysteria,  and  is  often 
associated  as  a  direct  result  with  the 
eating  of  indigestible  or  fermentable 
food. 

(5)  Examination  of  the  Rectum.— In- 
spection of  the  cmal  regio7i  may  reveal 
condylomata,  ulceration,  fissure,  hemor- 
rhoids, or  pruriginous  eruptions,  which, 
by  causing  pain,  insomnia,  or  loss  of 
blood,  may  be  responsible  for  neuras- 
thenic or  anaemic  conditions.  Prolapse 
of  the  rectum,  if  found,  may  be  signifi- 
cant of  pertussis,  prolonged  vomiting, 
the  presence  of  scybalous  masses,  or  the 
presence  of  other  causes  of  rectal  tenes- 
mus {q.  v.). 
Digital  examination  of  the  rectum  may  not  only  afford  valuable 
diagnostic  information  with  reference  to  the  causation  of  certain 
general  conditions  as  Just  described,  but  in  addition  may  confirm 
the  diagnosis  in  various  local  lesions  which  are  usually  first  encoun- 
tered by  the  internalist.  The  latter  are :  Impaction  of  the  rectum 
with  dry  and  hard  scybalous  masses,  or  impacted  gallstones  or  for- 
eign bodies ;  the  tumour  of  appendicitis,  which  may  be  felt  when  the 


Fig.  149. — To  show  the  method  of 
determining,  by  auscultatory 
percussion,  that  a  tumour  be- 
longs to  the  colon.  If  the  tu- 
mour involves  the  wall  of  the 
colon  the  percussion  notes  over 
points  A,  B,  and  C  differ,  but  C 
resembles  A  much  more  nearly 
than  B,  over  small  intestine,  re- 
sembles A.  Circle  =  chest  piece 
of  stethoscope. 


EXAMINATION  OF  LIVER  AND  GALL  BLADDER 


461 


appendix  is  unusually  long  and  depends  into  the  pelvis,  usually  to 
the  right ;  the  tumour  of  intussusception  or  a  bleeding  polypus;  and 
malignant  tumour  or  infiltration  of  the  rectum  causing  bloody  mu- 
cous diarrhoea  and  enlarged  secondarily  infected  lymph  glands. 

For  the  examiner  the  osmic  unpleasantness  of  a  digital  explora- 
tion of  the  rectum  may  be  almost  entirely  done  away  with  by  the 
use  of  a  cot  for  the  examining  finger,  made  of  rubber  tissue,  suffi- 
ciently thin  to  allow  an  almost  unimpeded  sense  of  touch  (Delatour). 
The  cotted  finger  may  be  lubricated  and  washed  as  if  uncovered. 

IV.    THE    LIVER    AND    GALL    BLADDER 

Topographical  Anatomy  of  the  Liver. — The  general  shape 
of  the  liver  is  that  of  a  wedge.  It  lies  with  its  base  or  thick  end 
in  the  right  hypochondriac  region.  Its  upper  surface  fits  neatly 
into  the  vault  of  the  diaphragm ;  its  loiuer  surface  rests  upon  a  bed 
composed  of  the  stomach,  duodenum,  transverse  colon,  and  small  in- 
testines. Its  anterior^  lateral,  and  posterior  aspects  are  in  relation 
for  the  most  part  with  the  abdominal  wall  and  lower  right  ribs. 


Lower  border 
of  lung 

Lower  border 
of  liver 
Gall  bladder 


Fig.  150. — Showing  the  jxiints  which  determine  the  size  and  position  of  the  normal  liver. 
Horizontal  shading  =  portion  of  liver  overlapped  by  lung;  vertical  shading  =  portion 
of  liver  overlapped  by  heart.     Compare  with  Fig.  152. 

(1)  Upper  Limits  of  Liver. — Mark  a  point  (.1,  Fig.  150)  at  the 
lower  edge  of  the  left  5th  rib,  between  the  parasternal  and  mammil- 


462 


THE  EVIDENCES  OF  DISEASE 


lary  lines  (about  2  or  2^  inches  to  left  of  left  edge  of  sternum).  Mark 
a  second  point,  B,  in  the  right  4th  interspace  in  the  mammillary  line. 
From  B  draw  a  line  to  the  left  convex  upward,  but  curving  down  to 
the  base  of  the  ensiform  cartilage,  from  which  it  is  prolonged  to  A. 
From  B  draw  also  an  almost  horizontal  line  to  the  right  and  poste- 
riorly, cutting  the  midaxillary  line  in  the  7th  space  and  the  scapular 
line  in  the  9th  space,  to  the  midspinal  line.  The  entire  line,  front, 
side,  and  back,  corresponds  to  the  upper  limit  of  the  liver. 

(2)  Lower  Limits  of  Liver.— Mark  a  point,  C\  in  the  median  line, 
a  handbreadth  (about  3i  to  4  inches)  below  the  base  of  the  ensiform 
cartilage.     This  will  lie  somewhat  above  the  halfway  point  between 

the  ensiform  appendix 
and  the  umbilicus.  Mark 
another  point,  D,  at  the 
lower  edge  of  the  9th 
right  costal  cartilage, 
and  a  third,  E^  at  the 
edge  of  the  left  costal 
arch,  on  a  level  with  the 
lower  border  of  the  6th 
rib.  Draw  a  line  from 
point  D  upward  and  to 
the  left,  through  point 
(7,  at  which  the  inter- 
lobar notch  should  be 
indicated,  then  bending 
upward  through  point 
E  to  point  A.  From 
point  D  draw  a  line 
backward  to  the  right, 
cutting  the  10th  inter- 
space in  the  midaxillary 
line  (Fig.  151),  from 
which  it  joins  the  spine 
at  the  level  of  the  11th  rib.  The  entire  line,  front,  side,  and  back, 
corresponds  to  the  lower  limit  of  the  liver. 

One  may  note  that  the  left  lobe  lies  to  the  left  of  the  median 
line  and  extends  nearly  to  the  left  nipple ;  the  interlobar  notch  lies 
in  the  median  line ;  the  liver,  in  the  right  mammillary  line,  extends 
vertically  downward  from  a  point  just  below  the  nipple  to  the  costal 
margin ;  and  that  the  lower  border  of  the  liver  on  the  right  cor- 
responds nearly  to  the  costal  edge.  In  the  aged  the  lower  edge  of 
the  liver  may  lie  one  space  above  the  indicated  limit ;  in  infants  and 


Fig.  151. — Showing  the  surface  relations  of  the  lung, 
pleura,  and  liver  in  the  midaxillary  line.  Note  the 
manner  in  which  the  complementary  pleura  ovei- 
laps  the  liver. 


EXAMINATION  OF  LIVER  AND  GALL  BLADDER  453 

children  it  projects  about  an  inch  below  the  edge  of  the  ribs ;  in  the 
erect  position  the  liver  descends  half  an  inch  below  the  costal  arch. 

(3)  The  Gall  Bladder. — This  pear-shaped  organ  lies  just  internal 
to  the  9th  right  costal  cartilage  and  close  to  the  outer  edge  of  the 
right  rectus  (Fig.  150).  A  line  drawn  from  the  right  acromion 
process  to  the  umbilicus  crosses  the  costal  arch  about  at  the  point 
where  the  gall  bladder  lies. 

Physical  Examination  of  the  Liver  and  Gall  Bladder. 
— Certain  cardinal  symptoms  {q.  v.)  of  disease  of  the  liver  have  been 
considered  elsewhere — jaundice,  ascites,  stools,  pain,  and  tenderness. 

The  direct  physical  examination  of  the  liver  is  intended  mainly 
to  ascertain  its  shape,  size,  position,  consistence,  the  character  of  its 
accessible  surface,  and  the  presence  of  tumours.  Taken  in  order  of 
inverse  importance,  the  methods  are  : 

{a)  Inspection  of  the  Liver  and  Gall  Bladder.— Very  rarely  one 
can  detect  by  careful  inspection  and  a  good  light  the  lower  edge  of 
an  enlarged  liver  showing  as  a  distinct  linear  prominence  and  moving 
up  and  down  with  respiration.  More  frequently  it  is  possible  to  see 
pulsation  of  the  liver  {q.  v.).  Swelling  or  enlargement  of  the  viscus, 
if  very  considerable,  may  cause  a  visible  fulness  of  the  right  hypo- 
chondriac region  with  bulging  of  the  ribs. 

{b)  Auscultation  of  the  Liver  and  Gall  Bladder. — One  may  hear 
the  friction  sound  of  a  perihepatitis  over  the  right  hypochondriac 
region,  or  between  the  upper  and  lower  liver  lines  laterally  and  pos- 
teriorly. The  very  infrequent  venous  hum  or  murmur  in  enlarged 
veins  of  the  liver  or  in  cases  of  tricuspid  regurgitation  has  been  con- 
sidered. When  palpating  a  gall  bladder  containing  a  number  of  con- 
cretions, it  may  be  possible,  by  the  simultaneous  use  of  a  stethoscope 
placed  close  to  the  sac,  to  hear  the  resultant  rubbing  or  grating  con- 
tact of  the  stones. 

(r)  Percussion  of  Liver  and  Gall  Bladder. — In  order  to  percuss 
the  liver  over  i\\Q  front  and  side,  the  patient  should  be  lying  down; 
to  percuss  posteriorly,  sitting  or  standing. 

The  upper  portion  of  the  right  lobe  of  the  liver  is  overlapped  by 
the  right  lung,  and  a  very  small  area  of  the  left  lobe  is  similarly 
covered  by  the  heart  and  left  lung  (Fig.  150),  the  remainder  being 
in  direct  contact  either  with  the  ribs  or  the  anterior  wall  of  the 
abdomen.  As  percussion  over  the  covered  portion  of  the  liver  affords 
an  impaired  pulmonary  resonance  or  modified  dulness,  because  of  the 
interposition  of  the  lung  between  the  liver  and  thoracic  wall,  and 
similar  percussion  over  the  portion  which  is  in  parietal  contact  gives 
absolute  dulness,  one  recognises  clinically  two  areas.  The  first  is  the 
deep,  relative  or,  preferably,  the  covered  hepatic  dulness ;  the  second, 


464 


THE  EVIDENCES  OF   DISEASE 


the  superficial,  absolute,  or  exposed  dulness ;  the  two  together,  the 
entire  hepatic  dulness. 

In  percussing  the  liver  (Fig.  152)  it  is  necessary  to  determine  (1) 
the  upper  limit  of  covered  dulness,  (2)  the  upper  limit  of  exposed 
dulness,  and  (3)  the  lower  limit  of  exposed  dulness.  Percuss  down- 
ward, first  in  the  mammillary  line,  beginning  at  the  second  inter- 
space, then  in  the  midaxillary  line  from  the  fourth  interspace,  finally 
in  the  scapular  line  from  angle  of  scapula.     Then  percuss  from  below 

upward — in  the  mid- 
dle line  anteriorly 
from  the  umbilicus ; 
and  from  other  points, 
lateral  and  posterior, 
below  the  ribs. 

Ordinary  Percus- 
sion.— (1)  Upper  Lim- 
it of  Covered  Hepatic 
Dulness.  —  Starting 
with  the  pure  pul- 
monary resonance  of 
the  upper  thorax  and 
using  strong  percus- 
sion, a  careful  watch 
is  kept  in  passing 
down  for  the  first 
trace  of  impaired 
resonance  which  de- 
notes the  presence  of 
the  liver.  This  point 
is  normally  found  in 
the  4th  space  in  the 
mammillary  line,  the  7th  space  in  the  midaxillary  line,  and  the  9th 
space  in  the  scapular  line.  By  comparing  rib  with  rib  and  inter- 
space with  interspace,  it  may  be  quite  accurately  located. 

(2)  Upper  Limit  of  Exposed  Hepatic  Dulness. — Passing  down  from 
the  upper  limit  of  covered  dulness  with  gentle  strokes,  absolute  dul- 
ness will  be  met  with  under  normal  circumstances — in  the  mammillary 
line  at  the  6th  rib ;  midaxillary,  8th  rib ;  scapular,  10th  rib.  The 
ascertainment  of  the  upper  limit  of  the  exposed  hepatic  dulness  is 
practically  the  determination  of  the  lower  border  of  the  right  lung, 
the  respective  limits  coinciding.  Note  that,  in  the  midsternal  line, 
the  demarcation  between  the  exposed  heart  and  liver  dulness  can 
not,  as  a  rule,  be  determined.     By  auscultatory  percussion  it  is  occa- 


FiG.  152.- 


-Showing  the  results  of  percussion  over  a  normal 
liver  (and  heart). 


EXAMINATION  OF   LIVER  AND  GALL  BLADDER  465 

sionally  practicable.  It  may  be  obtained,  usually  with  suflBcient  cor- 
rectness, by  drawing  a  line  from  the  cardio-hepatic  angle,  the  junc- 
tion of  the  dulness  of  the  right  border  of  the  heart  with  the  upper 
limit  of  hepatic  dulness,  to  the  apex  of  the  heart. 

(3)  Lower  Limit  of  Hepatic  Dulness. — Gentle  percussion  down 
and  up  along  the  lines  previously  indicated  will  enable  the  line  to  be 
drawn  between  liver  dulness  and  tympanitic  resonance.  The  lower 
litnit  is  :  in  the  median  line  anteriorly^  3|  to  4  inches  (a  handbreadth) 
below  the  ensiform  appendix ;  in  the  niammillary  line,  as  a  rule,  the 
costal  margin ;  in  the  midaxillary  line,  the  10th  space ;  in  the  scap- 
ular line  it  fuses  with  the  dulness  of  the  right  kidney.  It  may  be 
difficult  to  find  the  lower  limit  in  the  median  line  in  front  because 
of  the  thinness  of  the  left  lobe  and  the  dulling  effect  of  the  muscular 
masses  of  the  recti. 

The  vertical  width  of  hepatic  dulness  is  normally :  in  the  mam- 
millary  line,  4  inches  ;  in  the  midaxillary,  6  inches  ;  in  the  scapular, 
3  inches.  In  elderly  persons  it  is  about  1  inch  less.  In  percussing 
over  the  exposed  portions  of  the  liver  a  sense  of  resistance  may  be 
perceived,  particularly  if  the  viscus  is  enlarged  or  its  consistence 
increased. 

Percussion  of  the  gall  bladder  is  possible  only  when  it  is  consider- 
ably distended  or  enlarged,  in  which  case  it  affords  an  area  of  dul- 
ness projecting  downward  and  inward  from  the  lower  hepatic  border 
and  continuous  with  the  dulness  of  the  latter.  In  some  instances 
the  transverse  colon  may  become  looped  over  the  neck  of  a  full  gall 
bladder,  lying  between  it  and  the  liver,  separating  its  dulness  from 
that  of  the  liver  by  a  tympanitic  interval. 

Auscultatory  Percussion  of  the  Liver. — The  limits  of  the  liver 
can  be  ascertained  with  sufficient  correctness  by  ordinary  percussion, 
but  if  unusual  accuracy  is  required,  or  if  the  origin  of  a  tumour  near, 
and  perhaps  belonging  to,  the  liver  is  to  be  determined  (Stengel), 
auscultatory  percussion  may  be  employed. 

(1)  To  determine  the  limits  of  the  liver  by  this  method  the  steth- 
oscope should  be  placed  over  the  middle  of  the  liver  area,  anteriorly, 
laterally,  and  posteriorly,  in  turn,  while  percussion  is  made  toward  it 
from  above  and  below,  following  the  lines  previously  described  for 
ordinary  percussion,  the  sounds  being  judged  by  the  usual  rules. 

(2)  To  determine  whether  or  not  an  adjacent  tumour  is  connected 
with  the  liver,  the  stethoscope  is  placed  over  a  nearby  portion  of  the 
organ  (Figs.  153  and  154),  and  percussion  made  from  several  direc- 
tions toward  and  upon  the  tumour.  If  the  latter  is  an  outgrowth 
from  the  liver,  the  note  over  it  will  resemble  in  intensity  and  quality 
that  which  is  obtained  from  the  liver  itself,  the  connecting  tissue 


466 


THE  EVIDENCES  OF  DISEASE 


Fio.  153. — If  a  nearby  tumour  is  connected 
with  the  liver,  percussion  note  B  (auscul- 
tatory) is  more  intense  and  clear  than  note 
A.,  resembling  C  (over  liver)  in  character. 
Circle  =  mouth  of  stethoscope. 


between  tumour  and  liver  conducting  the  sound  without  interrup- 
tion. If,  however,  a  tumour  originating  outside  of  the  liver  has  con- 
tracted extensive  adhesions  to  it,  or  has  come  to  involve  the  liver  as 
well  as  the  adjacent  organ  in  which  it  first  began  (e.  g.,  stomach),  it 
will  be  impossible  to  determine  which  viscus  is  the  more  involved. 

{d)  Palpation  of  Liver  and  Gall  Bladder. — For  palpation  of  the 
liver  the  patient  should  be  in  the  recumbent  position,  with  the  head 

and  shoulders  somewhat  raised 
and  the  knees  flexed  in  order  to 
relax  the  abdominal  muscles. 
Sitting,  preferably  at  the  right 
side  of  the  patient  and  facing  the 
couch,  the  (warmed)  right  hand 
is  laid  flat  upon  the  abdominal 
wall  below  the  right  costal  arch, 
the  fingers  pointing  upward  and 
somewhat  toward  the  median  line, 
their  tips  resting  just  outside  of 
the  border  of  the  right  rectus  in 
order  not  to  mistake  the  upper- 
most linea  transversa  for  the  edge 
of  the  liver. 

Seek  first  to  find  the  loiver 
edge  of  the  organ.  Depress  the 
fingers  and  upper  border  of  the 
hand  so  as 
to  push  up 
a  fold  of 
skin,  feeling 
at  the  same 
time  for  the 
resistant  he- 
patic edge. 
Cause  the 
patient  to 
take  a  se- 
ries of  deep 
respirations, 
pressing  the  fingers  inward  toward  the  end  of  expiration,  when,  if 
the  edge  of  the  liver  is  palpable,  it  may  be  felt  to  slip  under  the  fin- 
gers, as  it  moves  on  the  average  half  an  inch  up  and  down  with  the 
respiratory  movements.  As  the  liver  may  be  greatly  enlarged,  its 
lower  edge  must  be  sought  for  at  different  points  from  below  the 


Fig.  154.— If  the  tumour  (see  Fig.  153)  is  not  connected  with  the  liver  but 
with  some  adjacent  organ  (e.  g.,  stomach),  note  D  resembles  G  more 
than  it  resembles  F. 


EXAMINATION  OF   LIVER  AND  GALL  BLADDER  467 

umbilicus  up  to  the  costal  margin.  If  a  ridge  is  felt  and  one  is  un- 
certain whether  or  not  it  is  the  edge  of  the  liver,  the  notch  for  the 
gall  bladder  or  round  ligament  may  be  sought  for.  Note  the  charac- 
ter of  the  edge,  sharp  or  thick,  smooth  or  irregular. 

Next  palpate  the  surface,  not  only  of  the  left  lobe  in  the  epigas- 
trium, but  also,  if  the  liver  is  enlarged,  that  portion  of  it  which  pro- 
jects from  under  the  ribs.  Note  whether  it  is  smooth,  roughened,  or 
nodular,  or  presents  one  or  more  large  masses.  It  should  be  remem- 
bered that  inequalities  or  nodelike  irregularities  of  the  muscular  and 
fibrous  tissues  of  the  recti  and  abdominal  walls  may  be  mistaken  for 
abnormal  roughnesses  of  the  liver.  Note  also  its  consistence — hard, 
soft,  or  fluctuating — and  in  the  latter  case  seek  for  hydatid  thrill 
{q.  v.).  It  may  be  that  a  soft  friction  is  felt  during  respiration,  which 
is  best  perceived  posteriorly  (perihepatitis),  or  pulsation  of  the  en- 
larged organ  observed.  If  the  abdomen  is  distended  by  gas  or  fluid, 
the  liver  may  be  felt  by  "  dipping "  [q.  «;.),  unless  the  tumidity  is 
excessive. 

The  gall  bladder,  when  empty,  is  not  palpable.  If  distended,  it 
may  be  felt  as  a  smooth,  pear-shaped  tumour.  Unless  adhesions  have 
been  contracted  it  is  rather  freely  movable /row?  side  to  side  and  rises 
and  falls  with  respiration.  If  it  is  the  seat  of  a  malignant  growth,  it 
is  more  irregular  and  nodular  on  palpation  ;  and  if  it  contains  gall 
stones,  the  latter  may  give  a  sensation  resembling  "  a  bag  of  nuts  " 
(Hutchison). 

Diagnostic  Results  of  Physical  Examination  of  the 
Liver  and  Gall  Bladder. 

Enlargement  of  the  Liver. — The  increase  in  size  may  be  general  or 
local  and  circumscribed. 

A  general  increase  in  the  size  of  the  liver  may  be  due  to  passive 
congestion  (usually  from  valvular  cardiac  disease),  amyloid  disease, 
cancer,  fatty  infiltration,  hypertrophic  cirrhosis,  leucaemia,  hydatids, 
abscess,  gummata  or,  in  rare  instances,  Weil's  disease.  The  increase 
due  to  cancer  and  amyloid  disease  may  be  excessive,  the  lower  border 
of  the  enlarged  organ  reaching  considerably  below  the  umbilicus  and 
almost  filling  the  abdomen. 

Before  deciding  that  the  liver  is  actually  enlarged,  certain  sources 
of  error  must  be  eliminated. 

Enlargement  upward  must,  of  course,  be  judged  by  percussion.  If 
the  upper  limit  of  apparent  hepatic  dulness  is  found  above  the  nor- 
mal level,  the  extra  area  of  dulness  may  be  caused  by  consolidation 
of  the  base  of  the  right  lung,  or  by  an  effusion  into  the  right  pleural 
cavity.  This  question  must  be  decided  largely  by  the  history,  evi- 
dences of  pulmonary  rather  than  hepatic  disease  being  present,  ex- 


468  THE  EVIDENCES  OF  DISEASE 

cept  in  subphrenic  abscess  ;  possibly  by  auscultatory  percussion,  the 
stethoscope  being  placed  first  over  the  liver  area,  posteriorly  on  the 
right  side,  and  the  upper  limit  of  the  liver  defined  by  percussing  up- 
ward ;  then  placing  the  instrument  over  the  lung  and  purcussing 
downward,  attempting  to  determine  the  lower  pulmonary  border.  It 
is  also  to  be  borne  in  mind  that  the  liver  may  be  displaced  in  an 
upward  direction. 

Enlargement  downward^  if  judged  to  have  been  found  either  by 
percussion  or  by  palpation,  is  open  to  the  possibility  that  an  accumu- 
lation of  faeces  in  the  transverse  colon,  or  a  flattened,  hard,  cancerous 
or  tuberculous  omentum  may  give  rise  to  the  dulness,  or  may  resem- 
ble upon  palpation  the  lower  edge  of  a  large  liver.  A  feecal  mass, 
however,  is  apt  to  be  doughy  and  indentable,  while  a  tympanitic 
band  or  area  usually  intervenes  between  a  thick  omentum  and  the 
liver.  Apparent  enlargement  downward  may  be  caused  by  prolapse 
or  dislocation  of  the  liver. 

Circumscribed  enlargements  of  the  liver — e.  g.,  of  the  left  lobe — 
are  usually  due  to  abscess,  hydatid  cyst,  cancer,  or  gumma.  As  a 
source  of  embarrassment,  one  tjrpe  of  the  "  lacing  "  liver  may  here  be 
mentioned,  in  which  a  thin,  sometimes  thick,  movable  tongue  or  lap- 
pet from  the  anterior  portion  of  the  right  lobe  projects  below  the 
costal  border  for  a  distance  of  1  or  2  inches,  and  may  extend  as  far 
down  as  the  navel.  It  usually  moves  with  respiration,  by  careful 
palpation  is  found  to  be  continuous  with  the  liver,  and  can  be 
grasped  in  the  hand. 

Displacement  of  the  Liver. — The  liver  may  lie  above  or  beloiv  its 
normal  position. 

Displacement  upivard  may  be  due  to  pressure  from  below  by  large 
abdominal  tumours,  meteorism,  or  ascites.  It  may  be  drawn  upward 
by  collapse  or  retraction  of  the  right  lung,  or  allowed  to  ride  at  a 
higher  point  by  paralysis  of  the  diaphragm. 

Displacement  doivnivard  is  caused  by  downward  pressure  on  the 
diaphragm  by  emphysema  or  spasmodic  asthma,  large  right  pleural 
effusion  or  pneumothorax,  large  intrathoracic  tumour,  and  perhaps 
(affecting  mainly  the  left  lobe)  by  a  greatly  dilated  heart  or  a  large 
pericardial  effusion.  Subphrenic  peritonitis  (abscess),  a  collection 
of  pus  or  pus  and  gas  between  the  liver  and  diaphragm,  is  also 
responsible.  Finally,  the  liver  may  become  prolapsed  as  a  part  of  a 
■general  ptosis  or  falling  of  the  abdominal  viscera.  As  the  posterior 
border  of  the  liver  is  quite  firmly  moored,  the  descent  affects  mainly 
the  anterior  border,  which  drops  down  so  as  to  throw  the  superior 
surface  forward  and  downward  (see  following  paragraph). 

To  distinguish  between  enlargement  and  prolapse  of  the  liver,  it 


EXAMIXATION   OF  LIVER  AND  GALL  BLADDER  469 

is  necessary  to  consider  the  history  and  associated  symptoms  in  order 
to  determine  the  existence  of  a  thoracic  lesion  capable  of  causing 
descent  of  the  liver ;  or,  per  contra^  the  presence  of  some  disease 
causing  an  enlarged  liver.  In  downward  displacement  it  will  be 
found  that  the  upper  surface,  especially  of  the  left  lobe,  is  more 
than  usually  accessible  to  palpation,  and  its  rounded  shape  may  be 
felt.  Moreover,  a  prolapsed  liver,  because  of  its  separation  from  the 
diaphragm,  does  not  move  so  freely  with  respiration  as  the  normal  or 
enlarged  organ. 

Diminution  in  the  Size  of  the  Liver. — There  is  a  slow  and  pro- 
gressive lessening  in  the  size  of  the  liver  in  cirrhosis.  The  latter  is 
by  far  the  most  common  cause  of  hepatic  atrophy.  In  the  rare  cases 
of  acute  yellow  atrophy  the  liver  grows  rapidly  smaller  day  by  day. 

As  with  an  increase,  so  with  a  decrease,  in  the  size  of  the  liver 
one  must  guard  against  certain  possibilities  of  error.  If  a  marked 
emphysema  is  present,  the  inflated  lung  intrudes  into  the  comple- 
mentary pleura  between  liver  and  ribs,  pulmonary  resonance  thus 
encroaching  upon  the  tipper  limit  of  hepatic  dulness.  A  similar 
condition  is  found  in  right  pneumothorax.  The  loiuer  limit  of  liver 
dulness  may  be  raised,  and  the  vertical  measurement  of  the  liver 
area  diminished  by  distention  of  the  colon  and  small  intestines,  the 
coils  of  which  interpose  themselves  between  the  liver  and  the  ab- 
dominal wall ;  or,  with  extreme  rarity,  by  free  gas  in  the  peritoneal 
cavity. 

Irregularities  in  the  Shape  of  the  Liver. — In  rare  instances  the 
percussion  outline  of  the  liver  is  found  of  a  notably  abnormal  shape. 
In  such  cases  one  must  think  of  a  diaphragmatic  hernia  (extremely 
uncommon),  the  liver  lying  in  the  pleural  sac  ;  congenital  malforma- 
tion of  the  organ ;  or  a  disturbance  of  its  normal  relations  by  a 
rachitic  chest  or  the  deformity  of  Pott's  disease  of  the  spine.  An 
entire  absence  of  liver  dulness  may  be  due  to  transposition  of  the 
thoracic  viscera. 

Abnormal  Consistence  of  the  Liver  or  Roughness  of  its  Surfaces. — 
The  consistence  of  the  liver  may  be  found  to  be  increased  so  that  it 
feels  abnormally  dense,  hard,  and  resistant.  Such  a  condition  is 
indicative  of  cirrhosis,  carcinoma,  amyloid,  or  syphilitic  disease.  A 
fluctuating  or  elastic  swelling  in  or  at  the  lower  edge  of  the  liver,  if 
detected,  is  an  abscess,  an  hydatid  cyst,  or  a  gall  bladder  distended 
with  bile. 

The  surface  of  the  liver  is  smooth  in  amyloid  disease,  fatty  infil- 
tration or  degeneration,  and  passive  congestion ;  roughened  in  tuber- 
culous peritonitis ;  and  has  a  granular  feel  in  cirrhosis.  If  hard  nod- 
ules varying  in  size,  perhaps  with  a  central  depression  (umbilication), 
32 


470 


THE  EVIDENCES  OF   DISEASE 


are  found,  it  is  significant  of  cancer  ;  smooth,  slightly  elevated  promi- 
nences are  met  with  in  gummata  of  the  liver ;  and  one  or  more 
smooth  projections  may  be  felt  as  evidences  of  abscess  or  cyst.  If 
either  of  the  latter  is  suspected  to  be  present  exploratory  puncture 
{q.  V.)  may  be  made. 

V.    THE    PANCREAS 

Aside  from  the  scanty  signs  revealed  by  direct  physical  examina- 
tion of  the  pancreas,  other  diagnostic  points  {q-v.)  are  Pain,  Fatty 
Diarrhoea,  Glycosuria,  Ascites,  and  Jaundice. 


Fm.  155. — Showing  the  relations  of  the  pancreas. 

Topographical  Anatomy  of  the  Pancreas. — This  organ  lies  about 
3  inches  above  the  umbilicus,  midway  between  navel  and  ensiform 
appendix,  corresponding  to  the  level  of  the  2d  lumbar  vertebra.  It 
is  usually  6  inches  long.  It  is  deep  in  the  epigastrium,  lying  trans- 
versely across  the  spinal  column  with  its  head  resting  in  the  curve  of 
the  duodenum  and  its  tail  extending  to  the  spleen.  The  stomach 
hides  it  in  front.  Because  of  its  depth  and  surroundings,  it  is  rarely 
accessible  for  direct  examination. 

It  is  clinically  important  to  remember  the  close  relation  of  the 
head  of  the  organ  posteriorly  to  the  inferior  vena  cava,  the  portal 


PANCREAS— SPLEEN  47I 

rein,  and  the  common  bile  duct  (Fig.  155).  On  account  of  its  near- 
ness, a  cancer  or  other  gro^rth  affecting  the  head  of  the  pancreas 
may  press  upon  the  blood  vessels  mentioned,  giving  rise  to  oedema 
and  ascites ;  or  upon  the  bile  duct,  causing  persistent  jaundice. 

Physical  Examination  of  the  Pancreas. — Under  normal  circum- 
stances the  pancreas  can  not  be  palpated,  except  in  rare  instances 
of  extreme  emaciation.  The  most  important  physical  sign  of  pan- 
creatic disease  is  the  presence  of  a  median  tumour  in  the  epigas- 
trium, usually  midway  between  navel  and  ensiform  appendix.  The 
tumour  is  necessarily  deep  seated,  and  not  infrequently  nothing 
more  than  a  sense  of  resistance  can  be  perceived  by  the  palpating 
hand.  The  diseases  of  the  pancreas  in  which  either  a  tumour  or  a 
suggestive  feeling  of  resistance  is  present  are  acute  hemorrhagic 
and  suppurative  pancreatitis,  chronic  pancreatitis,  and  tumour,  solid 
(usually  carcinoma)  or  cystic. 


SECTION   XXXY 
EXAMIXATIOX   OF   THE   SPLEEN" 

The  physical  examination  of  the  spleen  is  concerned  mainly  with 
the  determination  of  its  size  and  position  by  inspection,  palpation, 
and  percussion.     In  rare  instances  auscultation  is  of  service. 

Topographical  Anatomy  of  the  Spleen. — The  spleen  is  of 
oval,  flattened  shape  (rarely  rhomboid)  and  lies  in  the  left  hypochon- 
driac region.  It  measures  on  the  average  3  by  5  inches.  It  reaches 
from  a  point  1^  incli  to  the  left  of  the  midspinal  line  posteriorly 
almost  to  the  midaxillary  line  laterally,  lying  along  the  9th,  10th, 
and  11th  ribs.  The  long  axis  is  parallel  with  the  ribs,  and  therefore 
runs  downward  and  forward  (Fig.  156).  The  lower  f  of  its  outer 
surface  are  parietal,  the  upper  ^  separated  from  the  ribs  by  the  dia- 
phragm'and  the  lower  border  of  the  left  lung.  It  is  bounded  poste- 
riorly by  the  kidney,  above  by  the  diaphragm,  and  its  remaining  por- 
tions are  in  contact  with  the  stomach,  colon,  and  small  intestines. 
Tlie  anterior  border  is  sharp  and  indented  by  from  2  to  4  notches. 

Physical  Examination  of  the  Spleen.— (1)  Inspection.— 
This  is  rarely  of  service.  If  the  organ  is  greatly  enlarged  it  may  be 
visible  as  a  protuberance,  extending  from  the  left  hypochondriac 
region  downward  and  inward  and  moving  with  respiration. 

(2)  Palpation  of  the  Spleen. — The  patient  should  be  in  the  recum- 
bent position.     Then  lay  the  (warm)  hand  flat  upon  the  abdomen, 


472 


THE  EVIDENCES  OF  DISEASE 


80  that  the  finger  tips,  by  exerting  pressure  and  pushing  up  a  fold  of 
skin,  lie  close  to  and  under  the  left  costal  margin  at  the  10th  carti- 
lage. The  edge  of  the  spleen,  if  sufficiently  enlarged,  may  then  be 
felt  without  furtlier  trouble.      If  not,  desire  the  patient  to  draw 

several  deep  breaths, 
when  the  sharp  sple- 
nic edge,  moving  with 
respiration,  will  be 
perceived  to  slip  or 
ride  over  the  ends  of 
the  fingers.  Still  fur- 
ther aid  may  be  ob- 
tained from  placing 
the  unoccupied  hand 
posteriorly  between 
the  ends  of  the  10th 
and  11th  ribs  and 
making  firm  pressure 
so  as  to  tilt  the  organ 
forward  and  make  it 
more  accessible. 

Under  normal  cir- 
cumstances the  spleen 
can  not  be  felt.  If 
increased  in  size,  the 
anterior  edge,  which 
is  always  directed 
downward  and  inward, 
is  sharp  and  usually 
smooth.  Notching  of 
this  border  is  generally  but  not  always  to  be  found.  A  point  of  some 
practical  importance  is  that  a  depression  or  space  in  which  the  finger 
tips  can  be  sunk  may  invariably  be  detected  at  the  posterior  border 
of  the  enlarged  organ,  between  it  and  the  erector  spinse.  Infre- 
quently the  spleen,  although  enlarged,  can  not  be  felt  owing  to  an 
unusually  strong  phreno-colic  ligament  which  prevents  its  protrusion 
from  under  the  ribs.  In  such  a  case  percussion  must  be  relied  upon 
to  declare  the  enlargement. 

The  question  sometimes  arises  as  to  whether  a  tumour  found  be- 
low the  left  costal  margin  is  an  enlarged  spleen  or  an  enlarged  kid- 
ney. The  discrimination  is  to  be  made  by  finding,  if  it  is  the  spleen, 
that  the  shape  is  oval,  that  it  moves  with  respiration,  that  it  is 
notched,  that  it  has  a  sharp  edge,  that  a  gap  exists  between  it  and 


Fig.  156. — Showing  tlie  surface  topography  of  the  spleen. 
Shaded  area  =  portion  overiapped  by  lung.  Numbered 
arrows  show  the  lines  along  which  percussion  should 
be  conducted. 


EXAMINATION  OF  SPLEEN 


473 


the  lumbar  muscles,  and  that  it  lies  in  front  of  the  colon — i.  e.,  that 
there  is  no  tympanitic  resonance  over  it.  On  the  other  hand,  the 
kidney  is  rounded  or  reniform,  never  has  a  sharp  edge  or  is  notched, 
moves  slightly,  if  at  all,  with  respiration,  and  is  overlaid  by  tympan- 
itic resonance  (Fig.  157). 

If  confusion  arises  between  an  enlarged  left  lobe  of  the  liver  and 
an  enlarged  spleen,  it  is  to  be  remembered  that  the  edge  of  the  spleen 
lies  at  a  lower  level  and  that  the  organ  can  be  tilted  forward  by 
pressure  over  the  left  lower  ribs  posteriorly. 

(3)  Percussion  of  the  Spleen.— The  patient  may  be  sitting  or 
standing,  or,  if  recumbent,  should  lie  partly  turned  to  the  right— 
i.  e.,  midway  between  the  dorsal  and  right  lateral  postures  —  in 
either  case  with  the  left  arm 
over  the  head.  The  percussion 
strokes  should  be  light,  ex- 
cept in  percussing  the  poste- 
rior portion  of  the  spleen 
where  its  dulness  merges  into 
that  of  the  left  kidney.  Per- 
cussion should  be  conducted 
along  the  following  lines  (i,  2, 
3,  and  ^  Fig.  156) : 

Anterior  Limit. — Begin  at 
the  costal  margin,  and  percuss 
along  the  10th  rib  until  the 
tympanitic  resonance  of  the 
stomach  is  replaced  by  dulness. 
Xormally  this  will  be  found  at 
the  midaxillary  line. 

Upper  Limit. — Begin  at  the  level  of  the  angle  of  the  scapula 
halfway  between  the  posterior  axillary  and  scapular  lines,  passing 
vertically  downward  until  the  pulmonary  resonance  is  impaired. 
Xormally  this  occurs  at  the  9th  rib. 

Lower  Limit. — Begin  below  the  border  of  the  ribs,  in  or  a  little 
behind  the  posterior  axillary  line,  and  percuss  vertically  upward 
until  tympanitic  resonance  is  dulled.  Normally  dulness  is  met  at 
the  11th  rib,  reaching  not  quite  down  to  the  margin  of  the  ribs. 

Posterior  Limit. — Begin,  using  strong  percussion,  at  the  mid- 
spinal  line  at  the  level  of  the  10th  rib,  and  percuss  along  the  latter. 
The  splenic  dulness  should  be  attained  1^  inch  from  the  median  line, 
but  it  is  always  difficult  and  rarely,  if  ever,  necessary  to  determine  it. 

If  splenic  percussion  is  successful,  the  area  found  is  oval  and 
measures  3  to  24  X  3  to  34  inches.     Practicallv,  the  vertical  extent 


-eoROEBor 

LUNG 

MARGIN  OF 

RIB5       _ 


Fig.  157. — If  a  tumour  ^shado'l  area  -  found  be- 
low the  left  costal  margin  is  an  enlarged  kid- 
ney it  will  be  overlaid  by  the  tympanicity  of 
the  colon,  as  in  this  cut.  If  it  is  an  enlarged 
spleen  the  tympanitic  colon  will  not  be  found 


474  THE  EVIDENCES  OF   DISEASE 

of  the  dull  area  is  sufficient  for  clinical  purposes.  If  it  exceeds  3^ 
inches  it  may  be  surmised  that  the  spleen  is  enlarged. 

There  are  certain  sources  of  error  in  percussion  of  the  spleen 
which  greatly  minimize  its  value  as  a  method  of  ascertaining  the 
size  of  the  organ,  as  follows :  Apparent  increase  in  the  size  of  the 
splenic  dulness  may  be  caused  by  left  pleural  effusion,  pulmonary 
basal  consolidation,  pleural  thickening  or  new  growth  of  lung  or 
pleura,  or  by  faecal  accumulation  in  the  splenic  flexure  of  the  colon. 
Apparent  decrease  in  the  size  of  the  splenic  dulness  may  be  due  to 
an  unusual  arching  of  the  diaphragm,  an  emphysematous  lung,  or 
a  left  pneumothorax,  crowding  the  spleen  away  from  the  ribs.  Dul- 
ness, if  entirely  absent,  may  be  a  corroborative  sign  of  the  rare  float- 
ing spleen. 

(4)  Auscultation  of  the  Spleen. — A  friction  sound  may  be  heard 
over  the  spleen  if  its  peritoneal  investment  is  inflamed  (perisplenitis), 
as  in  infarcts  due  to  a  septic  embolism  or  thrombus,  or  in  the  splenic 
abscess  following  such  infarctions.  Friction  sound  and  a  systolic 
bruit  have  been  noted  in  splenic  leucasmia  and  other  causes  of  great 
enlargement  of  the  organ. 

Results  of  the  Examination  of  the  Spleen. — Of  the  vari- 
ous methods  of  determiniug  the  size  and  position  of  the  spleen,  pal- 
pation is  by  far  the  most  important.  A  positive  diagnosis  of  splenic 
enlargement  should  never  be  made  unless  the  organ  can  be  felt. 
Practically,  if  palpable,  unless  dislocated,  it  is  enlarged. 

(1)  Acute  Splenic  Enlargement.— The  spleen  enlarges  more  or  less 
rapidly,  usually  only  to  a  moderate  extent,  as  a  consequence  of  infec- 
tious and  septic  processes.  Acute  enlargement,  therefore,  may  be 
due  to  typhoid  fever,  typhus  fever,  malarial  fever,  relapsing  fever, 
scarlet  fever,  smallpox,  diphtheria,  erysipelas,  acute  miliary  tubercu- 
losis, tuberculous  peritonitis,  erysipelas,  pneumonia,  epidemic  cerebro- 
spinal meningitis,  pyaemia  (including  septic  splenic  infarction  and 
abscess),  and  septicaemia. 

(2)  Chronic  Uniform  Splenic  Enlargement.— Uniform  enlargement 
of  the  spleen  takes  place  slowly  as  a  consequence  of  leucasmia  (spleno- 
medullary  form)  and  chronic  malaria  (ague  cake).  It  is  in  these  dis- 
eases that  the  organ  attains  its  greatest  size,  in  some  instances  nearly 
filling  the  abdominal  cavity.  Slow' enlargement  of  varying  degrees 
occurs  also  in  splenic  anaemia,  amyloid  disease,  cirrhosis  of  the  liver, 
rachitis,  pernicious  anaemia,  the  general  venous  congestion  of  cardiac 
disease,  and  in  passive  portal  congestion  from  hepatic  cirrhosis  or 
pressure  of  tumours. 

(3)  Irregular  or  Unequal  Splenic  Enlargement.— This  is  significant 
of  an  abscess  or  the  excessively  rare  carcinoma  or  hydatids  of  the  spleen. 


EXAMINATION  OF  THE  KIDNEYS  475 

(4)  Displacement  of  the  Spleen. — The  spleen  may  be  pushed  down- 
ward, so  that  its  edge  becomes  palpable,  by  left-side  pleural  effusion, 
pneumothorax,  emphysema,  or  thoracic  tumour.  That  the  edge  can 
be  felt  because  of  descent  and  not  because  of  enlargement,  is  not 
always  easy  to  determine.  The  existence  of  thoracic  disease,  and 
the  absence  of  ailments  capable  of  causing  an  increase  in  size,  will 
aid  in  the  discrimination.     Clinically  it  is  not  of  much  importance. 

K  floating  spleen,  due  to  congenital  laxity  of  its  ligaments  or  to 
overstretching  from  increased  size  and  weight  of  the  organ,  may  be 
encountered,  usually  in  women,  as  a  part  of  a  general  visceroptosis. 
It  may  descend  into  the  pelvis.  Ordinarily  it  is  recognisable  by  its 
mobility,  shape,  sharp  edge,  and  notches.  If  the  organ  has  con- 
tracted adhesions,  or  its  shape  is  altered  by  inflammatory  deposits 
upon  its  peritoneal  covering,  the  recognition  may  be  very  difficult. 

The  spleen  may  be  pushed  upward  by  tympanites  or  ascitic  fluid, 
or  pulled  in  the  same  direction  by  a  contracting  lung  or  the  shrink- 
age of  a  previously  inflamed  pleura  on  the  left  side.  Such  a  dis- 
placement is  only  of  importance  as  a  possible  explanation  of  a  per- 
cussion abormality. 

(5)  Combined  Enlargement  of  Liver  and  Spleen— Both  liver  and 
spleen  are  simultaneously  enlarged  in  passive  congestion,  hepatic 
cirrhosis,  leucaemia,  and  amyloid  disease. 


SECTION  XXXYI 
EXAMINATION   OF  THE  KIDXEYS,  URETEES,  BLADDER 

Heee  are  considered  the  results  to  be  obtained  from  the  physical 
examination  of  these  organs.  Other  evidences  {q.  v.)  of  disease  of 
the  urinary  organs  are  noted  elsewhere — viz..  Results  of  Urinalysis, 
Urination,  Pain,  and  Qi^dema. 

I.    KIDNEYS 

Topographical  Anatomy  of  the  Kidneys. — These  organs, 
2  in  number,  lie  against  the  posterior  abdominal  wall,  one  on  each 
side  of  the  spinal  column,  in  beds  of  fat  and  connective  tissue. 
They  have  a  characteristic  (reniform)  shape.  The  upper  end  of  the 
left  kidney  is  in  contact  with  the  spleen,  the  right  with  the  liver. 
The  right  kidney  lies  about  4  an  inch  lower  than  its  .companion. 
Each  kidney  is  about  4  inches  long,  2  to  2^  inches  in  breadth,  and  1 
inch  in  thickness. 


476 


THE  EVIDENCES  OP  DISEASE 


The  normal  surface  relations  which  it  is  clinically  important  to 
have  in  mind,  may  be  found  as  follows  : 

(I)  Anteriorly. — Prolong  the  mammillary  line  on  each  side  down- 
ward (or  draw  a  vertical  line  upward  from  the  middle  of  Poupart's 
ligament)  until  it  intersects  a  horizontal  line  through  the  umbilicus 
(Fig.  158).  Or  measure  and  mark  on  the  horizontal  umbilical  line 
2  points,  one  3  inches  to  the  right,  the  other  3  inches  to  the  left,  of 
the  median  line  of  the  abdomen.  From  the  intersections  of  the 
horizontal  umbilical  and  the  mammillary  lines,  or  from  the  points 
marked,  measure  upward  1  inch  on  the  right,  1^  inch  on  the  left, 

mammillary  line,  and  in- 
dicate by  short  horizontal 
lines.  The  lower  ends  of 
the  kidneys  lie  at  the  level 
of  the  short  horizontal 
lines, and  the  organs  them- 
selves extend  upward  and 
somewhat  inward  for  4 
inches.  One  third  of  the 
kidney  lies  to  the  outer, 
f  to  the  inner  side  of  the 
vertical  lines. 

(2)  Posteriorly. — Draw 
2  horizontal  lines  across 
the  back  (Fig.  159),  the 
first  at  the  level  of  the 
tip  of  the  spinous  process 
of  the  11th  dorsal  verte- 
bra, the  second  at  the 
level  of  the  tip  of  the  spinous  process  of  the  3d  lumbar  vertebra. 
On  each  side  draw  2  vertical  lines  from  the  upper  to  the  lower 
horizontal  line.  The  first  vertical  line  should  lie  1  inch  from  the 
median  line,  the  second  vertical  line  2f  inches  farther  away.  The 
outer  parallelograms  thus  outlined  correspond  to  the  normal  loca- 
tion of  the  kidneys.  The  lower  ends  of  these  organs  (right  lower 
than  left)  lie  1  to  1|  inch  above  the  iliac  crests.  About  ^  of  their 
upper  ends  are  covered  by  the  11th  and  12th  ribs.  The  spleen 
overlaps  the  upper  extremity  of  the  left,  the  liver  of  the  right, 
kidney. 

Physical  Examination  of  the  Kidneys. — Of  the  ordinary 
methods  of  physical  examination,  inspection  is  seldom  of  value,  pal- 
pation is  indispensable,  percussion  is  untrustworthy  and  of  little 
use,  and  auscultation  is  never  employed. 


Fig.  158. — Showing  the  normal  surface  relations  of  the 
kidneys  anteriorly,  and  the  method  of  determin- 
ing these  relations. 


EXAMINATION  OF  THE  KIDNEYS 


477 


Lower  border  of  lungs 
Level  of  spine  of  11th 

dorsal  vertebra 
Lower  border  of  liver 


_  _  Level  of  spine  of  3d 
lumbar  vertebra 
Tympanitic  colon 


(a)  Inspection  of  Kidneys. — A  large  tumour  of  the  kidney  is  prac- 
tically the  only  direct  renal  physical  sign  which  may  become  visible. 
In  such  a  case  the  growth  may  fill  one  or  the  other  anterior  lumbar 
and    corresponding 

portion  of  the  um-  • 

bilical  region.  The 
ribs  on  the  affected 
side  will  be  bulged 
outward  and  afford 
an  indication  as  the 
original  point  of 
origin  of  the  neo- 
plasm. Sarcoma  of 
the  kidney  in  chil- 
dren, or  perhaps  a 
very  large  hydro- 
nephrotic  or  cystic 
kidney  in  the  adult, 
are  the  most  usual 
causes  of  a  visible 
renal  enlargement. 
In  some  cases  a 
perinephric  abscess 
may  become  visible 
as  a  swelling  in  one 
or  the  other  poste- 
rior lumbar  region. 

(b)  Palpation  of 
the    Kidneys.  —  To 
palpate  the  kidney 
let  the  patient  lie  in  the  dorsal  position,  head  slightly  raised,  knees 
drawn  up,  and  feet  supported. 

(1)  Slip  one  hand  under  the  back  so  that  it  rests  upon  the  two 
lower  ribs  and  the  lumbar  space  immediately  below  them.  The  other 
hand  is  to  be  laid  flat  upon  the  abdomen  in  front,  resting  just  below 
the  costal  margin,  to  the  outer  side  of  the  rectus,  in  the  mammillary 
line.  Desire  the  patient  to  take  deep  and  slow  respirations.  By 
firm  pressure  during  expiration,  with  the  fingers  in  front  acting 
against  equally  firm  counter  pressure  by  the  posterior  hand,  an  at- 
tempt is  made  to  grasp  the  firm,  rounded  kidney  between  the  two 
hands.  If  the  kidney  is  normal  in  size  and  position,  its  lower  ex- 
tremity may  be  palpated,  provided  that  the  abdominal  walls  are  not 
too  thick  (palpable  kidney).     If  it  can  be  felt  to  slip  down,  like  a 


FiQ.  169. — Showing  surface  relations  of  kidneys  posteriorly ;  also 
the  combined  percussion  dulness  (shaded  area)  of  liver, 
spleen,  kidneys,  and  thick  muscles  of  the  back ;  also  that 
if  the  colon  is  empty  of  fseces  and  distended  with  gas  the 
lower  and  a  part  of  the  outer  border  of  the  kidney  can  be 
outlined  by  percussion.  Lines  of  percussion  indicated  by 
arrows  on  right  kidney. 


478  THE  EVIDENCES  OF  DISEASE 

"  pea  in  a  pod,"  so  that  its  entire  length  is  accessible,  especially  if  it 
can  be  pushed  down  to  the  horizontal  umbilical  line,  it  is  a  movable 
kidney.  If  it  can  be  displaced  into  the  lower  half  of  the  abdomen, 
pushed  across  the  median  line,  or  displaced  in  any  direction,  it  is  a 
floating  kidney.  It  should  be  remembered  that  a  failure  to  find  the 
kidney  at  its  normal  site  may  be  due  to  the  fact  that  it  is  elsewhere 
in  the  abdomen,  and  search  should  be  made  accordingly.  The  kid- 
ney may  or  may  not  move  slightly  with  respiration. 

(2)  Another  method  is  to  grasp  the  flank  with  the  full  grip  of  one 
hand,  the  thumb  resting  under  the  costal  margin  and  the  fingers  pos- 
teriorly, when  the  kidney  (the  patient  breathing  deeply)  may  be 
seized  and,  if  movable,  felt  to  slip  downward,  where  it  may  be  held  by 
the  grasping  hand,  palpated  by  the  other  hand,  and  finally  made  to 
slip  back  into  its  former  position. 

It  is  sometimes  helpful  to  let  the  patient  stand,  leaning  well  for- 
ward and  supporting  the  weight  by  the  hands  resting  upon  a  chair 
or  table,  while  the  abdominal  muscles  are  relaxed  and  the  breathing 
is  quiet  and  easy.  The  methods  of  palpation  just  described  may  then 
be  employed. 

In  addition  to  abnormal  mobility  of  the  kidney,  enlargement  of 
the  organ  may  be  detected  by  palpation  anteriorly ;  and  in  rare  in- 
stances the  renal  artery  may  be  felt  pulsating  if  the  kidney  is 
seizable. 

(c)  Percussion  of  the  Kidney. — It  is  possible  in  some  cases  to 
determine  the  lower  and  a  part  of  the  outer  border  of  each  kidney, 
contrasting  their  dulness  with  the  tympanicity  of  the  ascending  and 
descending  portions  of  the  colon  which  lie  immediately  anterior  to 
the  kidneys  (Fig.  159).  But  the  thickness  of  the  lumbar  muscles 
(Fig.  160),  the  amount  of  perirenal  fat,  and  the  possible  packing  of 
the  colon  with  non-resonant  faecal  matter,  render  the  results  very 
uncertain  as  compared  to  palpation. 

To  percuss  the  kidneys,  the  patient  may  be  placed  in  one  of  two 
positions,  either  of  which  will  relax  the  lumbar  muscles  and  mini- 
mize their  influence  upon  the  percussion  stroke.  He  may  lie  upon  the 
face  with  one  or  more  thick  pillows  placed  under  the  abdomen  so  as 
to  moderately  arch  the  back ;  or,  perhaps  better,  he  may  be  placed 
midway  between  the  prone  and  the  lateral  position,  the  examiner 
facing  the  patient's  back  and  percussing  the  kidney  of  the  upper- 
most side. 

Beginning  in  the  middle  of  the  area  in  which  the  kidney  is  nor- 
mally found  (Fig.  159),  percuss  outward,  using  vigorous  strokes 
until  the  renal  dulness  is  replaced  by  the  tympanitic  resonance 
of  the  colon,  thus  determining  the  lower  portion  of  the  outer  bor- 


EXAMINATION  OF  THE  KIDNEYS 


479 


der  of  the  organ.  Starting  from  the  same  area,  percuss  downward 
until  a  similar  change  occurs,  indicating  the  lower  border  of  the 
kidney. 

Diagnostic  Besults  from  the  Physical  Examination  of 
the  Kidneys. — (1)  If  the  percussion  dulness  is  increased,  and  the 
examiner  is  reasonably  certain  of  the  accuracy  of  his  results,  it  may 
be  inferred  that  the  kidney  is  enlarged  by  tumour  or  other  cause  of 


Fig.  160.— Horizontal  section  through  kidney  and  lumbar  muscles,  showing  the  difficulty 

of  kidney  percussion. 

increased  size  of  the  organ.  If  the  dulness  is  greatly  lessened  or  ab- 
sent, a  movable  kidney  is  to  be  suspected.  In  either  case  abdominal 
palpation  is  decidedly  more  reliable. 

(2)  A  movable  right  kidney — and  in  the  majority  of  cases  it  is 
the  right — may  require  to  be  discriminated  from  a  distended  gall 
bladder.  This  may  be  accomplished  by  remembering  that  if  it  is 
the  kidney  it  will  be  freely  movable  in  all  directions ;  may  be  carried 
down  toward  the  pelvis,  and  held  there  during  forcible  expiration ; 
may  be  pushed  backward  and  upward  toward  its  normal  position, 
where  it  tends  to  remain  and  elude  further  jialpation  ;  moves  slightly, 
if  at  all,  with  respiration ;  and  that  an  area  of  tympanitic  percussion 
(colon)  may  be  found  between  it  and  the  costal  margin.  On  the 
other  hand,  the  gall  bladder — which,  when  distended,  may  resemble 
the  kidney  very  nearly  in  size  and  shape — moves  with  respiration ; 
can  be  moved  from  side  to  side,  or  in  various  radii  of  a  small  circle 
having  the  neck  of  the  bladder  as  its  centre ;  and,  if  pushed  back- 
Avard,  away  from  the  abdominal  wall,  tends  to  spring  forward  to  its 
former  position  when  the  pressure  is  removed.  Finally,  unless  the 
colon,  above  which  it  usually  lies,  has  become  looped  over  the  neck 


480  THE  EVIDENCES  OF  DISEASE 

of  the  gall  bladder  (an  infrequent  happening),  there  is  no  tympanitic 
band  between  it  and  the  lower  border  of  liver  dulness. 

(3)  The  kidney  may  be  found  to  be  enlarged,  or  there  is  an 
obscure  swelling  or  sense  of  resistance  upon  palpation  anteriorly ;  or 
bulging  and  indistinct  swelling  in  the  region  of  the  kidney  poste- 
riorly. In  such  a  case  one  must  bear  in  mind  the  possible  causes  of 
its  enlargement  or  of  closely  related  tumidity.  Such  causes  are  pyo- 
nephrosis, hydronephrosis,  cystic  disease,  echinococcus,  carcinoma, 
sarcoma,  and  perinephric  abscess. 

The  tumours  of  pyonephrosis,  and  hydronephrosis  or  renal  echi- 
nococcus are  alike — rounded,  globular,  perhaps  fluctuating — and  may 
attain  a  large  size.  Multiple  large  cysts  of  the  kidneys  can  be  felt 
as  rounded  masses.  Malignant  tumours  of  the  kidney  may  grow  to 
dimensions  occupying  one  half  of  the  abdomen,  may  be  somewhat 
movable,  and,  if  of  rapid  growth,  a  sense  of  fluctuation  may  be  per- 
ceived. If  in  doubt  as  to  whether  or  not  a  tumour  in  the  left  renal 
region  involves  the  kidney  and  is  not  an  enlarged  spleen,  the  position 
of  the  descending  colon  should  be  ascertained  by  percussion,  inflating 
it  if  necessary  by  pumping  in  air  through  a  large  catheter  or  colon 
tube.  If  the  colon  lies  in  front  of  the  tumour  (Fig.  157),  it  is  renal 
and  not  splenic.  Perinephric  abscess  affords,  in  some  cases,  a  dis- 
tinct tumour,  in  others  a  bogginess  or  induration  in  the  interval 
between  the  last  rib  and  the  iliac  crest.  An  enlarged  kidney  tends 
to  develop  toward  the  front ;  a  perirenal  abscess  to  bulge  backward 
and  become  palpable  posteriorly. 

The  differential  diagnosis  between  the  various  causes  of  renal 
enlargement  must  be  made  by  an  attentive  consideration  of  the 
accompanying  signs  and  symptoms,  an  examination  of  the  urine,  and, 
in  some  instances,  by  the  use  of  the  aspirator. 

II.    BLADDER    AND    URETERS 

It  is  not  within  the  scope  of  this  work  to  describe  the  methods  of 
examining  the  urinary  bladder  or  the  ureters.  The  use  of  the  cysto- 
scope  and  the  catheterization  of  the  ureters,  in  men  as  well  as  in 
women,  is  occasionally  of  great  use  to  the  internalist  in  the  diagnosis 
of  suppurative  disease  of  the  kidney  or  vesical  new  growths,  but  the 
special  skill  required  for  such  manipulations  is  as  yet  confined  to 
a  few. 

The  presence  of  irritation  or  inflammation  of  the  urinary  bladder 
as  an  indication  of  renal  calculus,  spinal-cord  disease,  and  pyelitis 
should  be  remembered.     (See  also  Urination,  page  139.) 


NERVOUS  SYSTEM— THE  NEUEONE  481 

SECTION  XXXTII 
EXAMIXATIOX   OF   THE  XERVOUS  SYSTEM 

The  examination  of  the  nervous  system  and  the  diagnosis  of  its 
diseases  requires  an  intimate  acquaintance  with  neural  anatomy  and 
physiology.  With  the  exception  of  one  or  two  brief  references,  the 
subject  can  not  be  dealt  with  here. 

The  Neurone. — Modern  investigation  has  framed  a  conception  of 
the  nervous  system  which  differs  greatly  from  that  in  vogue  not 
many  years  ago.  At  present  it  is  conceived  as  an  aggregation  of  an 
enormous  number  of  units — the  neurones. 

A  neurone  consists  of  (1)  a  cell  hody^  (2)  dendrites,  and  (3)  an 
axo7ie  (Fig.  161). 

The  cell  body  from  one  of  its  poles  gives  off  the  dendrites,  which 
are  usually  numerous  and  relatively  short,  except  in  some  of  the  sen- 
sory neurones.  The  axone  or  axis-cylinder  process  passes  out  from 
the  body  of  the  cell,  and  becoming  what  was  formerly  termed  a  nerve 
fibre,  may  be  continued  for  long  distances,  giving  off  collaterals  at 
right  angles.  The  axone  finally  cleaves  into  a  number  of  fine 
branches,  forming  the  end  brush  or  terminal  arborization.  So  also 
may  the  collaterals.  The  whole  of  this  structure — cell  body,  den- 
drites, axone,  collaterals,  and  end  brushes — is  a  neurone. 

One  neurone  is  anatomically  independent  of  all  other  neurones, 
but  is  functionally  related  by  contact.  The  end  brushes  of  one  neu- 
rone intermingle,  but  do  not  anastomose  (or  but  rarely),  with  the 
dendrites  of  another,  like  the  branches  of  contiguous  trees. 

The  dendrites  are  celhilipetal  in  function  (i.  e.,  bring  impulses  to 
the  cell  body) ;  the  axones  are  celhilifugal,  carrying  impulses  aivay 
from  the  cell  body.  The  cell  bodies  are  the  containers  and  gen- 
erators of  nerve  force,  the  dendrites  conduct  it  to  the  cell  body  from 
other  cells,  and  the  axones  distribute  it. 

The  well-being  of  the  processes  of  the  neurone  (dendrites  and 
axone)  depends  upon  their  connection  with  the  cell  body  and  the 
integrity  of  the  latter.  If  the  cell  body  is  injured  by  accident  or 
disease  the  processes  degenerate,  or  if  a  process  is  severed  from  the 
cell  body  the  separated  part  undergoes  degeneration — i.  e.,  the  cell 
body  is  trophic  for  its  processes.  Conversely,  a  cell  separated  from 
its  processes  undergoes  a  sligliter  but  still  perceptible  degeneration. 

Central  and  Peripheral  Neurones. — Starting  from  the  large  cell 
bodies  of  the  motor  area  of  the  brain  cortex,  efferent  impulses,  which 
are  from  this  source  motor,  but  from  other  centres  may  be  secretory. 


DENDRITES' 


u 

R 
0 
N 

E 


B 


^ 


V_ 


End  organ 

in  muscular  fibre 


Carry  impulses  to  the  cell 
Degenerate  if  separated  from  it 


Is  the  container  and  generator  of 

nerve  force 
Is  trophic  for  dendrites  and  axones 


Carries  impulses  from  the  cell  body 
Degenerates  if  separated  from  it 


A  •  Upper  or  cerebral  motor 

NEURONE 

Exercises  an  inhibitory  con- 
trol OVER  B 


i  Intermingles  but  does  not  unite  with 
-<  dendrites  of  neurone  to  which  it 
(     carries  impulses 


B  -  Lower  or  peripheral  mo- 
tor neurone 

Exercises  trophic  influence 
over  and  maintains  tonus 
of  muscles 


Fig.  161.— The  neurone  (diagrammatic). 


THE  NERVOUS  SYSTEM  483 

trophic,  or  inhibitory,  travel  down  the  axones  which  run  from 
the  cortical  cell  bodies  to  the  cell  bodies  in  the  cranial  nerve 
nuclei  and  the  anterior  horns  of  the  spinal  cord,  their  end  brushes 
surrounding  and  transferring  impulses  to  the  latter.  The  latter  in 
turn  send  off  axones  which,  leaving  the  nuclei  and  the  cord  in 
the  motor  cranial  nerves  and  in  the  anterior  roots  of  the  spinal 
nerves,  are  finally  distributed  by  way  of  the  peripheral  nerves  to  the 
voluntary  muscles. 

It  is  thus  evident  that  cortical  motor  impulses  must  pass  through 
at  least  two  sets  of  neurones,  the  primary,  central,  or  higher  level 
neurones  (cortex  to  anterior  horns,  or  to  nuclei  of  motor  cranial 
nerves),  and  the  secondary,  peripheral,  or  lower  level  neurones  (an- 
terior horn  or  cranial  nuclei  to  muscles).  These  are  sometimes  re- 
ferred to  respectively  as  the  upper  and  lower  segments  of  the  motor 
path  (Fig.  162). 

The  upper  and  lower  motor  neurones  are  not  entirely  independ- 
ent. The  upper  neurones  exercise  a  constant  controlling  influence 
over  the  lower.  The  lower  neurone  is  just  as  constantly  sending 
impulses  to  the  muscle  in  which  its  axone  terminates,  and  the  nutri- 
tion, the  reflex  irritability,  and  the  tone  or  tension  of  the  muscle 
depend  upon  the  steady  reception  of  such  impulses.  Practically,  the 
lower  neurone  plus  the  muscle  forms  a  nutritive  unit. 

It  must  be  clearly  understood  that  although  the  cell  bodies  of 
the  nuclei  of  the  motor  cranial  nerves  lie  in  the  substance  of  the 
medulla,  they  are  as  distinctly  peripheral  as  those  of  the  anterior 
horns  of  the  spinal  cord. 

Motor  and  Sensory  Paths. — The  direct  motor  path,  for  all  volun- 
tary impulses,  from  the  motor  area  of  the  brain  (Fig.  43),  and  the 
indirect  motor  path,  for  the  co-ordination  of  muscular  movements 
and  the  higher  reflex  and  automatic  movements,  are  shown  in 
Fig.  162. 

The  direct  sensory  path,  through  which  pass  the  sensations  of 
touch,  pain,  and  temperature,  and  the  indirect  sensory  path,  which 
is  concerned  Avith  the  sensations  from  the  muscles,  joints,  and  vis- 
cera, are  shown  in  Fig.  163. 

Spinal  Cord. — The  surface  relations  of  the  spinal  cord  are  shown 
in  Fig.  164;  the  relation  of  the  spinal  segments  and  their  nerves  to 
the  spinous  processes  of  the  vertebras  in  Fig.  165 ;  and  certain  facts, 
with  reference  to  the  names,  functions,  and  diseases  of  the  parts  of 
the  cord,  in  Figs.  166,  167,  168,  and  169. 

It  is  further  requisite  for  the  clinician  to  know  the  segmental 
localization  of  the  motor,  sensory,  reflex,  and  other  functions  of  the 
cord,  as  follows : 


HORIZONTAL  SECTION 

or  THE  LEFT 

INTERNAL 

CAPSULE 


VcKTICAL   SECTION 

OF  INTERNAL 

CAPSULE. 


HORIZONTAL  SEC- 
TION OF  CRUS. 


CEREBELLUM  AND 

INDIRECT  MOTOR 

PATHWAY. 


MOTOR  DECUSSATION 
IN  MEDULLA. 


HORIZONTAL 

SECTION  OF 

THE  SPINAL 

CORD. 


DIRECT  PYRAM- 
IDAL TRACT. 


ANTERIOR  ROOT 
OF  SPINAL 
NERVE. 


ANTERIOR  ROOT 

OF  SPINAL 

NERVE. 


BLACK  FfBRES- INDIRECT  PATHWAY. 

BLUE=  PERIPHERAL  H.OWF^R^   NEURONE 
RED  =  CENTRAL (UPPER)  NEURONE 
Fig  162. — Motor  Pathways.     Direct  motor  path  (in  red)  (for  voluntary  impulses)  runs 

from  cortex,  via  corona  radiata,  internal  capsule,  crus,  pons,  medulla,  crossed  and  direct 
pyramidal  columns,  to  motor  cells  of  anterior  horn;  the  cranial  nerve  motor  fibres  (in 
(red)  cross  at  various  levels  in  crus,  pons,  and  medulla.  Indirect  motor  path  (in  black) 
(for  muscular  co-ordination  and  higher  rellex  and  automatic  movements)  runs  from  cor- 
tex to  pons  nuclei,  to  cerebellum,  to  lateral  fundamental  column,  via  the  peduncles,  tlie 
fibres  terminating  at  various  levels  in  the  anterior  horn. 
484 


CORTHX 


SENSORY  BRANCH 
TO   MOTOR  CELL 
IN  ANTERIOR 
HORN. 


Each  cell  of  the  ganglia  of 
the  posterior  roots  of  the  spinal 
cord  (or  of  the  cranial  nerve 
nuclei)  gives  off  two  main  pro- 
cesses. One,  the  dendrite,  goes 
to  the  sensory  end  organ  In  the 
skin  or  elsewhere,  bringing  im- 
pressions to  the  cell,  and  con- 
stituting the  peripheral  sensory 
nerve  fibre  ;  the  other,  the  ax- 
one,  enters  the  cord  through  the 
posterior  root  (or  runs  from  the 
cranial  nerve  nuclei  Inward), 
coming  into  relation  with  other 
neorones. 


3Lw£  =  i:;rect  sensory  pathway. 

RED  =  INDIRECT  SENSORY  PATHWAY. 

"DENDRITES. 

Fig.  163. — Sensoky  Pathways.  The  direct  sensory  path  (in  blue)  (for  touch,  pain,  and  tem- 
perature) runs  from  posterior  root  across  the  cord  to  antero-lateral  column,  to  tegmentum 
of  crus,  to  optic  thalamus,  to  corte.x.  The  indirect  sensory  paths  (in  red)  f  for  co-ordi- 
native  sensations  from  muscles,  joints,  and  viscera)  run  upward  on  same  side,  via  the 
direct  cerebellar  tract  and  the  posterior  column,  decussating  at  upper  part  of  cord,  to 
cerebellum,  to  optic  thalamus,  to  cortex. 

33  485 


486 


THE  EVIDENCES  OP  DISEASE 


Segmental  Motor  Localization  in  the  Cord. — One  must  distinguish 
carefully  between  the  motor  functions  of  a  segment  and  those  of  the 
peripheral  nerve  or  nerves  of  which  the  axones  coming  from  a  par- 
ticular segment  may  form  a  part.  Each  segment  may  be  regarded  as 
a  unit  possessing  certain  motor,  sensory,  trophic,  vasomotor,  and 
reflex  functions,  with  reference  to  the  peripheral  distribution  of  the 
nerve  roots  which  jsass  off  from  and  enter  it.  A  segment  is  named 
after  the  pair  of  nerves  which  arise  from  it,  and  not  from  the  verte- 
bra at  the  level  of  which  it  lies.     Any  peripheral  nerve  may  contain 


Fio.  164. — Showing  the  relation  nf  the  spinal  oord  to  the  dorsal  surface  of  the  trunk ;  the 
relative  length  of  the  cervical,  dorsal,  lumbar,  and  sacral  portions;  and  the  position  of 
the  cervical  and  lumbar  enlargements. 

fibres,  motor  or  sensory,  from  several  different  segments,  and,  indeed, 
this  is  the  case  in  the  majority  of  the  cerebro-spinal  nerves.  Conse- 
quently, movements,  not  individual  muscles  or  nerves,  are  represented 
in  the  gray  matter  of  each  segment,  and  the  determination  of  the 
exact  position  of  focal  (circumscribed  or  limited)  lesions  of  the  cord 
depends  largely  upon  the  discovery  of  the  deficient  action  of  a  group 
or  groups  of  muscles  controlled  by  definite  segments  of  the  oord, 
from  which  deficiency  one  may  infer  the  existence  of  disease  in  the 
controlling  segment. 


ROOTS 


SPINOUS  PROCESS 


EXITS 


C    I       ARISES 
II     ARISES 

III  ARISES 

IV  ARISES 
V 

VI 

VII 

VIII       „ 
D  I 
II 

III 

rv 

V 
VI 

VII 
VIII 

IX 

X 

XI 
XII 


M 

?} 


S  I 

II 
III 

IV 


ABOVE  ATLAS 
OPPOSITE  ATLAS 

AT  ATLAS 

BETViEEN  2nd  &  3rd  SPINE    . 

OPPOSITE  3rd  SPINE 

„  4th 

5th  « 

-.  6th  „ 

6th 

7th  „       . 

/,        1st  DORSAL  spme. 

2nd 


3rd 
4th 
5th 
eth 
7th 
8th 
9th 
10th 
11th 


ii 


tz"---- 


a  lit  LUMBAR 


Black  Dots  =  Points  of  Origin. 
Circles  =  Points  of  Exit. 
C  =  Cervical.  D  =  Dorsal. 

L  =  Lumbar.  S  =  Sacral. 


BETWEEN  ATLAS  &  OCCIPUT 
ABOVE  ATLAS 


ABOVE 

3rd 

CERVICAL  SPINE 

" 

4th 

n               n 

.. 

5th 

,. 

" 

6th 

„ 

" 

7th 

//               // 

„ 

1st 

DORSAL  SPINE 

BETWEEN  lat  &  2nd  DORSAL  SPINE 


2nd, 
3rd.. 

3rd       „           „ 
4th       ..           „ 

4th  „ 

5th        „           „ 

5th., 

6th        •<           „ 

6th  „ 

7th        „ 

7th  „ 

8th        ,1 

8th  „ 

9th        ..           u 

9th  „ 

10th       „           „ 

10th  „ 

11th       „           •• 

11th  & 

12th       „ 

BETWEEN  12th 

DORSAL  & 

Ut  LUMBAR     „ 

1st  &  2nd       „ 

2nd,, 

3rd       „ 

3rd,, 

4th        ., 

4th  „ 

5th 

BETWEEN  5th 

LUMBAR  4 

lat  SACRAL      ,. 

1st  &  2nd        „           „ 

2nd,. 

3rd       ,. 

3rd,, 

4th 

4th  „ 

Sth 

Fig.  165. — Diagram  showing  tlie  relation  of  the  segments  of  the  spinal  cord,  and  of  the  roots 
and  exits  of  the  spinal  nerves,  to  the  spinous  processes  of  the  vertebrse. 

487 


MARGINAL  ZONE, 

OR 
LISSAUER'S  TRACT. 


Fig.  166.— Showing  the  tracts  of  the  spinal  cord  and  their  varied  nomenclature.     Ked 
motor  (or  efferent).    Blue  =  sensory  (or  afferent). 
488 


z'  •-  S3 

^   CO    S 

=  S  Ji- 

S    >   CO 

£  o  p   . 
tr  Qo  Q- 1— 

•^  -»:  u.  a: 


»:^  ^-^  /J^  '^^- 


Fig.  167. — Showinjr  tlie  functions  of  the  various  tracts  of  the  spinal  cord.     Red  =  motor 
(or  elferent).    Blue  =  sensory  (or  afferent).    Compare  with  Fig.  166. 

489 


PAIN  AND  TEM 
PERATURE  SENSE. 


REFLEX  AND 
VISCERAL. 


Fig.  168. — Showing  the  functions  of  the  fibres  of  the  anterior  and  posterior  roots,  and  their 
relations  to  the  horns  and  columns  of  the  spinal  cortl.  Redrawn  and  modified  from 
Dana.    Compare  Figs.  166  and  167. 


FiQ.  169. — Showing  the  parts  and  columns  of  the  spinal  cord  and  some  of  the  diseases 
which  affect  them.     Compare  with  Fig.  168 ;  also  with  Figs.  166  and  1C7. 
490 


SENSORY 

Occiput  - 

Neck- 
Shoulder  - 

Musculo-spiral   i 

nerve \ 

Median  nerve  - 
Ulnar  nerve. 


CORD 


Thorax, 


Epigastrium  - 


Abdomen 


Umbilicus  - 


Gluteal  and  in-  ) 

guinal  regions  f 

Anterior   / 

Thigh  ^P^^  t 

and    <  External  , 

aspect  ,- 

"'P       Posterior  ( 

i       aspect  )■ 

)  Internal    i 
aspect  f 
Anterior    j 
aspect  f 

Foot  — 


n    ^ 


^   6 


n  7 


10 


II 


/2 


■0  / 


fl  ^ 


0^ 


Scrotum,  penis- 
Rectum,  bladder- 


MOTOR 

[  Diaphragm 
I  Levator  angull 
scapulae 

Sterno-mastoid 
Scaleni 
Neck  muscles 
Trapezius 

Supraspinatus 

Supinator  longus 
Rhomboids 

Teres  minor 

Deltoid 

Infraspinatus 

Biceps 

Subscapularis 

Coraco-brachialis 
Deep  shoulder  mus- 
cles 
Serratus  magnus 
Brachialis  anticus 
Pectoralis  major 
Extensors  of  wrist 

and  fingers 
Teres  major 
Latissimus  dorsi 
Flexors    of     wrist 

and  fingers 
Triceps 

Extensorsof  thumb 
Muscles  of  thenar 

and    hypothenar 

eminences 
Interossei,  lumbri- 

cales 
Intercostals 
Muscles    of     back 

and  abdomen 

Adduction  of  hip 

Quadriceps 
Sartorius 

Dio-psoas 

External    rotators 

of  hip 
Hamstring  muscles 
Calf  muscles 
Abduction  of  hip 
Glutei 
Peronei 
Small    muscles   of 

foot 
Anterior  tibial  mus- 
cles 
Perineal  muscles 

Bladder 
Rectum 


Fig.  170.— Showing  the  location  of  the  spinal  segments  for  sensibility  and  motion. 
Based  on  Jakob  (sensorv)  and  Starr,  Mills,  Sachs,  and  Dana  (motor). 

491 


492 


THE  EVIDENCES  OF  DISEASE 


The  following  table  *  (Starr,  Mills,  Sachs,  Dana,  Thoeburn)  shows 
the  muscles,  their  normal  function,  the  evidences  of  their  deficient 
action,  the  nerves  which  innervate  them,  their  representation  in  the 
medulla  and  the  segments  of  the  cord,  and  the  diseases  in  which 
they  are  commonly  involved  (see  also  Fig.  170). 

Muscles  of  Tongue,  Palate,  and  Pharynx 


name  of 

MUSCLE. 


Normal  function. 


Sjmptomi  of  deficient 
action. 


Innervated  by 


Represented  in 


Diseaws  in  which 

muscle  ia  commonly 

involved. 


G  e  n  i  o  - 
glossus. 

Styloglos- 


Lingua 1 
muscle 
proper. 


Az ygo  s 
uvulae. 


Levator 
palati. 


Pa  la  t  o- 
p  h  a  r  y  n- 
geal  mus- 
cles. 


Stylo -pha- 
ryngeus. 


Const  ric- 
tors  o  f 
pharynx. 

Laryngeal 
muscles. 


Pushes  tongue 
to  opposite 
side. 

Raises  tongue 
backwardand 
upward. 


All  movements 
of  the  tongue 
itself. 


Shortening  of 
uvula. 


Raises  the  ve- 
lum palati. 


Prevent  food 
from  passing 
toward  upper 
part  of  phar- 
ynx and  pos- 
terior nares. 
Helps  to  draw 
larj-nx  up- 
ward so  as  to 
be  closed  by 
epiglottis  and 
overtopped 
by  tongue. 
Help  to  push 
food  into  gul- 
let. 

Movements  of 
vocal  cords  in 
respiration 
and  in  articu- 
lation. 


Tongue  when  pro- 
truded deviates  to 
paralyzed  side. 
Tongue  can  not  be 
moved  backward 
or  hollowed  out 
(action  deficient 
in  many  healthy 
subjects). 
When  lying  in 
mouth  deviation 
to  healthy  side  ; 
when  protruded, 
deviates  to  para- 
lyzed side ;  if  one 
or  both  halves  are 
atrophied  tongue 
looks  shrivelled. 
Uvula  deviates 
toward  sound 
side;  if  both  sides 
are  paralyzed 
there  are  nasal 
tone  and  regurgi- 
tation through 
nose. 

Arch  can  not  be 
raised  in  the  into- 
nation of  '•ah"  ; 
if  paralysis  is  bi 
lateral  flapping  of 
arch  and  regurgi- 
tation of  food 
through  nose. 
Regurgitation  of 
food;  nasal 
speech. 


Imperfect  degluti- 
tion ;  food  gets 
into  windpipe. 


Food  is  swallowed 
very  imperfectly: 
sticks  in  throat. 
Hoarseness  and 
d  i  ffl  c  u  1 1  y  in 
breathing:  laryn- 
goscopicexamina- 
tion  reveals  false 
position  of  vocal 
cords. 


The      twelfth 
nerve    (hypo- 
glossal). 
The      twelfth 
nerve. 


The      twelfth 
nerve. 


Probably  pha- 
ryngeal plex- 
us :  seventh 
nerve  (?). 


As  above. 


Medulla. 
Medulla. 


Medulla. 


The  fifth  nerve. 


Glosso  -  pha- 
ryngeal. 


Pharyngeal 
plexus. 

Recurrent  la- 
ryngeal nerve 
excepting  the 
crico  -  thyroid 
muscle. 


Medulla. 


Medulla. 


Pons . 


Medulla. 


Medulla. 


Medulla. 


Bulbar  pal- 
sies (acute 
and  chron- 
ic) :  in  spe- 
cific and  tu- 
berculous 
diseases  of 
base  ;  dj's- 
trophi  es 
(rare). 


As  above. 


As  above. 


Basilar    affec- 
tions. 


Bulbar  affec- 
tions and  dis- 
eases of  the 
base. 


Diseases  of  the 
base  (bulbar). 

Bulbar  trou- 
bles (similar 
symptoms 
maj'  be  caused 
by  tumours 
and  foreign 
bodies  in  lar- 
ynx). 


*  Dana.    Textbook  of  Nervous  Diseases,  4th  edition.  New  York,  1897. 


THE  NERVOUS  SYSTEM 


493 


Muscles  of  Head  and  Neck 


NAME   OF 
MCSCLK. 


S  te  r  n  o- 
c  1  e  ido- 
mastoid. 


Rectus 
capitis 
an t icus 
major. 

Rectus 
capitis 
anticus 
minor. 

Rectus 
capitis 
lateralis. 


Scaleni 
anterior 
medius, 
et  pos- 
terior. 


Longus 
colli.        J 


Normal  foau^km. 


Symptonu  of  deficiost 
action. 


Raises  and 
turns  face  to 
opposite  side ; 
head  inclines 
to  same  side : 
if  both  mus- 
cles act  con- 
jointly head  is 
brought  for- 
ward. 


To  flex  head . . 


To  flex  head 


Slight  rotation. 


Elevate  ribs 
when  verte- 
bral column 
is  fixed ;  aid 
in  inspira- 
tion ;  slight 
lateral  flex- 
ion. 

Flexion  of  ver- 
tebral col- 
umn. 


Inability  to  raise 
head  from  bed,  or 
other  horizontal 
position,  if  both 
musclesare  affect- 
ed ;  if  one  muscle 
is  affected,  no 
marked  change  of 
position,  unless 
opposite  muscle 
is  contractured ; 
spasm  of  muscle 
frequent;  bead  in- 
clined to  one  side. 
Can  not  flex  head  i 
so  as  to  bring 
chin  on  chest. 


Deficient      rota-  ] 
tion        scarcely  | 
noticeable,     un- 
less   sterno-clei- 
do-mastoids  are  I 
diseased.  J 

Deficient  inspira- 1 
tory  movement! 


Imperfectflexion 
of  upper  spine,   j 


luwrratcd  by 


Spinal    acces- 
sor}-. 


BepcvMotcd  in 


DiteaM*  in  wUdi 

muida  i<  cumroonlj 

inTolred. 


MeduUa     and  i  In  bulbar  and 


Upi 


Upper 


Lower    cervi- 
cal nerves. 


Lower    cervi- 
cal nerves. 


second  and 
third  cervical 
segments. 


Uppercervical 
segments. 


Lowercervical 
segments. 


cervical  -  cord 
affections ;  in 
later  stages  of 
progressive 
m  u  s  c  u  1  a  r 
atrophies ;  oc- 
casionally in 
neuritis. 


Diseases  of 
the  cervical 
region  (mye- 
litis, menin- 
gitis, tu- 
mour ;  pro- 
gressive 
wasting  of 
muscles). 


Muscles  of  Shoulders  and  Upper  Extremity 


NAME    OF 
MUSCLE. 


Normal  function. 


Trapezius. 
1.  Clavic- 
ular por- 
tion (re- 
spiratory; 
outer 
third  o  f 
clavicle  to 
occipital 
bone). 


2.  MiAdle 
portion 
(from 
acromion 
and  outer 
spine  o  f 
scapula  to 
ligament, 
n  u  c  h  SB 
and  u  p- 
per  dorsal 
spines). 


Pulls  head 
backward;  ro- 
tates slightly 
toward  side  of 
muscle.  so 
that  chin  is 
turned  to  op- 
posite side  : 
contraction  of 
both  clavicu- 
lar portions 
bends  head 
b  a  c  k  w  a  rd  ; 
slight  eleva- 
tion of  shoul- 
ders :  aids  in 
deep  inspira- 
tion. 

Raises  shoul- 
der blade  : 
elevation  of 
acromion 
(clavicle  goes 
along). 


Syniptoms  of  deficient 
action. 


Innervated  by 


Represented  in 


Spinal    acces- 
sory. 


Deficient  back- 
ward movement 
of  head  ;  not 
marked  as  a  rule 
because  deep 
muscles  perform 
this  function : 
shoulder  does  not 
move  during  in- 
spiration. 


Acromion  de-    Spinal    acces- 

pressed  by  weight  sory  nerve 
of  upper  extrem- 
ity :  inner  upper 
angle  may  be 
pulled  upward  by 
levator  anguli 
.scapulae:  internal 
lower  angle  is 
nearer  to  median 
line. 


Medulla  and 
second  and 
third  cervical 
segments. 


As  above. 


tNseani  in  which 

muscle  is  commonly 

involved. 


Progressive 
muscular 
wasting ;  dis- 
eases of  me- 
dulla and  up- 
per cervical 
cord  ;  clavic- 
ular portion 
'  least  frequent- 
ly involved. 


As  above. 


494 


THE  EVIDENCES  OF  DISEASE 


Mtisclea  of  Shoulders  mid   Upper  Extremity  {continued) 


N.i31E   OF 

MUSCLE. 


8.  Lower 
portion 
and  ad- 
ductor. 


Rhomboids 


Levator 
a  n  gu 1 i 
scapulae. 


Serratus 
magnus. 


Deltoid 
(three  di- 
visioDB). 


Infraspi-  ] 
natus.      ! 

Teres  f 
minor.    J 

Subscap- 
ularis. 


Monnal  fuactioo. 


Adduction  of 
scapula 
toward  me- 
dian line. 


Oblique  move- 
ment of  scap- 
ula from  be- 
low, upward 
and  inward, 
so  that  infe- 
rior angle  is 
brought  near- 
er the  medi- 
an line  ;  hold 
spinal  margin 
of  scapula 
down  to  tho 


Draws  superi- 
or inner  angle 
of  scapula  up- 
ward ;  aids  in 
shrugging  of 
shoulders. 
Rotation  of 
should  e  r 
blade  out- 
ward,  and 
slight  eleva- 
tion of  acro- 
mion ;  holds 
inner  margin 
of  scapula  to 
thorax: 
brings  arm 
from  horizon- 
tal to  vertical 
position. 


To  raise  arm 
to  horizontal 
position,  and 
forward,  out- 
ward, or  back- 
ward ;  move- 
ments possi- 
ble only  if 
scapula  is 
fixed  by  ac- 
tion of  serra- 
tus and  tra- 
pezius. 

Rotator  hu- 
meri posticus 
(  Duchenne )  ; 
rotate  arm 
outward. 
Rotatorhume- 
ri  anticus 
( Duchenne  ^  ; 
rotates  arm 
inward. 


Symptonu  of  dtftici..'Qt 
actioD. 


Margin  of  scapula 
is  about  10  centi- 
metres distant,  in- 
stead of  being  .5  or 
6  centimetres  dis- 
tant from  median 
line  :  loss  of  ab- 
ductor may  be 
covered  up  by 
action  of  rhom- 
boids ;  rounding 
of  back. 

Deep  groove  be- 
tween inner  mar- 
gin of  scapula  and 
thorax  :  if  serra- 
tus is  normal,  this 
groove  disap- 
pears if  arm  is  ex- 
tended forward  ; 
shoulder  blade 
can  not  be  approx- 
imated to  median 
line.  (According 
to  Duchenne,  this 
can  be  effected  by 
upper  portion  of 
latissimus  dorsi.) 
Isolated  paralysis 
rare. 


Scapula  pulled  up- 
ward ;  lower  inner 
angle  nearer  the 
median  line:  arm 
can  not  be  raised 
above  horizontal 
position :  if  arm  is 
stretched  f  or  wa  rd 
scapula  is  re- 
moved from  tho- 
rax ('•  winged 
scapula  ") ;  dur- 
ing abduction  of 
arm,  scapula  is 
moved  nearer  to 
median  line,  and 
crowds  trapezius 
and  rhomboids 
forward. 

Can  raise  shoulder 
but  not  arm  ; 
shoulder  flattened 
(atrophy):  groove 
bet  ween  aero  mion 
and  head,  of  hu- 
merus :  each  di- 
vision of  deltoid 
may  be  paralyzed 
singly. 


Arm   can   not  be 
moved  outward. 
Difficulty  in  writ- 
ing (Duchenne). 

Arm  can  not  be 
moved  inward  : 
scapula  is  rubbed 
against  ribs. 


Innemttod  by 


Spinal    acces 
sory  nerve. 


Fifth  cervical. 


Third  and  fifth 
cervical 
nerves. 


Posterior  tho- 
racic nerve. 


Rt;pre«eDted  in 


Diseaso  in  which 

muscle  is  coniiuonly 

involvtd. 


Circumflex.. 


Suprascapu-  1 

lar. 

Circumflex. 


Subscapular 
nerve. 


Medulla  and 
second  and 
third  cervical 
segments. 


Fourth       and    As  above, 
fifth    cervical 
segments. 


Second      and  D  y  s  t  r  o  p  hies 

fourth  (?)  cer-  and     cervical 

vical          seg-  diseases, 
ments. 


Fifth  and    Progressive 

sixth  cervical    muscularatro- 
segments.  phies        (dys- 

trophies) :  neu- 
ritis of  part  of 
the  brachial 
plexus  :  after 
traumatic  in- 
juries to  shoul- 
der; in  cervi- 
cal-cord affec- 
tions. 


Fourth,    fifth,'  As  above:  also 

and  sixth  cer-  in  Erb's  form 

vical  seg-  of    ol)stetrical 

ments.  paralysis. 


Fourth,    fifth.    As  in  case  of 
and  sixth  cer-     deltoid, 
vical  seg- I 
ments. 


THE  NERVOUS  SYSTEM 


495 


Muscles  of  Shoulders  and  TJpper  Extremity  (continued) 


NAME   OF 
MUSCLE. 


Supraspi- 
natus. 


Latissimus 
dorsi. 


Teres  ma- 
jor. 


Pectoralis 
major. 


Nonnml  fnnctioa. 


Helps  to 

Steady  shoul- 
der joint  and 
to  elevate  arm 
forward  and 
outward ;  out- 
er angle  of 
scapula  is  de- 
pr^sed. 
Pulls  the  arm 
when  raised, 
downward 
and  back- 
ward ;  if  arm 
i.s  at  rest  up- 
per  j)ortion 
brings  scap- 
ula nearer  the 
median  line  ; 
united  action 
of  upjjer  third 
of  both  mus- 
cles causes 
extension  of 
dorsal  trunk  ; 
single  action 
causes  lateral 
movement  of 
trunk. 

Rotates  raised 
humerus  in- 
ward ;  adduc- 
tion of  arm  to 
thorax ;  slight 
elevation  of 
shoulder. 
Clavicular 
portion  de 
presses 
merus 
raised 
tion  to 
zontal  ; 
duction 
arm,  as  in 
giving  a  bless- 
ing ;  sternal 
portion  de- 
presses arm 
c  o  m  p  1  etely, 
and  if  arm  is 
at  rest  draws 
acromion  for- 
ward and 
backward. 


hu- 
from 
posi- 
hori- 

ad- 
of 


Symptotni  of  deficient 
action. 


buMTTStad  by 


RcprMentad  in 


Suprascapular.  Fourth   cervi- 
cal. 


According  to  Du- 
chenne,  humerus 
is  separated  still 
farther  from  acro- 
mion, if  supra- 
spinatus  is  aCFect- 
ed  in  addition  to 
deltoid. 


Arm  can    not  be  Sub  scapular,  '  Sixth  and  sev- 
moved  back  ward;  also  branches  I  enth  cervical, 
insufficient  exten-  |  of  dorsal  and  I 
sion     of      dorsal  lumbar 
spine ;  trunk  can  nerves     pass- 
not  be  moved  lat-  ing     through 
erally.  muscle 


DiaeatM  in  wliicli 

mnscl*  ii  oommooly 

involTcd. 


Very  few  symp- 
toms; action  sup- 
plied by  other 
muscles. 


Imperfect  adduc- 
tion of  arm ;  pa- 
ralysis can  be  dis- 
covered best  by 
extending  arm's 
and  trying  to 
press  volar  sur- 
faces again  st  each 
other. 


Subscapular. 


Anterior   tho- 
racic. 


Seventh  cervi- 
cal. 


Fifth,  sixth, 
and  seventh 
cervical. 


As  above. 


As  in  progress- 
ive atrophies 
and  dystro- 
phies ;  in  cer- 
vico-dorsal  le- 
sions ;  in  neu- 
ritis. 


As  above. 


Amyotrophies 
and  dystro- 
phies, chiefly ; 
also  in  lesions 
of  brachial 
plexus. 


Muscles  of  Arm,  Forearm,  and  Hand 


NAME   OF 

MUSCLE. 

Triceps 


Biceps. 


Nonnal  function. 


Extends  fore- 
arm ;  long 
head  of  tri- 
ceps, and  cor- 
aco-brachialis 
help  to  keep 
head  of  hu- 
merus in  posi- 
tion. 

Flexion  and 
supination  of 
forearm. 


Symptoou  of  deficient 
action. 


Innen'ated  bv 


Represented  in 


Diteaaet  in  wliich 

moscle  is  commonly 

involved. 


Arm  can  not  be 
extended  except 
by  its  own  weight ; 
if  long  head  of  tri- 
ceps is  affected 
subluxation  of 
head  of  humerus 
occurs  easily. 

Flexion  deficient, 
but  can  be  carried 
I  out    m    part    by 
other  muscles. 


Musculo-spiral.!  Sixth,  seventh,  ~1  Poliomyelitis 


Musculo- cuta- 
neous. 


eighth    cervi- 
cal segments. 


Fourth,    fifth, 
sixth  cervical. 


and  other 
affections  of 
I  cervical 
I  cord ;  trau- 
I  matic  inju- 
i  ries :  amyo- 
I  trophies  and 
dystrophies 
'  (triceps  es- 
I  capes  in 
1  many  pe- 
i  r  i  p"h  e  r  a  1 
J    palsies). 


496 


THE  EVIDENCES  OF   DISEASE 


Muscles  of  Arm,  Forearm,  and  Hand  (continued) 


NAME    OF 
MUSCLE. 


Supinator 
longiLs. 


Supinator 
brevis. 


Extensor 
carpi  radi- 
alislongus 
et  brevis. 


Extensor 
carpi  ul- 
uaris. 


Extensor 
digitorum 
commu- 
nis. 

Extensor 
indicis. 

Extensor 
minimi 
digiti. 

Flexor  car- 
pi radialis 

Flexor  car- 
pi ulnaris. 

Palmaris 
longus. 


Flexor 
digitorum 
sublimis. 

Flexor 
digitorum 
profun- 
dus. 


Interossei 
and  lum- 
bricales. 


Normal  function. 


Flexes  fore- 
arm and  aids 
in  pronation. 


Supinates 
hand  when 
forearm  is  ex- 
tended. 
Extens  i  on 
and  abduc- 
tion of  wrist ; 
the  shorter 
muscle  has 
pure  exten- 
sion action 
only. 

Extension  and 
abduction  of 
wrist. 


1 

Extension  of 

I    first      pha- 

J-  langesofall 

fingers  and 

abduction. 

J 

Flexion  of 
wri.st  and  pro- 
nation. 

Flexion  of 
wrist  and  su- 
pination. 
Flexion  of 
wrist  only. 


Flexes  second 
phalanx 
toward  first. 

Flexes  last 
twophalanges 
toward  first. 


Abductionand 
adduction  of 
fingers  if  first 
phalanges  are 
extended ; 
fiexion  of  first 
phalanges 
and  simulta- 
neous exten- 
sion of  second 
and  third  pha- 
langes. 


SymptonM  of  defident 
action. 


Flexion  and  pro- 
nation deficient ; 
muscle  does  not 
stand  out  promi- 
nently if  arm  is 
fiexed  and  at- 
tempt is  made  by 
another  to  extend 
it  forcibly ;  if  mus- 
cle is  atrophied 
arm  is  spindle- 
shaped. 

Deficient  supina- 
tion of  hand. 


Wrist  can  not  be 
flexed  dorsally 
(extended)  or  ab- 
ducted; flattening 
of  forearm. 


Wrist  can  not  be 
fiexed  dorsally  or 
adducted;  '•  drop- 
wrist  "'  is  charac- 
teristic of  paraly- 
sis of  extensors. 
First  phalanges 
can  not  be  ex- 
tended nor  fingers 
abducted  ;  grasp 
is  weak  because 
flexor  muscles  are 
shortened  and 
can  not  contract 
forcibly. 
Deficient  flexion  . . 


Flexion  and  supi- 
nation impaired. 

Flexion  impaired; 
no  anomalous  po- 
sition of  hand 
from  paralysis  of 
wrist  as  hand  falls 
by  its  own  weight ; 
the  flexors  of  fin- 
gers may  act  as 
substitutes. 
Second  phalanx 
can  not  be  flexed. 


Last  two. phalan- 
ges can  not  be 
flexed. 


Fin'gers  can  not 
be  abducted  or 
adducted  ;  inter- 
osseous spaces 
are  very  marked ; 
"Main  en  griffe" 
due  to  extension 
of  first  phalanges 
and  fiexion  of  sec- 
ond and  third  pha- 
langes. 


Innervated  by 


Musculo-spiral 


Musculo-spiral 


Musculo-spiral 


As  above . 


Musculo-spiral. 


Median. 


Ulnar , 


Median. 


Median . 


Ulnar  and  me- 
dian. 


Ulnar,  which 
also  supplies 
third  and 
fourth  lum- 
bricales;  me- 
dian supplies 
first  two  and 
sometimes 
third  lumbri- 
cales. 


B«preunted  in 


Diseases  in  which 

mu&cie  is  commonly 

involved. 


Fourth,     fifth    As  above ;  in- 


cervical. 


Fifth  cervical. 


Seventh  cervi- 
cal. 


Seventh  cervi- 
cal. 


Seventh  cervi- 
cal. 


Eighth    cervi- 
cal. 

Eighth    cervi- 
cal. 

Eighth    cervi- 
cal. 


Eighth    cervi- 
cal. 


Eighth    cervi- 
cal. 


Eighth  cervi- 
cal, first  dor- 
sal. 


volved  in  pe- 
ripheral neu- 
ritis (traumat- 
ic), not  in  lead 
palsy. 


Diseases  as 
above ;  also  in 
peripheral  pal- 
sies. 

As  before  ;  es- 
peciallyinneu- 
ritis. 


As  above. 


As  above. 


As  above. 
As  above. 
As  above. 


As  above. 


As  above ;  mus- 
cle should  be 
tested  with 
special  care  in 
cases  of  trau- 
matic injuries. 
As  above:  of- 
ten the  first 
muscles  to  be 
affected  in 
p  r  o  g  r  e  s  sive 
spinal  atro- 
phies. 


THE  NERVOUS  SYSTEM 
Muscles  of  Arm,  Forearm,  and  Hand  (conUrmed) 


497 


NAME   OF 

MUSCLE. 


The  n  a  r 
muscles: 

Extensor 
pollicis 
brevis. 


Extensor 
pollicis 
longus. 


Abductor 
pollicis 
longus. 


Abductor 

Eollicis 
revis. 

Opponens 
pollicis 
and  outer 
portion  of 
the  flexor 
brevis. 

Abductor 
pollicis 
brevis; 
flexor 
brevis  and 
adductor. 


Flexor 
pollicis 
longus. 


Monnal  fonctjon. 


Extends  first 
phalanx  and 
abducts  meta- 
carpal bone ; 
acts  with  ad- 
ductor poUicis 
longus. 

Extends  both 
phalanges  of 
thumb ;  also 
adduction  of 
m  e  t  a  c  a  rpal 
bone  and 
backward 
movement  of 
thumb. 

Abduction  of 
m  e  t  a  c  a  rpal 
bone ;  aids  in 
flexion  of 
band. 


Opppoiition 
'■    of  thumb. 


SymptoDu  of  <le6ci«it 
mctJoD. 


Impairment  of  ex- 
tension and  ad- 
duction ;  flatten- 
ing of  ball  of 
thumb. 


Deficient  exten- 
sion and  adduc- 
tion; second  pha- 
lanx is  flexed 
toward  first. 


Deficient  abduc- 
tion of  metacar- 
pal bone  ;  if  this 
muscle  and  ex- 
tensor pollicis 
brevis  are  para- 
lyzed adduction 
results. 


No     o  p  p  o  s  i  tion 
movement. 


\ 

Flex  first  pha-  No  flexion;  if  mus- 
lanx  and  ex-  j  cles  are  paralyzed 
tend  second  |  and  atrophied, 
phalanx  (like  |ape  hand  is 
1  n  t  e  r  o  s  seii,  formed, 
also  have  an 
abduction  and 
adduction  ac- 
tion. 

Flexes    end    No  flexion  of  end 
phalanx.  phalanx. 


lonernktcd  by 


Musculo-spiral. 


Musculo-spiral. 


Musculo-spiral. 


Musculo-spiral 


RapKMot«d  in 


Median. 


Median      and 
ulnar. 


Median. 


First  dorsal , 


First  dorsal . 


First  dorsal. 


DiHuet  in  which 

muacle  ia  commonly 

involved. 


First  dorsal . 


As  before; 
more  especial- 
ly in  amyotro- 
phies and  neu- 
ritis. 


As  above. 


As  above. 


As  above. 


As  above. 


As  above. 


Muscles  of  Back  and  Lower  Extremities 


NAME   or    MUSCLE. 


Erector  spince;  sacro- 
lumbalis:  lougissi- 
mus  dorsi. 

Abdominal  muscles  . . . 


Quadratus  lumborimi. 

Adductor  muscles 

Sartorius 

Quadriceps  femoris  . . , 


Ilio-psoas 

Tensor  fasciae  latse . . . 


Innemted  by 


Dorsal  nerves.    Second  to 
twelfth  dorsal  segments. 


Dorsal  nerves.    Second  to 
twelfth  dorsal. 


Lumbar  nerves . 


Obturator    nerve,    great 

sciatic  and  crural. 
Crural.      Third     lumbar 

segment. 
Crural.    Third  lumbar 


Crural    (lumbar   plexusl. 

Fourth  lumbar. 
Superior  gluteal.    Fourth 

lumbar. 


Symptoms  of  deficient  action. 


Lordosis  of  lower  spine;  perpendicular  line 
from  shoulder  falls  behind  os  sacrum  ; 
unilateral  palsy  causes  deflection  of  spine 
toward  sound  side. 

Lordosis  with  protrusion  of  nates  and  abdo- 
men :  other  actions  deficient ;  can  not 
straighten  up  from  recumbent  position 
without  as.sistance  of  bands. 

Lateral  movements  of  lower  vertebrae  im- 
perfect. 

No  adduction;  thigh  rolls  outward. 

Flexion  impaired ;  acts  imperfectly. 

Leg  can  not  be  extended;  to  test  it  ask  pa- 
tient, who  is  lying  down  with  hip  bent,  to 
stretch  out  the  leg;  when  patient  is  sitting 
down  to  extend  leg. 
1  Flexion  difficult :  in  bed  thigh  can  not  be 
\     flexed;  difficulty  rising  from  horizontal 
position. 


— C  VI 


CVIII 


Fig.  I71.-Diagram  of  skin  areas  corresponding  to  the  different  spinal  segments. 
Combined  from  Head's  diagrams  by  Osier. 
498 


Fig.  172. — Diagram  of  skin  areas  corresponding  to  the  diflFerent  spinal  segmeniB 
Combined  from  Head's  diagrams  by  Osier. 

499 


500 


THE  EVIDENCES  OF  DISEASE 


Muscles  of  Back  and  Lower  Extremities  (continued) 


NAME    OF    MUSCLE. 


External  rotators :  1 

Pyriformis.  i 

Genielli.  T 

Quadratus  femoris.  J 

Internal  obturator,  f 

External  obturator,  f 


Gluteal  muscles , 


Biceps;  semitendino- 
sus  and  seminrem- 
branosus. 

Gastrocnemius  (also 
plantarius  and  so- 
leus). 

Anterior  tibial  muscles 
(tibialis  anticus,  ex- 
tensor digitorum, 
and  extensor  pollicis 
longus). 

Peroneus  long^us 


Posterior  tibial  muscle 


Peroneus  brevii> 


Interossei  pedis  et  lum- 
bricales. 


Adductor;  flexor  bre- 
vis  and  abductor  hal- 
lucis. 


Innervatsd  by 


Sacral  plexus  (muscular 
branches).  Fifth  lum- 
bar. 

Obturator  nerve  (lumbar 

plexus), 
f  Inferior  gluteal   (sacral 
I     plexus).    First  and  sec- 
-j     ond  sacral. 
I  Gluteal  superior.    First 
t    and  second  sacral. 
Sciatic.      Fifth     lumbar 

segment. 


Internal  popliteal, 
lumbar. 


Fifth 


Anterior     tibial.       Fifth 
lumbar  and  first  sacral. 


Peroneal.  First  and  sec- 
ond sacral  segments. 

Posterior  tibial  nerve. 
First  and  second  seg- 
ments. 

Peroneal.  First  and  sec- 
ond segments. 

Posterior  tibial.  First 
and  second  segments. 


Posterior     tibial.      First 
and  second  segments. 


Symptoms  of  deficient  action. 


Deficient  outward  rotation;  leg  turned  in- 
ward. 


No  extension  of  thigh;  great  difficulty  in 
climbing;  no  abduction  of  thigh;  waddling 
gait,  exaggerated  movement  of  pelvis. 


Deficient  flexion;  action  of  quadriceps  may 
cause  excessive  extei  sion :  in  standing 
thigh  is  flexed  to  excess;  trunk  moved 
backward. 

Deficient  flexion  of  foot;  heel  can  not  be 
raised;  can  not  stand  on  tiptoes. 

Deficient  extension;  "  dropfoot,"  toes  scrape 
floor;  to  clear  this,  excessive  flexion  at 
knee  and  hip;  contracture  of  flexors  and 
pes  equinus  or  equinovarus. 

Deflcient  abduction;  plantar  arch  lessened; 
increased  by  contracture.  Flat  foot;  walk- 
ing tiresome. 

1 

I  Deficient  abduction  or  adduction;  deformi- 

(     ties  result  from  deficiencies. 

Abduction  and  adduction  of  toes  deficient: 
paralysis  of  interossei ;  hj-perextension  of 
first  phalanges ;  second  and  third  flexed 
(clawed  foot). 

Deficient  flexion  of  toes;  foot  can  not  be 
pushed  off  ground  easily. 


Segmental  Sensory  Localization  in  the  Cord. — Figs.  171,  172,  and 
173  represent  the  skin  areas  which  correspond  to  the  different  spinal 

segments  (compare  with  Figs.  174  to  179). 
It  is  obvious  that  if  areas  of  angesthesia 
are  found  to  exist,  which,  when  mapped 
out,  correspond  to  the  areas  in  the  dia- 
gram, one  may  infer  the  situation  of  the 
causative  lesion  in  the  cord. 

The  automatic  centres  of  the  cord  (Fig. 
195)  are  found  in  the  gray  matter  on  either 
side  of  the  central  canal.  They  are  so 
arranged  that  each  responds  in  a  special 
manner  to  a  definite  stimulus  (excito- 
reflex). 

The  Peripheral  Nerves. — The  peripheral 
nervous   system   includes    the   12   cranial 
Fig,  173.— Cutaneous  areas  of  the  (cerebral)  and  31  pairs  of  spinal  nerves, 
iiead  and  neck  supplied  by  the  ^jth  their  root  ganglia  and  end  organs, 

2d,  3d,   and  4th  cervical   —  &       &  e         ' 

ments  of  the  spinal  cord. 


and  also  the  so-called  sympathetic  nervous 


THE  NERVOUS  SYSTEM 


501 


Bystem.  It  should  be  borne  in  mind  that  the  latter,  embracing  the 
cranial,  vertebral,  and  peripheral  ganglia,  is  simply  a  part  of  the 
peripheral  apparatus. 


External  cutaneous 

( 

1. 

Genito-cruhal 

i 

Anterior  crural 

i 

External  popliteal 

Ilio-inquinal 


Long  saphenous 


Fig.  174. — Showing  the  distribution  of  the  sensory  nerves  of  the  skin,  anterior  aspect  of 

trunk  and  leg. 

(1)  The  motor  functions  of  the  cranial  nerves  are  summarized  in 
the  following  table  :  muscles. 

Sphincter  iridis.     Ciliary  muscles. 

III.  Ceanial  (Motor  oculi) 

84 


Levator  palpebrae  superioris.     Rectus 

internus  in  convergence. 
Rectus  superior.     Rectus  inferior. 


502 


THE  EVIDENCES  OF   DISEASE 


Muscles. 

(  Obliquus  inferior. 

IV.  Cranial  (Patheticus) -j  Obliquus  superior. 

'  (Upper  facial  group.) 

,TT   n<              /  *    „ „\                             ^  Rectus  externus.     Rectus  internus  of 

VI.  Cranial  (Abducens) ]  .       .,    .    , 

(  opposite  side  in  lateral  movements. 

I  Associated  movement  of  levator  pal- 

V.  Cranial  (Trigeminus) ■]  pebrje. 

(  Muscles  of  the  lower  jaw. 

VII.  Cranial  (Facial) Facial  muscles. 

XII.  Cranial  (Hypoglossal^ \  ^«^^f  ^^^j*^^  ^^^"P- 

(  Muscles  of  tongue. 

IX.  Cranial  (Glosso-pharyngeal)   \        i  Muscles  of  pharynx. 

X.  Cranial  (Pneumogastric) [■  •  •  ^  Muscles  of  esophagus. 

XI.  Cranial  (Spinal  accessory)  . . .  ;        '  Muscles  of  larynx. 


Fig.  175. — Showing  the  distributiou  of  tliu  -liixjin  ut;rv(.s  of  the  skin,  posterior  aspect  of 

trunk. 


With  reference  to  the  motor  function  of  the  mixed  spinal  nerves^ 
it  may  be  desirable  to  know  the  spinal  nerve  by  which  a  given  muscle 


THE  NERVOUS  SYSTEM 


503 


receives  its  motor  supply.  This  may  be  ascertained  by  consulting 
the  first  and  fourth  columns  of  the  table  on  pages  492-500.  On  the 
other  hand,  the  muscles  innervated  by  a  given  nerve  may  be  deter- 
mined (for  the  trunk  and  limbs)  by  the  following  table  (Hutchison 
and  Rainy)  : 


Upper  Limb. 


PoSt-THORACIC 

SUPEASCAPULAR  .  .  . 

Ex.  ANT.  Thoracic. 
Int.  ant.  Thoracic. 

musculo-cutane- 

ous 


Subscapular 
Circumflex  . 


MUSCULO-SPIRAL.  . .   ^ 


Post-Interosseus  .  < 


Median 


Median  and  Ulnar 
(jointly) 


Ulnar 


Serratus  magnus. 
(  Supra-spinatus. 
(  Infra-spinatus. 
f  Pectoralis    major 
J      (upp.  part,  low. 
1      part). 
[  Pectoralis  minor. 

(Coraco-brachialis. 
Biceps. 
Bracnialis      anti- 
cus. 
i  Subscapularis. 
<  Teres  major. 
(  Latiss.  dorsi. 
j  Deltoid. 
'(  Teres  minor. 
Triceps. 
Ext.     carp.     rad. 

long. 
Supinator  long. 
'  Supinator  brevis. 
Ext.     carp.    rad. 

brev. 
Ext.  carp.  uln. 
Ext.  comm.  digit. 
Ext.  ossis  metac. 

poll. 
Ext.  primi.  intern. 

poll. 
Ext.    secund.    in- 
tern, poll. 
Ext.  indicis. 
Ext.  minimi 

digiti. 
Pronator  radii 

teres. 
Palmaris  longus. 
Opponens  pollicis. 
Abductor  pollicis. 
Flexor  longus 

pollicis. 
Flexor  carpi  radi- 

alis. 
Plexor       sublim. 

digit. 
Flexor  brevis  pol- 
licis. 
Flexor    carpi    ul- 

naris. 
Adductor  pollicis. 
Muscles   of    little 

finger. 
Interossei. 


Trunk  and  Lower  Limb. 


Intercostals.  . 

Branches  of 
Lumbar 

Nerves. 
Genito-crural  , 


Anterior 
Crural 


Obtueatoe. 


Small  Sciatic. 
Sup.  Gluteal  . 

Great  Sciatic. 
Int.  Popliteal 


Plantars 


Ext.  Popliteal. 


Intercostals. 

Rectus  abdominis. 

External  oblique. 

Erector  spina?. 

Quadratus      lumbo- 
rum. 

Cremaster. 

Sartorius. 

Pec  tine  us. 

Rectus  femoris. 

Vastus  externus. 

Vastus  internus. 
y  Crureus. 
'  Gracilis. 

Adductor  longus. 

Adductor  brevis. 

Adductor  magnus 
(with  sciatic). 

Gluteus  maximus. 
j  Gluteus  medius. 
/  Tens.  vag.  femoris. 

Biceps  femoris. 

Seraitendinosus. 
■I   Semimembranosus. 

Adductor  magnus 
(with  obturator). 
f  Gastrocnemius. 

Soleus. 

Tibialis  posticus. 

Flex.  comm.  digit. 

Flex.  long,  hallucis. 
'  Flex.  brev.  hallucis. 

Flex.  brev.  digit. 

Abductor  hallucis. 

Adductor  hallucis. 

Ext.  brevis.  digit. 

Interossei. 
'  Tibialis  anticus. 

Ext.  prop,  hallucis. 

Ext.  digit,  longus. 

Peroneus  longus. 

Peroneus  brevis.  • 


Long  saphenous 


Anterior 
tibial 


Internal    External 
plantar     plantar 


External  plantar 
(Br.  post,  tibial) 


Internal  plantar 
(Br.  post,  tibial) 


Anterior 
tibial 


Long 
saphenous 


Internal  plantar 


External  saphenous 


External  plantar 


Long  saphenous 


Musculo-cutaneous 
(Br.  ext.  popliteal) 


Posterior  tibial 
Anterior  tibial 


Internal  plantar 


Fio.  179. — Showing  the  distribution  of  the  sensory  nerves  of  the  skin  of  the  foot 

505 


506 


THE  EVIDENCES  OF  DISEASE 


(2)  For  the  sensory  distribution  of  the  cranial  nerves,  see  Cranial 
Nerve  Functions ;  for  that  of  the  mixed  spinal  nerves,  see  Figs.  174 
to  179,  inclusive. 


Middle  cerebral 


Sylvian 
Posterior  cerebral 


Anterior  cerebral 


Lenticulo  optic 


Lenticulo-striate 
set  of  arteries 


Internal  carotid 


Basilar 


Vertebral 


Fig.  180. — Showing  the  arteries  at  the  base  of  the  brain.    One  of  tlie  lenticulo-striate  set  is 
called  the  "  artery  of  cerebral  hemorrhage."     Slightly  modified  from  Dercum. 


Fig.  181.— Showing  the  portions  of  the  cerebral  hemispheres  supplied  by  the  anterior, 
middle,  and  posterior  cerebral  arteries.     Kedrawn  from  Dana. 

Blood  Supply  of  the  Brain.— (See  Figs.  180  and  181.)     Certain 
practical  points  are  worthy  of   remembrance — viz.,  that  when  the 


NERVOUS  SYSTEM— DEGENERACY  507 

arteries  are  diseased  one  of  the  vessels  of  the  lenticulo-striate  group 
ruptures  more  frequently  than  the  others — the  artery  of  cerebral 
hemorrhage ;  that  in  consequence  of  the  manner  of  its  origin  the  left 
common  carotid  is  more  readily  entered  by  an  embolus  than  its  fel- 
low ;  and  that,  having  entered,  the  embolus  is  usually  arrested  in  a 
branch  of  the  middle  cerebral,  because  the  latter  is  an  almost  direct 
continuation  of  the  internal  carotid. 

THE  EXAMINATION  OF  THE  NERVOUS  SYSTEM 

An  examination  of  the  nervous  system  requires  an  investigation  of 
the  temperament,  the  diathesis,  the  presence  of  degeneracy,  the  con- 
dition of  the  intellect  and  of  speech,  and  the  state  of  the  motor 
and  sensory  functions,  including  the  reflexes  and  the  electrical  irri- 
tability of  the  muscles. 

Certain  of  these  elements  {q.  v.)  in  the  diagnosis  of  diseases  of  the 
nervous  system  have  already  been  considered — viz..  Temperament ; 
Diathesis ;  Facial  Expression ;  Emotional  State ;  Intellection,  includ- 
ing mental  confusion,  defective  memory,  delusions,  delirium,  and  dis- 
turbances of  consciousness  (stupor,  coma,  etc.) ;  Insomnia ;  and  Dis- 
orders of  Speech  (aphasia,  etc.). 

DEGENERACY 

There  are  certain  anatomical,  physiological,  and  psychic  pecul- 
iarities (stigmata  or  marks)  which  may  be  encountered  as  evidences 
of  a  congenital  and  usually  hereditary  neuropathic  diathesis  or  con- 
stitution. This  condition — termed  degeneration  or  degeneracy — is 
an  eccentric  departure  from  what  is  commonly  recognized  as  the  aver- 
age normal  type.  As  seen  in  this  country,  it  has  been  made  the  sub- 
ject of  special  study  by  Dana  and  Petersen. 

Anatomical  Stigmata. — The  physical  or  somatic  imperfections 
of  development  are : 

Cranium  and  Face. — Asymmetrical  cranium,  extremely  small  head 
(microcephalus),  unusual  configuration  of  the  skull,  lack  of  ordinary 
symmetry  of  the  two  sides  of  the  face,  a  very  high  and  narrow  fore- 
head, and  excessively  projecting  (prognathous)  or  very  large  jaws. 

Palate  and  Uvula. — Defects  or  deformities  of  the  palate  and 
uvula,  especially  a  high  and  narrow  arch  of  the  hard  palate,  and  a 
marked  longitudinal  ridge  on  the  latter  (torus  palatinus). 

Eyes. — Abnormally  narrow  palpebral  fissure  ;  lack  of  strength  in 
the  ocular  muscles  (muscular  insuflSciency  or  asthenopia,  squint) ; 
high  grades  of  astigmatism,  and  nystagmus  (rapid  turning  of  the 
eyes  from  side  to  side  or  vertically). 


508  THE  EVIDENCES  OF   DISEASE 

Ears. — Placed  in  unusual  positions,  poorly  shaped  or  unsymmetri- 
cal ;  absence  of  lobe,  the  lower  part  of  the  ear  directly  adherent  to 
the  head ;  and  noticeably  conchoidal  or  shell-shaped. 

Miscellatieous. — Imperfect  or  badly  set  teeth  ;  defects  in  shape  or 
size  of  lips  and  tongue ;  unusual  shortness  of  height ;  excessively 
long  or  short  fingers,  arms,  or  legs ;  small,  atrophic,  or  ill-formed 
genitals ;  absence  of  hair,  or  great  hairiness ;  or  any  congenital  atro- 
phy of  muscles  or  other  anatomical  deformities. 

Physiological  Stigmata.  —  These  are :  Some  forms  of  tic 
(muscular  twitching)  or  tremor,  hypersensitiveness  or  lack  of  sensi- 
tiveness of  the  skin  and  special  senses,  defective  speech — stammer- 
ing, etc.,  perversion  of  the  sexual  instinct,  and  inability  to  endure 
emotional  and  nervous  strain. 

Psychic  Stigmata. — These  are  :  Exaggerated  egotism,  excess- 
ive self-consciousness,  absence  of  will  power  and  emotional  control, 
disturbances  of  the  sense  of  personality,  and  feeble,  erratic,  or  ill- 
balanced  mental  activity. 

According  to  the  number,  degree,  and  kind  of  the  characteristics 
of  degeneracy  presented  by  the  individual,  three  classes  of  degener- 
ates are  recognised. 

(1)  Superior  Degenerates. — Moderate  degeneracy  is  often  asso- 
ciated with  unusual  mental  (usually  artistic)  endowments,  and  the 
geniuses  of  the  world  have  almost  always  exhibited  some  of  the  stig- 
mata mentioned.  A  combination  of  brilliant  mentality  and  degen- 
erate characteristics  constitutes  a  superior  degenerate.  Such  per- 
sons may  be  absolutely  sound  in  mind  and  enjoy  average  good  health. 

(2)  Inferior  Degenerates. — This  class  comprises  those  who  present 
not  only  the  evidences  of  degeneracy,  but  are  also  erratic,  morbid, 
eccentric,  criminal,  or  insane. 

(3)  Debiles. — This,  the  lowest  class,  consists  of  those  who  are 
weak-minded,  imbecile,  or  idiotic. 

The  most  significant  of  the  anatomical  stigmata  are  asymmetrical 
or  oddly  shaped  crania ;.  abnormal  palates,  found  in  10  percent  of 
normal  individuals,  and  46  to  80  per  cent  of  degenerates  ;  and  defect- 
ive or  badly  set  ears  (found  in  20  to  64  per  cent  of  degenerates)  or 
teeth. 

With  reference  to  the  diagnostic  and  prognostic  value  of  the 
degenerative  characteristics,  it  must  be  borne  in  mind  that  otherwise 
normal  individuals  may  possess  2  or  3  of  the  anatomical  stigmata, 
in  which  case  their  presence  is  of  no  significance.  If,  however,  a 
patient  exhibits  a  striking  combination  or  unusual  number  of  the 
various  stigmata,  one  should  look  for  evidences  of  insanity,  hysteria 
major,  epilepsy,  or  neurasthenia.     Such  diseases  occurring  in  degen- 


EXAMINATION  OF  MUSCLES 


509 


erates  have  a  decidedly  less  promising  prognosis.  If  a  child  is  born 
of  two  degenerates  it  is  likely  to  be  more  aberrant  than  either  of  its 
procreators. 

EXAMINATION   OF  THE    MUSCLES  WITH    REFERENCE 
TO  THEIR   NUTRITION,  TONE,  AND   MOTOR   POWER 

Nutrition  of  the  Muscles. — By  grasping  the  muscles  it  may 
be  determined  whether  they  are  normally  large  and  firm  or  whether 
they  are  flabby  and  small.  A  diminution  in  their  size  is  termed 
atrophy;  an  increase,  hypertrophy.  If  either  change  is  present  it 
may  involve  all  the  muscles  of  a  limb  (diffuse  atrophy  or  hypertro- 
phy), or  1  or  2  muscles  (circumscribed  atrophy  or  hypertrophy). 
In  judging  the  size  or  volume  of  the  muscles,  corresponding  sides 
should  be  compared,  and,  when  possible,  tape-line  measurements  of 
the  circumference  of 
the  limb  are  to  be  made. 
The  upper  arm  and 
calf  may  be  measured 
at  the  point  of  great- 
est girth ;  the  forearm 
about  1  inch  below  the 
inner  condyle  ;  the 
thigh  about  6  inches 
above  the  patella. 

Atrophy  (Fig.  182) 
may  occur,  to  a  slight 
extent,  simply  from  dis- 
use of  the  muscles,  and 
without  change  in  the 
electrical  irritability ;  if 
marked  (especially  if 
the  diminution  is  rapid) 
and  presenting  the  re. 
action  of  degeneration 
it  is  indicative  of  a  le- 
sion of  the  lower  motor 
neurones  ;  if  marked 
and  without  change  in 
its  electrical  reactions 
it  is  usually  indicative  of  primary  disease  of  the  muscles  (dystro- 
phies), or  chronic  disease  of  the  joints. 

Hypertrophy  may  be  true  or  false.     True  hypertrophy  is  distin- 
guished not  only  by  increased  size,  but  also  by  increased  strength. 


Fig.  IS'2. — An  old  case  of  infantile  spinal  paralysis  of  the 
entire  left  lower  extremity,  showing  extreme  atrophy 
of  the  thigh  and  leg,  and  a  very  characteristic  defor- 
mity of  the  foot  (Holt). 


610 


THE  EVIDENCES  OF  DISEASE 


and  is  found  in  muscles  which  have  been  much,  but  not  over,  used. 
It  occurs  also  in  Thomsen's  disease.  Pseudo-hypertrophy  presents 
increased  size  but  lessened  power — e.  g.,  pseudo-hyper  trophic  paraly- 
sis in  which  the  calf  muscles  in  particular  are  apparently  bulky  (Fig. 

183),  owing  mainly  to  an  over- 
growth of  the  fatty  and  in- 
terstitial elements,  the  mus- 
cular fibres  having  undergone 
atrophy. 

Tone  of  the  Muscles. — 
The  normal  tension  of  a  muscle 
at  rest  is  slight  but  perceptible. 
The  muscular  tone  is  deter- 
mined partly  by  palpation,  but 
mainly  by  the  degree  of  resist- 
ance offered  to  passive  motion 
of  the  limb.  An  increased 
tonus  or  tension,  usually  with- 
out atrophy^  of  muscles  which 
are  paralyzed  so  far  as  volun- 
tary effort  is  concerned  (spastic 
paralysis)  is  an  important  sign 
of  disease  of  the  upper  neu- 
rones, and  if  long  continued 
constitutes  one  form  of  con- 
tracture {q.  V.) ;  the  opposite 
condition  —  an  abnormal  lax- 
ness  or  flaccidity,  usually  with 
atrophy — of  paralyzed  muscles 
is  significant  of  lesions  involv- 
ing the  lower  neurones. 

Testing  the  Motor  Pow- 
er.— The  patient  should  be  de- 
sired to  sit  up,  to  move  each 
limb  in  turn,  to  walk,  thus  en- 
abling the  examiner  to  detect 
existing  gross  defects  of  motil- 
ity. If  the  patient  is  comatose 
the  limbs  should  be  lifted  separately  and  allowed  to  fall  upon  the 
bed.  If  the  coma  is  complete,  it  may  be  a  matter  of  some  difficulty 
to  determine  the  existence  of  paralysis — e.  g.,  a  hemiplegia  — but  it 
may  be  found  that  one  or  more  extremities,  if  paralyzed,  will  fall 
in  a  more  distinctly  limp  and  helpless  manner  than  others.     If  the 


Fig.  183. — Pseudo-muscular  hypertrophy,  show- 
ing to  a  moderate  degree  the  large  calves 
and  gluteal  regions  with  a  marked  lordosis 
(Holt).  From  a  photograph  by  Dr.  M.  A. 
Starr. 


EXAMINATION  OF   MUSCLES  51^ 

patient  be  conscious,  any  loss  of  power  is  readily  discovered  by  caus- 
ing him  to  resist  passive  motions  designed  to  bring  the  suspected 
muscles  into  play.  The  loss  of  power  may  vary  from  a  slight  impair- 
ment (parents)  to  an  absolute  loss  of  voluntary  action  (paralysis, 
nearly  or  quite  complete).  The  degree  of  impairment  may  be  accu- 
rately measured  by  a  dynamometer,  but  for  ordinary  purposes  it 
can  be  sufficiently  well  estimated  by  the  hand.  Always  compare 
corresponding  muscles  on  opposite  sides  of  the  body. 

One  also  observes  any  abnormal  muscular  movement  (page  514). 

The  power  of  individual  muscles  may  be  ascertained  as  follows  : 

(1)  Shoulder,  Arm,  Hand,  and  Fingers. — Deltoid. — Request  the  patient  to 
raise  the  arms  laterally  to  a  horizontal  position.  Inability  so  to  do  indicates 
deltoid  paralysis. 

Pectoral  Muscles. — Stretch  out  the  arms  straight  in  front,  and  then  approxi- 
mate the  hands  against  resistance  by  the  examiner,  meanwhile  watching  both 
heads  of  the  pectoral  muscle. 

Latissimus  Dorsi. — Raise  the  arms  laterally  to  a  level;  then,  while  keeping 
them  fully  extended,  bring  the  arms  downward  and  backward,  as  if  to  make 
the  hands  meet  behind  the  sacrum.  The  examiner  standing  behind  the  patient 
resists  the  movement. 

Serrattis  Magnus. — Desire  the  patient  to  push  with  his  hands  against  those 
of  the  examiner.  If  the  serratus  has  lost  its  power  the  scapula  will  project, 
and  the  digitations  of  the  muscle,  which  ordinarily  should  be  visible,  will  not 
be  seen. 

Trapezius. — Ask  the  patient  to  raise  the  shoulders  as  close  to  his  ears  as 
possible  against  the  pressure  of  the  examiner's  hands.  This  will  demonstrate 
the  strength  of  the  upper  part  of  the  trapezius.  The  middle  and  lower  portions 
are  tested  by  desiring  him  to  bring  the  scapulae  as  close  together  as  possible. 

It  is  hardly  possible  to  detect  paralysis  of  the  levator  anguli  scapulae  and 
rhomboids  unless  the  trapezius  is  also  involved. 

Biceps. — Let  the  patient  flex  his  extended  arm,  his  elbow  resting  on  the 
observer's  left  hand,  while  the  latter's  right  hand,  grasping  the  wrist  of  the 
patient,  offers  the  necessary  resistance.  Also  supinate  the  hand  against  re- 
sistance. 

Triceps. — The  triceps  may  be  tested  as  is  the  biceps,  excepting  that  the 
previously  flexed  arm  is  to  be  extended  against  resistance. 

Supinator  Longus. — Test  as  for  the  biceps,  except  that  the  hand  should  be 
midway  between  supination  and  pronation.  If  the  muscle  is  paralyzed,  it 
will  fail  to  become  conspicuous  on  the  radial  side  of  the  upper  part  of  the 
forearm. 

Flexors  of  the  Wrist. — Grasping  the  patient's  hand,  the  palm  being  upward, 
desire  him  to  bend  the  hand  up  toward  his  forearm  against  resistance. 

Extensors  of  the  Wrist. — The  patient's  hand  being  held  palm  downward,  he 
is  required  to  bend  it  backward  against  resistance.  Moderate  weakness  of  the 
extensors  of  the  wrist  may  be  manifested  by  asking  him  to  squeeze  the  exami- 
ner's hand,  in  which  case  the  wrist  will  become  involuntarily  flexed,  the  weak- 


512 


THE  EVIDENCES  OP  DISEASE 


Fig.  184.— Wrist-drop, 


ened  extensors  being  unable  to  counteract  the  flexors.     Marked  or  complete 
paralysis  of  the  extensors  is  wrist-drop  (Fig.  184). 

Flexors  of  the  Fingers. — Because  of  the  usual  difference  in  the  strength  of 
the  two  hands,  the  examiner  should  cross  his  forearms  and  place  his  right  hand 

in  the  right  hand  of  the  patient,  and  vice  vei'sa. 
Then  let  the  patient  squeeze  the  hands.  If  the 
observer  keeps  his  own  fingers  extended  and 
bunched  loosely  together,  he  will  be  able  to 
withstand  a  very  hearty  grasp  without  discom- 
fort. 

Adductor  Pollicis. — Ask  the  patient  to  pinch, 
with  his  thumb  and  forefinger,  one  of  the  ex- 
aminer's fingers. 

Opponens  Pollicis. — Desire  the  patient  to  ap- 
proximate the  ends  of  the  little  finger  and  the 
thumb. 

The   interosseous  and   lumbrical  muscles  of 
the  hand  flex  the  proximal  phalanges,  and  ex- 
tend the  middle  and  terminal  phalanges.     The 
dorsal  interossei  abduct,  the  palmar  adduct,  the 
fingers  from  and   toward  a  longitudinal  line 
drawn  through  the  centre  of  the  middle  finger. 
Test  by  making  tlie  patient  separate  and  ap- 
proximate the  fingers,  and  flex  the  proximal  phalanges,  keeping  the  middle 
and  terminal  phalanges  extended.     Paralysis  of  these  muscles  causes  the  "  claw 
hand  "  previously  considered  (q.  t).). 

(2)  Trunk  Muscles. — Paralysis  of  the  diaphragm  {q.  v.)  has  been  described. 
The  erector  muscles  of  the  spine  are  examined  by  causing  the  patient  to  lie 
face  downward,  and  asking  him  to  raise  the  head  and  shoulders  without  assist- 
ance from  the  hands.  Unless  paralyzed,  the  erectors  become  clearly  visible 
during  the  attempt.  The  abdominal  muscles  are  tested  in  a  similar  manner, 
except  that  the  patient  lies  in  the  dorsal  position  while  making  an  effort  to 
raise  the  head. 

(3)  Neck  Muscles. — Practically  one  examines  the  sterno-cleido-mastoid  mus- 
cle alone.  If  the  patient  is  lying  down  request  him  to  raise  the  head ;  or  if 
sitting  up  to  turn  the  head  as  far  as  possible  to  the  right  and  left,  with  or 
without  resistance  offered  by  applying  the  hands  to  the  sides  of  the  head ;  or  to 
bend  it  forward  against  pressure  upon  the  forehead.  If  the  muscle  is  not  para- 
lyzed it  stands  out  prominently. 

(4)  Muscles  of  the  Eye. — See  page  198. 

(5)  Muscles  of  the  Face. — The  occipito-frontal  raises  the  eyebrows  and  de- 
velops horizontal  wrinkles  in  the  forehead.  The  corrugator  supercilii  produces 
vertical  wrinkles  over  the  root  of  the  nose.  The  orbicularis  palpebrarum  shuts 
the  eyes,  lightly  or  tightly.  The  orbicularis  oris  closes  the  lips,  or  if  contract- 
ing strongly,  closes  and  protrudes  them.  The  levatores  and  zygomatic  major 
lift  the  upper  lip  and  the  angles  of  the  mouth.  The  buccinator  preserves  the 
tension  of  the  cheeks  when  blowing.  Facial  paralysis  {q.  v.)  is  described  else- 
where. 


EXAMINATION  OP  MUSCLES  513 

(6^  Muscles  of  Tongue,  (7)  Palate,  (8)  Pharynx,  (9)  Larynx,  and  (10)  Mastica- 
tion (see  Index). 

(11)  Muscles  of  the  Lmcer  Extremity. — Flexors  of  Thigh. — The  patient  lying 
upon  his  back,  ask  him  to  raise  the  leg  up  from  the  bed,  the  knee  being  kept 
straight.  This  determines  the  strength  mainly  of  the  ileo-psoas,  partly  of  the 
quadriceps. 

Extensors  of  Thigh. — The  leg  being  kept  straight  and  the  patient  lying 
upon  his  back,  raise  the  foot  and  ask  him  to  bring  it  down  upon  the  bed  against 
resistance.  This  determines  the  strength  of  the  gluteus  maximus  and  partly  of 
the  hamstring  muscles. 

Abductors  of  Thigh. — Fetch  the  leg  across  the  middle  line  and  desire  the 
patient  to  carry  it  toward  the  outer  side  against  resistance,  thus  testing  mainly 
the  gluteus  medius. 

Adductors  of  the  Thigh. — Carry  the  leg  outward  and  cause  the  patient  to 
bring  it  back  to  the  middle  line  against  resistance,  thus  testing  the  adductors 
longus,  brevis,  and  magnus. 

Inrotators  of  the  Thigh. — With  the  patient  prone  (face  downward),  flex  the 
knee  to  a  right  angle,  grasp  the  foot  and  oppose  resistance  while  he  inrotates 
the  thigh,  testing  mainly  the  gluteus  minimus. 

Outrotators  of  the  Thigh. — Similarly  test  the  power  of  outrotation,  thus 
determining  the  condition  of  the  obturators,  pyriformis,  gemelli,  and  quadra- 
tus  femoris. 

Flexors  of  Knee. — The  patient  lying  upon  his  face,  desire  him  to  bend  the 
knee  while  the  examiner  resists  the  movement  hy  pressure  upon  the  heel,  thus 
ascertaining  the  power  of  the  biceps,  semimembranosus,  and  semitendinosus. 

Extensors  of  Knee. — With  the  patient  in  the  dorsal  position,  flex  the  knee 
and  by  pressure  on  the  sole  of  the  foot  resist  his  endeavour  to  extend  the  knee. 
The  quadriceps  femoris  is  the  principal  muscle  concerned. 

Plantar  Flexors  {Extensors)  of  the  Foot. — With  the  leg  straight,  resist,  by 
pressure  upon  the  sole  of  the  foot,  the 
patient's  endeavour  to  bring  the  tarsus 
in  a  line  with  the  leg,  thus  testing  the 
gastrocnemius,  soleus,  peroneus  longus 
and  brevis. 

Dorsiflectors  of  the  Foot. — With  the 
leg  straight,  resist  the  patient's  attempt  Fig.  185.— Foot-drop, 

to  bend  up  the  foot,   thus  testing  the 

tibialis  anticus  and  the  peroneus  tertius.     Marked  paralysis  of  these  muscles 
causes  "foot-drop"  (Fig.  185). 

Muscles  of  the  Foot. — The  flexors,  extensors,  iiiterossei,  and  lumbricals  of 
the  toes  are  examined  in  a  similar  manner  to  those  of  the  fingers.  There  is  a 
form  of  claw  foot  analogous  to  the  claw  hand. 

Having  investigated  the  condition  of  the  individual  muscles  and 
muscle  groups  as  Just  described,  and  comparing  the  results  of  the 
examination  with  the  table  on  page  503,  it  may  be  found  that  the 
paralyzed  muscles  correspond  to  the  supply  of  a  single  nerve — e.  g., 
musculo-spiral  or  great  sciatic — or  to  the  segmentary  distribution, 


514  THE  EVIDENCES  OP  DISEASE 

according  to  the  tables  on  pages  492  to  500 ;  or  constitute  a  hemi- 
plegia, paraplegia,  or  monoplegia. 

MOTOR    DISTURBANCES 

An  examination  of  the  motor  functions  (mainly  of  the  muscles) 
may  reveal  an  increase  or  exaggeration  of  normal  motility  (spasm), 
or  a  lessening  and  perhaps  an  entire  absence  of  motor  power 
(paralysis). 

I.  Increased  Motility  (Spasm) 

Spasm  or  an  abnormal  degree  of  muscular  contraction  may  be 
tonic — continuous,  and  lasting  from  minutes  to  months ;  or  clonic — 
contraction  and  relaxation  rapidly  alternating.  The  term  convulsion 
(or  fit)  is  commonly  applied  to  spasm  involving  the  majority  of  the 
skeletal  muscles ;  while  if  the  contractions  concern  a  single  muscle 
or  group  of  muscles  it  is  called  a  local  convulsion,  or  simply  a  spasm. 
If  a  paralyzed  voluntary  muscle  is  continuously  in  a  state  of  abnor- 
mal tension  it  is  said  to  be  spastic. 

General  convulsions  have  been  considered  elsewhere  (page  71). 
The  local  spasms  or  abnormal  muscular  movements  which  possess 
a  varying  diagnostic  importance  and  should  be  sought  after,  are  : 

{a)  Tremor. — This  is  a  more  or  less  continuous  quivering  or 
trembling,  especially  of  the  extremities,  due  to  a  species  of  clonic 
spasm  affecting  a  single  group  or  many  groups  of  muscles.  Tremor 
of  the  eyeballs  is  nystagmus  {q.  v.).  A  muscle  is  physiologically 
maintained  in  a  condition  of  moderate  tension  by  rhythmic  impulses 
passing  down  from  the  motor  cell  bodies  at  the  rate  of  about  12  to 
the  second.  Ordinarily  the  resulting  muscular  contractions  are  im- 
perceptible, but  if  the  strength  of  the  impulses  is  increased  the  mus- 
cular movements  may  be  seen  or  felt  as  a  tremor.  If  the  rhythm 
and,  especially,  the  rate  remain  the  same  it  is  a  fine  tremor,  8  to  12 
per  second.  If  the  disturbance  is  greater,  every  second  impulse  may 
be  lacking  and  coarse  tremor  (4  to  6)  results. 

(1)  To  test  a  patient  for  the  presence  of  tremor,  direct  him  to 
hold  out  his  arms  with  the  fingers  extended  and  separated.  Usually 
both  the  hand  and  the  arm  tremble.  Tremor  which  is  too  slight  to 
be  seen  may  be  felt  by  placing  the  observer's  hand  against  the  tips 
of  the  patient's  fingers.  Tremor  of  the  facial  muscles  may  be  made 
manifest  by  causing  the  patient  to  shut  the  eyes  tightly  or  to  show 
the  upper  teeth ;  of  the  tongue,  by  its  protrusion.  Passive  tremor  is 
present  while  the  affected  muscles  are  at  rest,  but  during  volitional 
motion  it  diminishes  or  may  stop  entirely.  Intention  tremor  begins 
or,  if  present,  increases,  upon  voluntary  movement ;  it  is  best  tested 


INCREASED  MOTILITY,   OR  SPASM  515 

by  handing  the  patient  a  glass  of  water,  desiring  him  to  hold  it  a 
moment  and  then  carry  it  slowly  to  his  mouth,  observing  the  effect 
of  the  performance.  Segmental  tremor  is  that  which  involves  a 
limited  portion  of  an  extremity — e.  g.,  fingers,  or  one  hand  and  its 
fingers.  Whether  a  tremor  is  fine  or  coarse  can  usually  be  estimated 
after  a  little  experience,  but  for  accurate  results  special  laboratory 
instruments  are  required.  Coarse  and  irregular  tremor  may  be  con- 
fused with  moderate  choreiform  movements. 

(2)  The  diagnostic  associations  of  tremor  are  iji  general  as  fol- 
lows :  Intention  tremor  is  often,  but  by  no  means  always,  due  to 
organic  disease  ;  conversely,  passive  tremor  is  commonly  functional. 
Coarse  tremor  is  generally  an  evidence  of  organic  disease  or  paralysis 
agitans,  but  is  also  seen  in  serious  alcoholism  and  hysteria.  Tremor 
of  the  facial  muscles,  lips,  and  tongue  is  indicative  of  marked  neu- 
rasthenia, paresis,  or  alcoholism. 

Following  are  some  of  the  special  conditions  or  diseases  in  which 
tremor  is  a  noticeable  symptom  : 

It  is  normal  in  persons  of  a  nervous  temperament  under  excite- 
ment or  alarm,  and  is  sometimes  marked,  even  in  robust  individuals, 
after  violent  or  long-continued  exercise,  but  in  both  cases  is  tempo- 
rary. It  exists  apparently  as  a  constitutional  peculiarity  in  some 
persons  who  are  otherwise  in  good  condition,  becoming  more  distinct 
if  the  health  is  impaired.  Senile  tremor  (fine)  beginning  in  the 
hands  and  finally  spreading  to  the  neck  muscles  so  that  the  head 
becomes  involved,  is  not  infrequent,  but  rarely  occurs  under  the  age 
of  seventy. 

The  tremor  of  paralysis  agitans  (coarse  or  slow,  6  per  second) 
affects  the  four  extremities,  sometimes  the  head,  most  commonly  the 
hands.  The  thumb  and  forefinger  usually  present  the  movements 
characterized  as  "  bread  crumbling  "  or  "  pill-making."  The  tremor 
ceases  during  sleep  and  temporarily  during  voluntary  movement. 
Exophthalmic  goitre  is  attended  by  a  fine,  rapid  (12  per  second) 
tremor,  often  to  be  felt  but  not  seen.  It  is  an  important  early  diag- 
nostic sign.  Volitional  or  intentional  tremor  (coarse  or  slow)  is  espe- 
cially characteristic  of  disseminated  sclerosis,  most  marked  in  the 
hands  and  arms,  but  occurring  also  in  the  legs  and  head.  When  the 
patient  is  absolutely  quiet  the  tremor  may  disappear.  The  tremor  of 
hysteria  (rapid  or  fine,  8  to  12  per  second)  usually  affects  the  hands 
and  arms,  less  frequently  the  head  and  hands.  The  tremor  may  be 
volitional,  resembling  that  of  disseminated  sclerosis. 

Tremor  is  often  significant  of  the  overuse  of  tea,  coffee,  alcohol, 
and  tobacco,  as  well  as  poisoning  by  lead,  mercury  and,  less  fre- 
quently, arsenic  and  opium.     Alcoholic  tremor  affects  especially  the 


616 


THE  EVIDENCES  OP  DISEASE 


tongue  and  extremities.  It  may  be  fine  or  coarse,  and  often  mani- 
fests itself  only  upon  movement.  Tremor  is  an  important  symptom 
in  plumbism  and  mercurialism.  It  is  seen  also  in  opium  or  morphine 
eaters,  if  the  customary  supply  of  the  drug  be  stopped.  Cases  of 
hereditary  tremor  beginning  in  infancy  have  been  reported. 

(b)  Fibrillary  Tremor. — This  is  a  more  or  less  rhythmic  twitching 
or  tremor  confined  to  certain  fibres,  bundles  or  parts  of  a  muscle. 
Most  commonly  it  is  seen  in  the  tongue,  the  facial  muscles,  and  the 
muscles  of  the  extremities.  It  indicates  great  exhaustion  of  a  mus- 
cle or  wasting  of  the  muscle  from  lack  of  neurotrophic  influence,  as 
in  progressive  muscular  atrophy. 

(c)  Athetosis  or  Athetoid  Movements. — These  consist  of  continu- 
ous, deliberate,  somewhat  forcible  twisting  movements,  usually  of  the 

fingers  and  hands  (Fig. 
186),  less  frequently  of 
the  toes  and  feet,  and 
are  sometimes  painful. 
The  fingers  and  toes 
flex  and  extend,  the 
hands  are  pronated  and 
supinated.  While  the 
patient  is  awake  the 
movements  may  cease, 
but  only  for  a  short 
time.  They  are  much 
slower  than  those  of 
chorea. 

Athetosis  may  con- 
stitute a  separate  dis- 
ease, or  may  occur  in 
the  paralyzed  limbs  as 

Fig.  186.— Athetoid  movements.    Redrawn  from  Strumpell.    a  not  infrequent  result 

of  cerebral  paralysis  in 
children;  more  rarely  it  may  be  found  in  adults,  involving  the 
affected  side  (hemiathetosis)  in  hemiplegia  due  to  a  lesion  of  the 
thalamus  or  the  posterior  portion  of  the  internal  capsule. 

(d)  Localized  Convulsive  Seizures. — A  sign  which  may  be  of  great 
importance  is  the  so-called  Jacksonian  or  localized  epilepsy,  a  clonic 
convulsion  beginning  in  a  single  muscle  or  group  of  muscles — e.  g., 
the  face,  fingers,  or  toes — preceded  by  pain  or  tingling  in  the  part, 
extending  so  as  to  involve  the  entire  extremity  and  sometimes  more 
than  one.  The  convulsive  movements  are  usually  confined  to  one 
side.     The  patient  retains  consciousness  except  in  the  comparatively 


INCREASED  MOTILITY,   OR  SPASM  517 

infrequent  cases  in  which  general  convulsions  follow.  A  typical 
attack  of  this  kind  is  very  significant  of  a  localized  source  of  irrita- 
tion in  the  sensori-motor  zone  of  the  cerebrum.  The  causative 
lesion  may  be  brain  tumour,  softening,  localized  meningitis,  hemor- 
rhage, abscess,  and  injury.  It  may  follow  hemiplegia  in  children. 
That  localized  epilepsy  does  not  necessarily  imply  a  limited  lesion  is 
shown  by  the  fact  that  it  may  occur  typically  in  general  paresis  and 
uraemia. 

Here  also  may  be  mentioned  the  irregular  and  usually  moderate 
twitchings  of  various  muscles,  most  commonly  those  of  the  face, 
arms,  and  hands,  less  frequently  of  the  feet,  which  may  be  witnessed 
in  high  fever,  especially  in  the  gastro-intestinal  diseases  of  children  ; 
the  typhoid  status  {suhsultus  tetidinum),  uraemia,  meningitis,  jaun- 
dice, delirium  tremens ;  and  as  a  result  of  full  medicinal  doses  of 
strychnine,  particularly  in  neurotic  patients.  Picking  at  the  bed- 
clothes or  attempting  to  seize  invisible  objects  in  the  air  {carphologid) 
is  seen  in  the  typhoid  status  and  is  a  sign  of  serious  weakness,  per- 
haps of  impending  death. 

{e)  Choreic  Movements. — These  are  abrupt  twitchings  or  jerking 
movements  of  different  muscle  groups,  involuntary  and  without  an 
object.  Affecting  one  lateral  half  of  the  body  it  is  called  hemi- 
chorea.  A  child  suffering  from  chorea  appears  restless,  unsettled, 
and  fidgety.  If  the  choreic  movements  are  slight,  it  may  be  neces- 
sary, in  order  for  their  detection,  to  have  the  patient  lay  his  hands, 
palms  down,  upon  the  hands  of  the  examiner,  when,  after  a  short  wait, 
small  twitching  movements  of  the  fingers  may  be  perceived.  The 
handwriting  is  apt  to  be  impaired.  Ordinarily  choreic  movements 
cease  during  sleep,  are  often  diminished  by  voluntary  movement, 
and  always  increased  by  mental  excitement  or  bodily  fatigue.  Tics 
are  choreic  movements  of  certain  gi*oups  of  muscles  physiologically 
associated  for  the  performance  of  a  definite  function,  affecting  most 
commonly  the  muscles  of  expression,  less  frequently  those  of  speech, 
respiration,  and  locomotion. 

The  most  ordinary  cause  of  choreic  movements  is  the  acute  chorea 
of  children  (Sydenham's  C,  St.  Vitus's  Dance).  Other  affections 
which  present  choreic  movements  as  a  symptom  are  habit  spasm ; 
tic  convulsif  (Gilles  de  la  Tourette's  disease)  ;  chronic  (Hunting- 
ton's) chorea ;  saltatory  spasm  (Latah,  Jumpers)  ;  post-hemiplegic 
chorea  (hemichorea),  occurring  under  the  same  conditions  as  hemi- 
athetosis  {q.  v.) ;  rhythmic  chorea  (really  hysteria),  more  or  less 
regular  spasms  of  certain  muscle  groups,  e.  g.,  nodding  spasm  when 
the  neck  muscles  are  affected,  salaam  convulsions  when  the  ab- 
dominal muscles  are  involved ;  and  the  seldom  seen  electric  chorea 
35 


518 


THE  EVIDENCES  OF  DISEASE 


(Dubini).  Here  also  may  be  mentioned  a  peculiar  affection,  para- 
myoclonus multiplex,  characterized  by  either  constant  or  paroxysmal 
clonic  contractions,  sometimes  very  violent,  mainly  of  the  muscles 
of  the  extremities. 

(/)  Cramp. — If  a  localized  spasm  is  painful,  it  is  called  cramp. 
It  most  commonly  afEects  the  calf  muscles,  and  may  be  due  to  mus- 
cular exertion,  alcoholism,  nephritis,  gout,  diabetes  or  hysteria. 

{g)  Forced  Positions  or  Movements. — A  person  may  be  more  or 
less  suddenly  thrown  forward,  backward,  or  sideways,  or  forced  to 
move  in  a  circle,  by  involuntary  muscular  action  ;  or  by  a  tonic  con- 
traction, which  draws  the  head  and  trunk  to  one  side,  is  compelled 
to  lie  in  a  lateral  position.  Such  imperative  movements  or  positions 
are  significant  of  a  lesion  of  the  vermis  (or  middle  lobe)  of  the  cere- 
bellum. With  imperative  or  forced  movements  may  also  be  classed 
the  screaming,  laughing,  or  jumping  spasms  of  hysteria  and  epilepsy. 
{li)  Associated  Movements. — In  certain  cases  when  an  extremity 
is  paralyzed — e.  g.,  hemiplegia — movement  of  the  corresponding  un- 
affected limb  of  the  opposite  side  may  produce  similar  but  less  exten- 
sive movements  of  the  paralyzed  extremity. 

{i)  Myoidema. — A  smart  blow,  delivered  by  finger  or  hammer 
upon  a  muscle  near  its  tendinous  attachment,  may  under  certain 
circumstances  cause  a  sudden  localized  contraction  of  the  muscular 
fibres  (myoidema) ;  or,  if  the  belly  of  the  muscle  is  struck,  a  similar 
belt  of  contraction  may  appear  (idiopathic  muscular  sjjasm),  in 
either  case  lasting  only  a  few  seconds.  These  phenomena  are  evi- 
dences of  the  exaggerated  irritability  of  muscles  which  are  under- 
going rapid  wasting,  especially  in  phthisis. 

(/)  Tetany. — The  disease  known  by  this  name  {q.  v.)  is  a  par- 
oxysmal tonic  spasm  usually  confined  to  the  flexors  of  the  hands  and 

feet,  but  sometimes 
involving  the  mus- 
cles of  mastication 
(trismus).  Carpo- 
pedal  spasms  in 
rickety  children 
are  by  many  writers 
classed  as  a  mild 
tetany.  When  af- 
fecting the  upper 
extremities  the  fingers  assume  a  characteristic  position,  "  the  accou- 
cheur's hand  "  (Fig.  187).     In  the  foot  the  toes  are  strongly  flexed. 

A  form  of  tonic  cramp  of  the  muscles,  which  is  not  tetany,  char- 
acterizes Thomsen's  disease  (myotonia).    The  cramp  occurs  only  upon 


Fi(i.  187.— Hand  of  tetany. 


INCREASED  MOTILITY,   OR  SPASM 


519 


voluntary  movement,  the  muscles   stiffening  and  responding  very 
slowly  to  the  behest  of  the  will.     A  similar  localized  condition  may 
be  seen  in  writer's  cramp,  the  muscles 
becoming  rigid  when  called  upon  to  act.- 

{k)  Catalepsy.  —  This  is  a  peculiar 
form  of  muscular  rigidity  or  increased 
muscular  tonus  affecting  the  voluntary 
muscles.  An  affected  limb  may  be 
moved  with  but  slight  resistance,  and 
will  maintain,  in  opposition  to  gravity, 
for  an  hour  or  even  longer  the  position 
in  which  it  has  been  placed,  the  so- 
called  "  waxy  flexibility  "  {cerea  flexi- 
bilitas).  It  is  a  condition  which  is 
most  frequently  seen  as  a  symptom  of 
hysteria,  hypnosis,  or  that  form  of  psy- 
chosis known  as  melancholia  attonita. 
Earely  it  may  occur  in  connection  with 
brain  tumour  and  meningitis. 

(0  Contractures.  —  A  contracture 
(Fig.  188)  is  a  tonic  muscular  spasm  of 
long  standing.  The  spasm  may  be  so 
slight  that  the  resistance  of  the  affected 
part  to  passive  motion  is  hardly  per- 
ceptible, or  so  strong  that  movement 
becomes  impossible.  If  the  contrac- 
tured  extremity — finger,  arm,  foot,  or 
leg — be  suddenly  extended  by  the  ex- 
aminer, a  curious  "  check"  may  be  felt.  Fig.  ISS.— Deformity  of  left  hand,  the 
In  contractures  of  considerable  duration       '""^^"•f  ^^  coutractures  follow  ing  an 

.      .         n    Ti     Ti         t  attack  of  hemiplegia  lour  years 

there   is   m   all   likelihood  an   actual   or         before;    child    seven    years    old 

anatomical  shortening  of  the  affected       (Holt), 
muscles. 

Contractures  are  most  commonly  seen  either  as  a  symptom  of 
hysteria  or,  affecting  the  palsied  muscles,  as  a  result  of  cerebral 
paralysis,  hemiplegia  {q.  v.)  in  particular.  If  functional,  the  'con- 
tracture disappears  during  sleep  or  anaesthesia;  if  of  organic  origin, 
it  will  persist.  Contractures  affecting  the  arms  may  be  seen  in 
chronic  hydrocephalus.  The  contracture  may  affect  the  paralyzed 
muscles  or  healthy  muscles  whose  antagonists  have  lost  their  con- 
tractility, or  may  be  present  in  the  strongest  muscles  of  a  paralyzed 
group.  Contractures  and  spastic  rigidity  of  the  muscles  are  further 
considered  in  connection  with  the  various  forms  of  paralysis  {q.  v.). 


520  THE   EVIDENCES  OF  DISEASE 

II.    Decreased  Motility  (Paralysis) 

A  partial  or  total  loss  of  voluntary  motor  power  is  called  2mraly- 
sis.  A  partial  loss  is  often  termed  paresis  (not  to  be  confused  with 
general  paresis  of  the  insane).  Amyosthenia  is  a  sudden,  usually 
temporary,  weakness  of  an  arm  or  of  both  legs,  and  is  a  symptom  of 
hysteria.  Hemiplegia  is  a  paralysis  of  one  lateral  half  of  the  body. 
Alternating  or  crossed  hemiplegia  signifies  paralysis  of  the  extremities 
of  one  side  and  the  facial,  ocular,  or  other  muscles  of  the  opposite 
side.  Diplegia  is  a  double  hemiplegia.  QuadrupUgia  is  a  paralysis 
of  all  four  extremities.  Paraplegia  used  without  qualification  means 
paralysis  of  both  lower  extremities.  Some  writers  speak  of  paralysis 
of  both  legs  as  paraplegia  inferior ;  of  both  arms  as  paraplegia  supe- 
rior. Monoplegia  is  a  paralysis  of  one  extremity—  e.  g.,  brachial  = 
of  the  arm,  crural  =  of  the  leg,  facial  =  of  the  face.  It  may  be  sin- 
gle or  double — e.  g.,  of  both  arms  =  double  brachial  monojjlegia  = 
also  paraplegia  superior. 

In  the  examination  of  a  case  of  paralysis  the  following  points 
must  be  determined :  (1)  The  limb  or  limbs,  the  muscle  or  muscle 
groups  involved — the  extent  of  the  paralysis.  (2)  Is  the  paralyzed 
limb  or  muscle  group  spastic  or  is  it  flaccid  ? — an  extremely  impor- 
tant point.  If  the  limb  resists  attempts  at  passive  motion  because 
of  existing  contraction  of  the  muscles,  or  if  the  muscles  contract  in 
opposition  to  the  attempted  movement,  the  paralysis  is  spastic.  If, 
on  the  other  hand,  the  member  is  limp,  the  muscles  are  lax,  and 
there  is  no  resistance  to  passive  motion,  the  paralysis  is  flaccid. 
(3)  Are  the  muscles  atrophied?  (4)  What  is  the  condition  of  the 
reflexes  {q.  v.)  ?  (5)  How  do  the  paralyzed  muscles  react  to  elec- 
tricity {([.  V.)  ?     (6)  Are  there  sensory  disturbances  [q.  r.)  ? 

{a)  Paralysis  according  to  its  Type. — Having  obtained  the  re- 
quired data  according  to  the  foregoing  scheme  in  a  satisfactory  man- 
ner, it  is  usually  possible  to  assign  all  cases  of  paralysis  to  one  of  two 
types^  viz.,  cerebral  or  spinal.  Such  an  assignment  does  not  in  all 
cases  imply  of  necessity  a  cerebral  or  spinal  lesion,  for  the  paralysis 
may  be  due  to  inflammation  of  the  peripheral  nerves  (neuritis),  or  to 
primary  disease  of  the  muscles  and  the  terminal  motor  filaments  em- 
bedded in  them  (intramuscular  paralysis  or  muscular  dystropliy),  or 
it  may  be  functional  (hysteria).  Nevertheless,  a  determination  of  the 
type  of  the  paralysis  is  a  clinical  prerequisite  to  a  more  particular 
diagnosis  of  the  exact  condition  upon  which  it  depends — a  diagnosis 
which  is  to  be  made  by  a  consideration  of  the  associated  symptoms. 

(1)  Upper  Neurone  {Central^  Cerebral.,  or  Spastic)  Paralysis. — The 
clinical  features  of  cerebral  paralysis  are  :  Hemiplegia^  partial  or  total, 


DECREASED  MOTILITY,   OR  PARALYSIS  521 

the  most  characteristic  distribution  of  this  type  of  paralysis.  The 
paralyzed  muscles  are  spastic,  and  contractures  may  develop.  The 
reflexes  are  exaggerated.  The  reaction  of  the  muscles  to  electric 
stimulation  is  normal.  Atrophy  of  the  muscles,  if  it  occurs,  is  slight, 
and  in  the  large  majority  of  cases  is  due  simply  to  their  disuse. 

The  cerebral  type  of  paralysis  is  due  to  lesions  affecting  the  cen- 
tral (upper)  motor  neurones.  The  destructive  lesion  may  involve  the 
cell  bodies  proper,  or  the  axones  in  any  part  of  their  length,  includ- 
ing the  terminal  end  brushes,  and  is  followed  by  a  secondary  degen- 
eration of  the  axis  cylinders  below  the  diseased  point  (descending 
degeneration).  It  should  be  clearly  understood  that  disease  affecting 
any  part  of  the  upper  motor  path  gives  rise  to  the  cerebral  or  spastic 
type  of  paralysis  (Figs.  191  and  197).  Thus  in  sclerosis  affecting  the 
lateral  pyramidal  columns  (Figs.  168  and  169),  although  the  disease  is 
in  the  cord  the  type  of  the  paralysis  is  cerebral,  because  the  pyram- 
idal column  is  composed  of  the  axis  cylinders  of  the  central  (cere- 
bral) neurones.  If  the  disease  extends  outside  of  these  columns,  the 
symptoms  of  the  peripheral  type  may  be  superadded,  one  usually 
predominating  according  to  the  course  of  the  malady. 

Cerebral  paralysis  is  spastic  and  attended  with  contractures,  be- 
cause the  peripheral  or  lower  neurones  are  deprived  of  the  controlling 
and  inhibiting  influence  of  the  central  neurones  (Fig.  161),  and  for 
the  same  reason  the  reflexes  are  exaggerated.  As  the  muscles  still 
receive  the  trophic  and  other  influences  of  the  peripheral  neurones, 
they  do  not  undergo  atrophy  and  degeneration;  consequently  the 
electrical  reaction  is  normal. 

As  the  most  common  causes  oi  cerebral  paralysis  are  unilateral, 
the  distribution  of  the  paralysis  is  usually  that  of  a  hemiplegia. 
The  paralysis  is  on  the  opposite  side  of  the  body  from  the  lesion, 
because  of  the  decussation  of  the  motor  (pyramidal)  fibres  in  the 
medulla. 

(2)  Loicer  Neurone  {Peripheral,  Spinal,  Flaccid,  or  Atrophic) 
Paralysis. — The  clinical  symptoms  of  peripheral  paralysis  are  :  Para- 
plegia, the  most  characteristic  variety  of  this  form  of  paralysis..  The 
paralyzed  muscles  are  flaccid,  having  lost  their  tone.  The  reflexes  are 
dinmiished  or  lost,  and  there  is  an  entire  or  partial  loss  of  response  to 
the  faradic  current,  with  a  partial  or  complete  reaction  of  degenera- 
tion to  the  galvanic  current.  Marked  atrophy  and  wasting  of  the 
paralyzed  muscles. 

Paralysis  of  the  peripheral  (spinal)  type  (Figs.  191  and  197)  may 
be  due  to  a  lesion  of  any  part,  cell  bodies  or  axones,  of  the  peripheral 
(lower)  motor  neurones,  including  those  of  the  cranial  motor  nuclei 
in  the  pons  and  medulla  (Figs.  189  and  190)  as  well  as  the  motor 


522 


THE  EVIDENCES  OF   DISEASE 


VNcrve. 


emeduli. 


cells  of  the  anterior  horns  of  the  spinal  cord.  Consequently  this 
type  is  seen  if  the  cell  bodies  are  involved,  as  in  anterior  poliomye- 
litis (Fig.  169)  or  polioencephalitis ;  or  if  the  peripheral  nerves  are 
diseased  as  in  neuritis.  If  the  disease  begins  primarily  in  the  mus- 
cles, involving  also  to  some  ex- 
tent the  nerve  endings  which 
they  contain,  as  in  the  muscular 
dystrophies,  the  paralysis  is  of 
the  spinal  type,  except  that  the 
reaction  of  degeneration  is  rarely 
observed,  and  an  apparent  en- 
largement (pseudo-hypertrophy) 
may  be  present  in  the  early  stages 
of  the  malady ;  the  muscles  in 
reality  being  atrophied. 

The  explanation  of  the  clin- 
ical symptoms  of  the  peripheral 
type  of  paralysis  lies  in  the  fact 
that  the  peripheral  motor  neu- 
rones and  the  muscles  which 
they  innervate  constitute  neuro- 
muscular trophic  units.  The  cell 
body  of  the  lower  motor  neurone 
not  only  maintains  the  tone  or 
tension  of  the  muscle,  but  also 
exercises  a  trophic  or  nutritive 
action  upon  the  latter.  If,  there- 
fore, the  integrity  of  the  cell 
body  or  its  axis  cylinder  is  im- 
paired by  injury  or  disease  the 
tonic  impulses  received  by  the 
muscle  cease  and  it  loses  its  tone 
— i.  e.,  becomes  flaccid — and  the 
reflexes  are  abolished.  Further- 
more, as  it  is  deprived  of  the 
necessary  trophic  influence,  atro- 
phy takes  place  and  it  presents 
the  reaction  of  degeneration. 
(3)  Summary  of  the  Diagnostic  Significance  of  the  Type  of  Paral- 
ysis.— The  cerebral  type  indicates :  A  lesion  of  the  motor  cortex  and 
pyramidal  tracts,  usually  unilateral  (hemiplegia),  sometimes  bilateral 
or  symmetrical  (diplegia,  especially  in  children) ;  or  an  aifection  of 
the  crossed  pyramidal  column  of  the  cord  (Figs.  166  and  167),  the 


Fig.  lS9.^Diiigranis  showing  the  relative 
positions  of  the  cranial  nerve  nuclei, 
posterior  aspect.     Redrawn  from  Merkel. 


DECREASED  MOTILITY,   OR  PARALYSIS 


523 


latter  being  to  all  intents  and  purposes  a  continuation  of  the  cere- 
bral motor  tract. 

The  spinal  type  indicates  :  Lesions  of  the  motor  cell  bodies  of  the 
medulla  and  pons  nuclei  (e.  g.,  bulbar  paralysis  and  ophthalmoplegias, 
classed  as  polioencephalitis).  Lesions  of  the  motor  cells  in  the  ante- 
rior horns  (e.  g.,  poliomyelitis,  acute  and  chronic).  Neuritis  of  the 
peripheral  nerves,  with,  in  the  acute  forms  at  least,  disturbances  of 
sensation  which  are  lacking  in  poliomyelitis  (an  important  differential 
symptom).  Muscular  dystrophies,  which,  as  the  paralysis  originates 
in  the  muscle  itself,  do  not  present  the  reaction  of  degeneration,  and 
there  is  apparent  hyper- 
trophy but  real  atrophy, 
wherein  they  differ  from 
poliomyelitis  and  neu- 
ritis. 

A  mixture  of  these 
types  may  be  found  in 
amyotrophic  lateral  scle- 
rosis where  there  is  rapid 
muscular  atrophy  with 
spasticity  and  exagger- 
ated reflexes,  the  disease 
involving  simultaneous- 
ly the  lower  ends  of  the 
upper  and  the  cell  bodies 
of  the  lower  neurones ; 
and  transverse  myelitis, 
in  which  the  muscles  in- 
nervated from  the  site 
of  the  lesion  exhibit  the 
spinal  type  (Fig.  191), 
while  below  the  level  of  the  lesion  the  spastic  variety  of  paralysis  is 
found. 

The  functional  paralyses  (hysteria,  strong  emotion)  are  usually 
flaccid,  but  do  not  exhibit  atrophy  or  the  reaction  of  degeneration, 
and  the  deep  reflexes  are  variable,  usually  preserved  or  exaggerated. 
The  presence  of  contractures  and  anaesthesias  and  the  peculiar 
psychic  condition  of  the  patient  are  serviceable  in  making  the  diag- 
nosis. Hysteria  is  capable  of  simulating  very  closely  nearly  every 
type  of  organic  disease. 

{b)  The  Distribution  of  the  Paralysis  with  reference  to  Topical 
Diagnosis  and  Particular  Forms  of  Disease. — As  a  rule,  if  the  paraly- 
sis is  unilateral  it  is  due  to  a  cerebral  lesion ;  if  bilateral,  to  disease 


Fio.  190.- 


-Diagram  showing  the  relative  positions  of  the 
cranial  nerve  nuclei,  lateral  aspect. 


524  THE  EVIDEXCES  OF  DISEASE 

of  the  spinal  cord,  except  in  the  diplegias  (double  hemiplegias)  of 
children. 

(1)  Hemiplegia. — Complete  paralysis  of  one  lateral  half  of  the 
body  (face,  arm,  and  leg),  unless  functional,  is  always  due  to  a  cere- 
bral lesion.  There  are  certain  varieties  of  this  form  of  paralysis 
which  serve  to  localize  the  causative  lesion. 

Complete  hemiplegia  (see  B,  Fig.  191)  is  caused  by  a  lesion  of  the 
knee  and  anterior  two  thirds  of  the  posterior  limb  of  the  internal 
capsule,  the  motor  fibres  from  the  sensori-motor  area  being  at  this 
point  gathered  into  a  narrow  band.  Consequently  a  comparatively 
small  lesion  will  involve  the  pyramidal  tract  fibres  which  have  a  very 
extensive  distribution  (face,  arm,  leg). 

Eight  hemiplegia  plus  aphasia  (page  246)  in  a  right-handed  indi- 
vidual indicates  that  the  lesion  further  involves  the  left  third  frontal 
convolution  (see  also  Figs.  42  and  43,  page  249). 

Hemiplegia  plus  hemianaesthesia  of  the  same  side  indicates  that 
the  lesion  has  encroached  upon  the  posterior  one  third  (sensory)  of 
the  posterior  limb  of  the  internal  capsule  (6',  Fig.  191). 

Hemiplegia  with  paralysis  of  the  third  nerve  on  the  opposite  side 
{H,  with  crossed  or  alternating  oculo-motor  paralysis)  indicates  a 
lesion  of  the  crus  (C,  Fig.  191)  involving  the  third  nerve  as  it  passes 
through  the  crus  to  emerge  at  the  inner  border  of  the  latter  (Fig.  27). 

Hemiplegia  with  crossed  (opposite)  facial  paralysis  signifies  a 
lesion  in  the  pons  involving  the  nucleus  of  the  seventh  or  facial 
nerve  (Z>,  Fig.  191).  The  facial  paralysis  in  this  case  is  of  the  flac- 
cid or  lower  neurone  type.  Hemiplegia  with  double  facial  paralysis 
is  extremely  rare,  and  is  caused  by  a  pons  lesion  involving  both  right 
and  left  facial  fibres  at  their  point  of  decussation.  Hemiplegia  with 
anarthria  (difficult  or  imperfect  articulation,  not  aphasia)  and  diffi- 
culty in  swallowing  is  due  to  a  lesion  of  the  bulb  (medulla).  Double 
hemiplegia  (diplegia),  is  due  to  bilateral  or  symmetrical  cerebral 
lesions,  and  is  of  notable  occurrence  in  children. 

In  the  majority  of  cases  hemiplegia  is  due  to  cerebral  hemor- 
rhage, embolism,  or  thrombosis,  associated  with  arteriosclerosis,  and 
followed  by  softening.  Syphilis  may  be  a  factor  in  the  vascular 
changes.  It  may  be  due  to  brain  tumour,  multiple  sclerosis  or 
sclerosis  of  one  hemisphere,  meningeal  hemorrhage  or  suppuration, 
inflammation,  Raynaud's  disease,  and  general  paresis  of  the  insane. 
It  may  be  functional  from  hysteria,  and  transient  from  uraemia.  It 
is  a  very  infrequent  event  in  the  last  stages  of  carcinoma  and  pul- 
monary tuberculosis,  and  2  cases  have  been  reported  (Jaxeway)  as  a 
result  of  the  injection  of  hydrogen  peroxide  into  the  pleural  cavity 
(oxygen  embolism).     An  acute  and  sudden  hemiplegia  is  usually  the 


LESION  CAUSING 
MONOPLEGIA  OF  LEG 


ORDINARY  HEMIPLEGIA. 
PARALYSIS  OF  SIDE 
OPPOSITE  TO  LESION. 


HEMIPLEGIA  OF  OPPO- 
SITE SIDE,  OCULO- 
MOTOR PARALYSIS  OF 
SAME  SIDE. 


HEMIPLEGIA  OF  OPPO- 
SITE SIDE,  PARALYSIS 
OF    FACE  AND    EXTER- 
NAL RECTUS  ON  SAME 

SIDE.  


UPt^ER   MOTOR   '=ATH=PED. 
LESIONS    OF    THIS    PATH 
CAUSE  SPASTIC  PARALYSIS. 


LC  '       '    "  ■■  - 

LESIONS    OF    THIS    PATH 
CAUSE  FLACCID  PARALYSIS. 


ORDINARY 
HEMIPLEGIA 


HEMIPLEGIA,  ARM 
MORE  THAN  LEG. 


HEMIPLEGIA 
WITH  HEMIATHE 
TOSIS  AND  HEMl- 
CHOREA. 


HEMIPLEGIA,  LEG 
MORE  THAN  ARM, 
WITH  HEMIANAES- 
THESIA,  HEMIOPIA, 
AND    DISTURBAN- 
ES  OF  HEARING, 
TASTE  ?  AND 
SMELL P 


ERIOR 
EXTREMITY 

OF  CAPSULE. 


SECTION  o^f"-  INTERNAL  CAPSULE 


III  N.  OCULOMOTOR. 

IV  N.  PATHETICUS. 
•V  N.  TRIGEMINUS. 


-  VI  N.  ABDUCENS. 

—  VII  N.  FACIAL. 


IX  N.  GLOSSOPHARYNGEAL. 
.  X  N.  PNEUMOGASTRIC. 
XI  N.  SPINAL  ACCESSORY. 


XII  N.  HYPOGLOSSAL. 


LESION   INVOLVING 
ANTERIOR  HORN  OR 
ROOT.  FLACCID  PAR 
ALYSIS  OF  MUSCLES 
AT  SITE  OF  LESION 


TRANSVERSE  LESION 
OF  CORD.  FLACCID 
PARALYSIS  OF  MUSC- 
LES LOCALIZED  AT 
LEVEL  OF  LESION. 
SPASTIC  PARALYSIS 
OF  MUSCLES  BELOW 
LESION.  


Fig.  191. — Showing  the  eftects  of  various  lesions  of  the  motor  path  in  the  brain  and  spinal 
cord.  The  upper  right-hand  sketch  shows  tlie  variations  in  symptoms  caused  by  a 
difference  in  the  antero-posterior  position  of  the  lesions  in  the  internal  capsule. 

525 


526  THE  EVIDENCES  OP   DISEASE 

result  of  hemorrhage,  embolism,  or  thrombosis ;  if  gradual  and  pro- 
gressive, of  unilateral  brain  tumour  or  an  island  of  sclerosis,  the  lat- 
ter, perhaps,  only  a  part  of  the  multiple  form. 

(2)  Paraplegia. — Paraplegia,  used  here  as  indicating  paralysis  of 
"both  legs,  may  be  due  to  spinal-cord  lesions  or  to  bilateral  disease 
{neuritis)  of  the  peripheral  nerves.  The  following  points  are  of 
service  in  the  discrimination. 

Spastic  paraplegias  are  almost  invariably  due  to  spinal-cord  lesions. 
Flaccid  paraplegias  may  be  due  to  spinal  disease  or  peripheral  neuritis. 
If  the  sphincters  of  the  bladder  and  rectum  are  involved,  the  lesion 
is  in  the  cord,  and  not  confined  to  the  peripheral  nerves. 

The  diseases  which  are  especially  characterized  by  spastic  para- 
plegia are  lateral  sclerosis,  spinal  meningitis,  pressure  from  Pott's 
disease  of  the  vertebrse,  hereditary  ataxic  paraplegia,  multiple  cere- 
"bro-spinal  sclerosis,  chronic  myelitis,  transverse  myelitis  (below  level 
of  lesion),  syphilis  of  the  cord,  combined  scleroses  (Putnam),  and  the 
spastic  cerebral  paralysis  of  children  when  the  legs  only  are  involved. 

Other  diseases  which  are  responsible  for  paraplegia,  for  the  most 
part  of  the  flaccid  type,  are  Landry's  paralysis,  Friedreich's  ataxia, 
hemorrhage  into  the  cord  or  the  spinal  meninges,  acute  polio- 
myelitis, tumour  or  tuberculosis  of  the  cord,  neuritis,  hysteria  and 
diphtheria.  Scurvy  and  rickets  may  give  rise  to  an  apparent  or 
pseudo-paraplegia.  There  is  a  senile  paraplegia  due  to  thrombosis 
or  embolism  of  the  spinal  arteries.  The  most  common  causes  of 
paraplegia  are,  perhaps,  alcoholic  neuritis  and  acute  poliomyelitis. 

The  differential  diagnosis  of  these  various  maladies  must  of  course 
be  made,  in  each  instance,  from  the  associated  symptoms. 

(3)  Monoplegia. — Brachial. — Paralysis  of  one  arm  is  rarely  due  to 
a  spinal  lesion.  Almost  always  it  is  caused  either  by  a  cerebral  lesion 
or  by  neuritis  of  the  nerves  supplying  the  arm. 

If  due  to  cerebral  disease  (hemorrhage,  embolism,  tumour,  etc.), 
the  paralysis  ia  of  the  spastic,  non-atrophic  type.  The  lesion  is 
almost  inevitably  cortical  or  lies  a  short  distance  below  the  cortex. 
A  lesion  in  the  internal  capsule  would  need  to  be  narrowly  limited, 
on  account  of  the  crowding  together  of  the  motor  fibres  at  this  point, 
to  cause  paralysis  of  the  arm  without  involving  the  face  and  leg  fibres 
as  well.     Like  other  paralyses,  it  may  be  due  to  hysteria. 

If  due  to  neuritis  involving  the  nerves  of  the  arm,  the  paralysis  is 
of  the  spinal  (lower  neurone)  type.  Neuritis  (of  various  origin)  may 
and  usually  does  affect  special  nerves  (e.  g.,  musculo-spiral,  median). 
Consequently  certain  groups  of  muscles  which  are  innervated  by  the 
inflamed  nerve  will  be  paralyzed,  other  groups  supplied  by  the  unin- 
volved  nerves  escaping — partial  brachial  monoplegia. 


SENSORY   DISTURBANCES 


527 


Bilateral  brachial  monoplegia  is  usually  due  to  the  neuritis  of 
lead  poisoning ;  possibly  to  crutch  pressure. 

Crural  Monoplegia. — Paralysis  of  one  leg  alone  is  rarely  caused 
by  a  cerebral  lesion.  If  its  cerebral  origin  can  be  established  (by 
concomitant  symptoms),  the  lesion  will  be  found  in  or  beneath  the 
cortex  in  the  paracentral  lobule  and  at  the  upper  end  of  the  fissure 
of  Rolando  (Fig.  42,  and  A,  Fig.  191). 

More  commonly  it  is  due  to  disease  of  the  cord,  or  neuritis  involv- 
ing the  nerves  of  the  leg.  The  spinal  causes  are  unilateral  myelitis 
or  anterior  poliomyelitis.  The  latter  in  particular  is  responsible  for 
loss  of  power  in  special  muscle  groups  or  individual  muscles.  Neu- 
ritis from  disease  or  traumatism  (blows,  pressure)  may  also  be  the 
source  of  a  limited  paralysis  of  the  leg  muscles.  A  pelvic  tumour 
by  pressure  on  the  crural  nerve  may  give  rise  to  paralysis ;  and  in 
locomotor  ataxia  the  function  of  certain  nerves  may  be  abolished.  A 
false  or  apparent  monoplegia,  usually  not  a  source  of  error,  may  arise 
from  painful  affections  of  the  limb — e.  g.,  rheumatism  or  phlebitis — 
by  interfering  with  its  normal  mobility. 

Facial  Monoplegia. — Upper  neurone  (cerebral)  paralysis  of  one 
side  of  the  face  (and  tongue)  is  due  to  a  lesion  of  the  lower  part  of 
the  anterior  central  convolution  (Fig.  42).  The  causes  of  facial 
paralysis  have  been  previously  discussed  in  detail  (page  169). 


SENSORY    DISTURBANCES 

Disturbances  of  certain  of  the  special  senses  (q.  v.)  have  already 
been  described — viz..  Sight,  Hearing,  Smell,  and  Taste — leaving  for 
consideration  the  cutaneous,  muscular,  articular  and  tendinous  sen- 
sibilities. For  the  sake  of  clearness  they  are  here  tabulated.  The 
table  is  based  upon  Dana's  classification. 

I  Contact'  [  ^'^^'"'''^  ^'''''^ 

i  ??!        \  (Special  Sense) 
i  Cold         ) 

Pain  Sense ( General  Sense) 


Tactile  Sense 


Temperature  Sense. 


Cutaneous  sensa- 
tions. 


Muscular  Sense  . . 

Articular  Sense . . 
Tendinous  Sense. 


chiefly  of  {Special  Sense) 

weight 

of  posture  {Special  Sense) 

of  posture  {Special  Sense) 


Largely  cutane- 
ous, also  muscu- 
lar. 
^  The  power  of 
CO  -  ordinating 
muscular  move- 
ments depends 
mainly  upon 
these  three  spe- 
cial senses. 


528  THE  EVIDENCES  OF   DISEASE 

A  general  or  common  sensation  appears  in  consciousness  to  have 
its  seat  in  the  body — e.  g.,  pain  ;  a  special  sensation  is  referred  men- 
tally to  some  external  agency — e.  g.,  the  pressure  of  a  weight. 

Methods  of  Examining  for  Sensory  Disturbances. — 
The  sensory  functions  are  examined  in  order  to  determine  whether 
they  are  abnormally  active,  absent  or  perverted.  In  testing  the 
cutaneous  and  pain  senses,  the  patient's  eyes  should  be  kept  strictly 
closed  or  blindfolded,  and  he  should  be  instructed  to  respond 
promptly  at  the  instant  he  perceives  the  sensation  required,  using 
always  the  same  word,  "Yes"  or  "^ow,"  but  otherwise  to  keep 
silent'.  Xote  the  promptness  of  the  response,  as  there  may  be  a 
delay  in  conduction.  The  time  elapsing  between  stimulus  and 
response  is,  under  normal  circumstances,  ^^  of  a  second ;  in  disease 
it  may  require  10  seconds.  In  testing  tactile,  temperature,  and  pain 
sensibility,  the  areas  in  which  disturbances  are  found  should  be  care- 
fully outlined.  It  is  often  necessary  to  go  over  the  whole  cutaneous 
surface  inch  by  inch  before  the  examination  can  be  considered  to 
have  been  thorough.  In  some  cases  it  is  necessary  to  examine  not 
only  the  cutaneous  surface,  but  the  mucous  membrane  of  the  nasal 
and  oral  cavities  and  the  external  genitalia. 

(«)  Tactile  Sense. — This  sense,  which  embraces  the  elements  of 
pressure  and  contact,  may  be  tested  as  a  ivliole  by  the  aesthesiometer 
— practically  a  pair  of  dividers  with  blunted  points.  In  default  of  a 
regulation  instrument,  ordinary  compasses  with  their  tips  guarded  by 
bits  of  adhesive  plaster,  a  hairpin,  or  the  heads  of  two  ordinary  pins, 
may  be  used.  The  patient's  eyes  being  closed,  the  points  are  to  be 
placed  upon  the  skin  suflBciently  wide  apart  to  be  recognised  as  a 
double  contact  and  gradually  brought  together  until  it  appears  to  the 
subject  that  he  is  being  touched  with  a  single  point  only.  Xote  also 
whether  one  point  is  felt  as  two  or  more :  and  whether  a  toucli  upon 
one  side  of  a  limb,  or  of  the  body,  is  felt  respectively  upon  the  other 
side  of  the  same  limb,  or  the  opposite  side  of  the  body.  The  sensi- 
bility varies  within  wide  limits.  If  the  distances  are  twice  as  great 
as  those  given  in  the  following  table  it  may  be  considered  abnormal : 


Tip  of  tongue 1  mm.  =  ^V  in- 

Tip  of  fingers 2  "  =  ^  " 

Lips 3  "  =  i  " 

Dorsal  surface  of  fingers  6  "  =  ^  " 
Tip  of  nose  and  forearm  8  "  =  ^  " 
Tip  of  toes,  cheeks,  eye- 
lids, temple 12  "  =4  " 


Back  of  hands. . .        30  mm.  =       H  in- 

Neck 35     "    =       If  " 

Forearm,  leg,  dor- 
sum of  foot  ...         40     "    —       I5  *' 

Back 60-^0    "    =2f-3i^  " 

Arm  and  thigh  . .         80    "    =       3^  " 


The  element  of  contact  or  touch  is  tested  by  drawing  the  tip  of 
the  finger,  a  pencil,  the  head  of  a  pin,  a  camel's-hair  pencil,  or  a 


SENSORY  DISTURBANCES  529 

small  cone  of  cotton,  lightly  over  the  skin,  desiring  the  patient  to 
answer  immediately  upon  feeling  the  touch.  To  avoid  unthinking 
or  mechanical  responses  by  the  patient,  it  is  desirable  from  time  to 
time  ostensibly,  but  not  actually,  to  touch  the  surface.  Symmetrical 
parts  should  be  compared.  The  power  of  localization,  dependent 
upon  the  tactile  sense  jilus  muscular  or  weight  sense,  is  determined 
by  touching  the  skin  with  the  finger  tip  and  asking  the  patient,  with 
his  eyes  closed,  to  put  his  own  finger  on  the  same  point.  He  should 
not  err  to  a  greater  extent  than  2  inches.  This  is  a  good  test  for 
slight  anaesthesia,  as  he  may  be  able  to  feel  the  touch  but  not  to 
localize  it. 

In  testing  the  other  element  of  tactile  sensibility,  viz.,  the 
cutaneous  pressure  sense,  the  extremity  or  part  to  be  examined 
must  lie  upon  a  table,  bed,  or  other  support,  so  as  to  eliminate  mus- 
cular action.  "Weighted  rubber  balls,  weights  held  by  a  wire,  shot 
cartridges  filled  to  different  levels  with  shot,  2  pill  boxes  (1  filled, 
1  empty),  or,  more  simply,  coins  differing  in  weight  but  preferably 
of  nearly  the  same  size,  may  be  laid  upon  the  part  and  the  patient 
requested  to  indicate  which  is  heavier.  This  sense  is  most  acute  on 
the  brow,  temples,  forearm,  dorsal  surface  of  hand,  and  abdomen. 
For  most  purposes  the  tactile  sensibility  can  be  determined  and  suf- 
ficiently measured  by  using  the  heads  of  two  pins. 

{h)  Temperature  Sense. — For  testing  this  sense  one  may  use  test 
tubes  containing  hot  and  cold  water.  Touch  the  surface  first  with 
one,  then  with  the  other,  desiring  the  patient  in  each  case  to  state 
whether  it  feels  hot  or  cold.  Observe  also  whether  there  is  a  reversal 
of  this  sense — i.  e.,  whether  he  calls  hot  "  cold,"  or  cold  "  hot,"  or 
both.  It  is  abnormal  if  temperatures  of  60°  to  65°  are  not  described 
as  cold,  or  those  of  85°  to  95°  as  warm.  In  some  instances  heat  and 
cold  of  moderate  degrees  will  be  painful. 

(c)  Pain  Sense. — The  point  of  a  pin,  needle,  pen,  sharp-pointed 
pencil,  or  the  faradic  current,  may  be  employed  to  determine  the 
acuteness  of  the  pain  sense.     It  may  be  absent  or  excessive. 

((/)  Muscular  Sense. — This  special  sense  is  to  be  tested  by  using 
weights,  as  in  the  examination  of  the  pressure  sense,  except  that  the 
limb  or  part  must  not  be  supported.  It  is  desirable  to  use  objects 
which  resemble  each  other  in  size  and  shape  but  differ  in  weight. 
First  a  light,  then  a  heavy,  object  may  be  placed  in  the  unsupported 
hand,  or  upon  the  dorsum  of  the  foot,  and  the  patient  be  required  to 
say  which  is  the  heavier. 

{e)  Articular  and  Tendinous  Sense. — To  test  this,  have  the  pa- 
tient's eyes  strictly  closed  or  blindfolded.  Then  taking  hold  of  one 
of  the  extremities,  flex,  extend  and  move  it  in  a  variety  of  direc- 


530  TH^   EVIDENCES   OP   DISEASE 

tions,  desiring  the  patient  to  imitate  these  motions  with  the  corre- 
sponding limb  of  the  opposite  side ;  or  place  one  limb  in  a  certain, 
posture  and  have  him  describe  the  position  in  which  it  remains. 

(/)  Ataxia. — Upon  the  muscular  sense,  by  which  is  ascertained 
the  amount  of  strength  to  be  employed,  and  the  articular  and  ten- 
dinous sense,  which  informs  the  sensorium  of  the  position  of  the 
various  limbs  and  parts  of  the  body,  depend  the  power  of  co-ordina- 
tion— i.  e.,  the  regular  and  smooth  co-operation  of  individual  muscles 
or  muscle  groups  which  is  requisite  to  accomplish  a  definite  action 
or  movement.  If  these  senses  are  dulled  or  abolished  the  condition 
of  ataxia  exists.  Other  factors  are  also  concerned — sight,  touch,  etc. 
— but  those  just  mentioned  are  the  most  important.  Ataxia  mani- 
fests itself  in  certain  disturbances  of  station  and  gait  or  other  volun- 
tary movements.  These  disorders  of  co-ordination  may  be  searched 
for  as  follows  : 

(1)  Ataxia  of  the  tipper  extremities  is  tested  for  by  asking  the 
patient,  his  eyes  being  closed,  to  touch  first  with  one  index  finger, 
then  with  the  other,  the  tip  of  the  nose,  the  lobe  of  the  ear,  the  cen- 
tre of  the  closed  eye,  or  the  end  of  an  indicated  finger  of  the  oppo- 
site hand  ;  or,  with  the  eyes  open,  to  thread  a  needle,  button  his  coat,. 
or  write.     If  these  attempts  are  successful  the  co-ordination  is  good. 

(2)  Ataxia  of  the  lower  extremities,  if  present,  may  be  exploited 
by  various  methods.  Eequire  the  patient  to  stand  with  closed  eyes, 
the  heels  together.  In  a  perfectly  healthy  person  the  swaying  of 
the  head  will  be  about  1  inch,  even  less  than  with  the  eyes  open. 
If  ataxia  is  present  the  swaying  will  be  very  noticeable,  and  the  pa- 
tient, if  not  prevented,  may  even  fall  down.  This  symptom  is  called 
static  ataxia  (or  the  "  Eomberg  symptom  ").  Ask  him  further  to 
walk  along  a  straight  line  (seam  of  carpet,  line  of  junction  of  floor 
boards),  or  to  walk  across  the  room  and  put  the  tip  of  a  forefinger, 
without  hesitation,  upon  some  indicated  spot  (a  mark  on  a  door, 
centre  of  a  picture,  mantel  ornament).  If  he  is  unable  to  follow  the 
line  or  touch  the  spot  he  has  motor  ataxia.  If  he  is  unable  to  walk^ 
desire  him,  with  his  eyes  open,  to  imitate  with  his  foot,  movements 
made  by  the  examiner's  hand  (e.  g.,  writing  in  the  air,  circles),  or 
with  closed  eyes  to  touch  with  the  big  toe  of  one  foot  a  stated  point 
(dorsum,  inner  malleolus)  of  the  other  foot. 

In  all  tests  for  ataxia  which  require  to  be  made  with  closed  eyes 
it  is  only  fair  that  the  patient  be  allowed  to  rehearse  once  or  twice 
the  actions  which  are  to  be  performed,  as  even  a  normal  person  may 
bungle  at  the  first  trial. 

There  is  a  special  form  of  ataxia,  the  "  cerebellar"  due  to  disease 
of  the  cerebellum,  especially  of  the  vermis  or  middle  lobe.      The 


SENSORY  DISTURBANCES 


531 


patient  walks  in  a  reeling,  drunken  manner,  with  short  steps  and 
feet  wide  apart — the  titubating  gait.  It  is  due  to  a  disturbance  of 
the  balancing  power  (equilibration)  over  which  the  cerebellum  pre- 
sides, and  is  distinguished  from  ordinary  ataxia  by  the  fact  that 
while  the  patient  is  in  bed  he  can  successfully  pass  the  available 
tests  described,  and  at  no  time  are  the  arms  ataxic. 

The  Diagnostic  Significance  of  Sensory  Disturbances. 
— The  disturbances  to  be  considered  are  : 

(a)  Anaesthesia. — This  term,  according  to  a  strict  definition,  indi- 
cates a  loss  of  tactile  sensibility,  but 
is  often  employed  to  denote  a  loss 
of  any  form  of  sensation.  The  dis- 
tribution of  tactile  anaesthesia  is 
somewhat  varied.  It  may  be  either 
functional  or  due  to  some  organic  le- 
sion. In  general,  the  most  important 
diseases  or  conditions  which  present 
anaesthesia  as  a  symptom  are  :  cere- 
bral lesions  causing  hemiplegia ;  hys- 
teria and  traumatic  neuroses  ;  disease 
of  the  posterior  column,  roots,  or 
horns  of  the  spinal  cord,  especially 
locomotor  ataxia ;  pressure  on  the 
cord ;  neuritis  (a  frequent  cause) ; 
leprosy  and  Morvan's  disease, 

(1)  HemiancBstJiesia,  as  its  name 
indicates,  is  a  loss  of  sensibility  con- 
fined to  one  lateral  half  of  the  body 
(Fig.  192).  When  found  it  is  in  the 
majority  of  cases  a  symptom  of  hyste- 
ria. It  usually  affects  the  left  side, 
and  terminates  very  exactly  at  the 
middle  line  of  the  body.  Not  infre- 
quently there  is  anaesthesia  of  the 
senses  of  hearing,  taste,  smell,  and 
sight  on  the  same  side.  The  next 
most  common  cause  is  a  lesion  (hemor- 
rhage, tumour)  of  the  posterior  third 
(retrolenticular  portion)  of  the  pos- 
terior limb  of  the  internal  capsule,  at 
which  point  the  sensory  fibres  pass  up- 
ward (G,  Fig.  191).  Under  such  circumstances  it  is  usually  incom- 
plete and  is  conjoined  with  hemiplegia  of  the  same  side.     Hemian- 


FiG.  192. — Showing  (shaded  area) 
heiiiianaesthesia ;  usually  affects 
left  side. 


532 


THE   EVIDENCES  OF  DISEASE 


assthesia  and  hemiplegia  on  the  same  side  j^^us  oculo-motor  paralysis 
of  the  opposite  side  (crossed  ocular  paralysis)  is  indicative  of  a  lesion 
in  the  crus  on  the  same  side  as  the  ocular  paralysis  (C,  Fig.  191). 
Anaesthesia  of  one  side  of  the  body  with  anaesthesia  of  the  opposite 
side  of  the  face  (crossed  facial  anaesthesia)  may  be  due  to  a  lesion  of 
the  upper  portion  of  the  pons.    Very  rarely  hemianaesthesia  is  indica- 


HySTEROGENIC    ZONES 


Bilateral  an/CSTHe- 
sia  of  lower  ex- 
tremities 


Fig   193. — Showing  (shaded  areas)  mono-an£esthesia,  bilateral   anaesthesia,  and  the  usual 
situation  of  hysterogenic  zones. 


tive  of  a  lesion  in  the  optic  thalamus,  or  a  large  cortical  or  subcor- 
tical lesion  of  the  parietal,  temporal,  or  occipital  lobes,  or  is  associated 
with  multiple  sclerosis  or  hemichorea.  An  incomplete  hemianaesthe- 
sia of  one  side,  with  partial  hemiplegia  of  the  opposite  side,  may 
occur  as  a  result  of  a  unilateral  lesion  of  the  spinal  cord. 


SENSORY  DISTURBANCES 


533 


(2)  Bilateral  ancesthesia  sometimes  amounting  to  a  double  hemi- 
anaesthesia,  but  generally  confined  to  the  two  lower  extremities  (Fig. 
193)  and  the  lower  part  of  the  trunk,  is  rarely,  if  ever,  due  to  a 
lesion  of  the  brain.  It  is  a  frequent  symptom  in  hysteria  or  the 
traumatic  neuroses.  If  hysterical,  the  skin  of  the  genitals  and  a 
triangular  area  on  the  sacrum  will  re- 
tain their  normal  sensibility.  Anaes- 
thesia of  the  lower  extremities,  if  in 
conjunction  with  varying  degrees  of 
paralysis,  is  usually  due  to  some  le- 
sion affecting  the  spinal  cord,  viz., 
injury  or  compression  of  the  cord  by 
dislocation,  fracture,  or  caries  of  the 
vertebrae ;  spinal  meningitis,  hemor- 
rhage into  the  cord  (rare)  or  menin- 
ges (anaesthesia  sudden),  tumour, 
myelitis,  and  locomotor  ataxia. 

(3)  Ancesthesia  of  irregular  dis- 
tribution is  due,  as  a  rule,  either  to 
hysteria  or  neuritis.  The  loss  of  sen- 
sibility may  involve  one  arm  (Fig. 
193)  or  one  leg,  or  one  side  of  the 
face  alone  (mono -anaesthesia),  or 
occur  in  multiple  and  scattered 
patches  in  any  portion  of  the  body 
(Fig.  194).  Anaesthesia  of  a  single 
extremity  rarely  originates  from  a 
cerebral  lesion,  but  when  arising  from 
this  cause  the  anaesthesia  is  most 
marked  at  the  terminal  portion  of 
the  limb  and  gradually  lessens  as  the 
trunk  is  approached ;  if  caused  by  a 
spinal  lesion  its  proximal  border  will 
present  a  sharp  line  of  demarcation. 
The  shape  and  location  of  isolated 
areas  of  anaesthesia  should  be  com- 
pared with  Figs.  171  to  173,  to  find 
if  they  correspond  to  definite  spinal 
segments ;  and  with  Figs.  174  to  179 

in  order  to  determine  whether  they  are  coterminous  with  the  area  of 
distribution  of  any  of  the  peripheral  nerves.  Single  or  multiple  cir- 
cumscribed patches  of  anaesthesia  are,  as  previously  stated,  usually 
'due  to  hysteria  or  neuritis.  If  to  the  former,  there  is  generally  a 
36 


Fig.  lO-l.— si,. 


634  THE  EVIDENCES  OP   DISEASE 

lack  of  correspondence  with  either  segmentary  or  peripheral  locali- 
zation; if  to  the  latter,  the  anaesthetic  area  or  areas  will  fit  the  area 
of  supply  of  one  or  more  of  the  sensory  cranial  or  the  mixed  spinal 
nerves — e.  g.,  trigeminal,  radial,  plantar,  etc. 

(b)  HypersBsthesla. — An  excessive  sensibility  to  tactile  and  other 
impressions  attends  a  considerable  number  of  diseased  conditions. 
Areas  of  hyperaesthesia  are  of  frequent  occurrence  in  hysteria  consti- 
tuting the  so-called  hysterogenic  zones — i.  e.,  tender  points  on  the 
chest,  the  lower  abdomen  and  the  back  (Fig.  193),  pressure  upon 
which  will  excite  and,  if  continued,  may  stop  a  hysterical  paroxysm. 
An  excessively  tender  and  painful  mammary  gland,  witliout  evidence 
of  tumour  or  inflammation,  is  the  "  hysterical  breast."  In  neurasthe- 
nia there  is  a  frequent  hyperaesthesia  of  localized  points  along  the 
spine  and  on  the  scalp  and  chest.  The  scaip  is  often  tender  follow- 
ing headaches  (especially  of  migranous  type),  and  facial  or  occipital 
neuralgias.  The  area  supplied  by  any  neuralgic  nerve  may  be  tem- 
porarily hyperaesthetic.  Tenderness  of  the  scalp  may  also  occur  at 
the  menopause  or  in  gouty  persons.  A  general,  sometimes  localized,, 
hyperaesthesia  may  be  present  in  epidemic  influenza,  typhoid  fever,, 
anaemia,  and  some  of  the  chronic  toxic  states,  especially  from  alcohol 
and  opium.  A  suggestive  and  early  symptom  of  rickets  is  a  diffuse- 
hyperaesthesia.  The  paralyzed  side  in  a  hemiplegia  may  be  slightly 
oversensitive,  and  in  some  cases  of  brain  tumour  there  is  a  marked 
and  extensive  hyperaesthesia.  In  unilateral  lesions  of  the  spinal 
cord  there  is  a  narrow  zone  of  hyperaesthesia  above  the  level  of  anaes- 
thesia on  the  side  of  the  lesion.  A  decided  hyperaesthetic  condition 
of  the  head  and  extremities  may  occur  at  the  onset  of  cerebro-spinal 
meningitis,  and  the  finding  of  hyperaesthetic  areas  in  locomotor 
ataxia  is  not  uncommon.  Inflamed  nerves  may  at  some  stage  of  the- 
disease  be  noticeably  hyperaesthetic.  Finally,  the  referred  tender- 
ness of  visceral  disease  has  been  described  (page  38). 

Loss  of  the  pressure  sense,  contact  sense  remaining,  may  be  ob- 
served in  locomotor  ataxia. 

Anaesthesia  dolorosa,  areas  which  are  acutely  painful  but  in  which 
there  is  tactile  anaesthesia  and  analgesia  (loss  of  pain  sense),  are  found 
in  compression  of  the  spinal  cord. 

(c)  Disturbances  of  the  temperature  sense  consist  in  a  loss  of  the 
cold  sense  or  the  heat  sense,  or  both,  or  a  condition  of  reversal  of 
sensation,  cold  being  called  "  hot  "  and  vice  versa.  Such  alterations 
from  the  normal  are  especially  characteristic  of  syringomyelia  (Figs. 
166  to  169),  and  to  a  less  extent  of  locomotor  ataxia  and  lesions  of 
the  medulla. 

(d)  Disturbances  of  the  pain  sense  comprise  hyperalgesia,  an  ex- 


SENSORY   DISTURBANCES  535 

cessive  sensibility  to  painful  stimuli ;  and  amtlgesia,  a  loss  of  sensi- 
bility to  pain.  Hyperalgesia  is  almost  synonymous  with  tenderness 
{q.  v.).  Analgesia  is  found  particularly  in  syringomyelia,  Morvan's 
disease  and  hysteria.  Syphilitic  disease  may  cause  a  loss  of  the  pain 
sense. 

{e)  Impairment  or  loss  of  the  muscular,  articular,  and  tendinous 
senses  constitutes  ordinary  as  distinguished  from  cerebellar  ataxia 
{q.  v.).  It  indicates  an  interruption  of  the  sensory  conducting  tracts 
for  such  impressions  (Figs.  163, 166  to  169).  It  is  seen  in  some  forms 
of  cerebral  disease,  especially  cortical  lesions  and  lesions  of  the  corpora 
quadrigemina,  crura,  and  pons.  It  is  thus  occasionally  seen  in  hemi- 
plegia. It  is  especially  characteristic  of  locomotor  ataxia,  and  may 
be  found  as  a  symptom  of  transverse  injury  or  disease  of  the  cord. 
To  a  slight  extent  it  is  present  in  multiple  neuritis. 

Of  these  separate  senses,  the  loss  of  all  of  which  causes  ordinary 
(both  static  and  motor)  ataxia,  it  may  be  noted  that  loss  of  weight 
sense  (muscular  anaesthesia)  may  be  found  alone  in  hysteria  and  cor- 
tical lesions ;  that  impairment  of  posture  sense  (articular  and  ten- 
dinous anaesthesia)  may  be  present  in  locomotor  ataxia  and  neuritis 
before  noticeable  ataxia  is  found ;  that  static  ataxia  involves  espe- 
cially muscular  and  articular  sensation ;  and  that  motor  ataxia  con- 
cerns particularly  articular  and  tendinous  sensations. 

Astasia-abasia — inability  to  stand  and  to  walk — is  a  symptom  of 
a  neurosis  akin  to  hysteria  rather  than  a  separate  disease.  There  is  no 
paralysis,  and  while  in  bed  the  movements  of  the  feet  and  legs  show 
no  incoordination ;  but  upon  attempting  to  stand  or  walk  the  legs 
give  way,  as  if  plastic,  and  in  some  cases  undergo  sudden  flexions  or 
dancing  movements.     Such  cases  occur  mainly  in  young  adults. 

(/)  Other  Irregularities  of  Sensation. — AUochiria,  transference  of 
sensation  so  that  a  touch  on  one  side  of  the  body  is  felt  ob  the  oppo- 
site side,  may  be  seen  as  a  symptom  of  hysteria,  locomotor  ataxia, 
disseminated  sclerosis,  and  myelitis.  Polywsthesia,  in  which  a  touch 
with  one  point  is  felt  as  two  or  more,  is  akin  to  and  of  the  same  sig- 
nificance as  allochiria.  Delayed  conductinn,  either  of  tactile  or  pain 
sensibility,  so  that  the  response  may  require  as  long  as  ten  seconds 
instead  of  the  normal  one  tenth  of  a  second,  may  be  found,  especially 
with  reference  to  pain,  in  locomotor  ataxia  and  various  paralyses  of 
peripheral  origin.  Eelated  to  delayed  conduction  and  of  similar 
moderate  suggestiveness  are  two  other  abnormalities,  viz.,  after-sen- 
saiion^  a  gradually  increasing  sense  of  pain  which  may  last  for  some 
minutes  after  a  pin  prick  ;  and  double  scnfdbih'fy  to  touch  and  pain, 
in  which  the  tactile  impression  is  first  perceived,  the  painful  impres- 
sion coming  to  consciousness  after  a  varying  length  of  time. 


536  THE   EVIDENCES  OF   DISEASE 


THE    REFLEXES 

The  reflexes  to  be  tested  are  tlie  cutaneous  or  superficial ;  the 
tendinous  or  deep  reflexes  ;  and  certain  organic  or  excito-rejlex  actions. 

All  of  these  reflexes  presuppose  the  travelling  of  a  stimulus  from 
the  periphery  along  the  afferent  nerve  to  the  motor  cells  in  the  cord 
or  medulla.  The  motor  cells  transform  the  received  stimulus  into 
an  impulse  which  is  reflected  to  the  periphery  along  an  efferent 
(motor)  nerve  to  certain  muscles,  which  in  consequence  contract  in- 
voluntarily. This  reflex  action  ordinarily  occupies  from  one  twelfth 
to  one  tenth  of  a  second.  The  superficial  or  cutaneous  reflexes  are 
elicited  by  irritating  the  skin  or  mucous  membrane,  thus  causing 
contraction  of  the  muscles  near  the  irritated  part ;  the  deep  or  ten- 
don reflexes  are  produced  usually  by  striking  the  tendon,  but  also  by 
sharp  percussion  of  the  muscle  or  the  periosteum  near  the  tendon. 
The  organic  or  visceral  reflexes  involve  a  definite  and  co-ordinate 
response  to  special  stimuli — e.  g.,  defecation. 

The  Superficial  (Cutaneous)  Reflexes. — («)  Method  of 
Examination. — The  cutaneous  reflexes  are  usually  tested  by  sharply 
stroking  the  skin  with  the  finger  or  a  pencil,  or  by  scratching,  tick- 
ling, pinching,  and  pricking,  or  the  application  of  heat  (hot  water), 
cold  (ice),  or  chemical  irritants.     The  superficial  reflexes  are  the  : 

Scapular. — Irritate  the  interscapular  region  and  the  scapular  muscles  con- 
tract. 

Ej)iga8tric. — Stroke  the  side  of  the  chest  downward  from  the  nipple,  and 
the  epigastrium  on  the  same  side  retracts. 

Abdominal. — Stroke  from  the  costal  margin  downward  in  the  mammillary 
line,  and  the  abdominal  muscles  contract  on  the  same  side. 

Cremasteric. — Stroke  the  upper  and  inner  part  of  the  thigh,  and  the  testicle 
(not  the  scrotum  alone)  on  the  same  side  draws  upward. 

Gluteal. — Stroke  the  skin  of  the  buttock,  and  a  contraction  of  the  gluteal 
muscles  on  the  same  side  will  follow. 

Plantar. — Stroke  or  tickle  the  sole  of  the  foot,  and  the  leg  jerks  upward  or 
the  foot  is  suddenly  dorsiflexed. 

The  foregoing  reflexes  depend  upon  the  spinal  cord  as  a  motor 
centre ;  the  following  upon  centres  in  the  medulla : 

Conjunctival  or  Lid  Reflex. — Touch  the  conjunctiva,  or  expose  the  eye  ab- 
ruptly to  a  bright  liglit,  and  the  eyelids  close  suddenly  by  contraction  of  the 
orbicularis  orbis.     The  trigeminus  is  the  afferent,  the  facial  the  efferent,  nerve. 

Pupillary— Skin  Beflex. — Stroking  skin  of  chin  or  neck  causes  dilatation  of 
the  pupils. 

Palatal. — Touching  the  raucous  membrane  of  the  palate  causes  the  latter 
to  draw  up.  The  glossopliaryngeal  is  the  afferent,  the  pneumogastric  or  spinal 
accessory  the  efferent,  nerve. 


THE  r?:flexes 


537 


(b)  Diagnostic  Signifi- 
cance of  the  Superficial 
Reflexes. — The  cutaneous 
reflexes  are  of  such  varia- 
ble occurrence  in  differ- 
ent individuals  that  their 
absence  is  not  of  much 
significance.  The  palate 
reflex  may  be  lost  in  hys- 
teria and  bulbar  paralysis. 
Diminished  plantar  reflex 
with  exaggerated  patellar 
tendon  reflex  is  some- 
what characteristic  of 
functional  paraplegia,  and 
the  superficial  refiexes  in 
general  may  be  absent  on 
the  affected  side  in  the 
early  stages  of  cerebral 
hemiplegia. 

The  presence  of  a  cu- 
taneous refiex  is  of  value 
because  it  demonstrates 
that  the  reflex  arc  (sen- 
sory nerve,  spinal  seg- 
ment, motor  nerve)  upon 
which  it  depends  is  in  a 
normal  condition.  The 
location  of  the  segments 
for  the  more  important  of 
these  reflexes  is  shown  in 
Fig.  195. 

The  Deep  (or  Ten- 
don) Reflexes. — There 
is  some  difference  of  opin- 
ion as  to  the  nature  of 
the  tendon  reflex.  That 
it  is  a  true  spinal  reflex 
is  denied  by  some  who 
attribute  it  to  an  abrupt 
stretching  by  the  blow, 
with  consequent  increase 
of  tension,  of  a  muscle 
which    is    already  tense, 


AUTOMATIC 
CENTRES 


CORO 


SUPERFICIAL  AND 
DEEP  REFLEXES 


Cilio-spinal 


Vasomotor 


Supinator  and 
biceps  jerk 


Genital  — 
(erection,  ejaculation; 


Bladder  and 
rectum 


Fig.  195. — Diacrram  showing  the  segmental  localization 
of  the  automatic  centres  and  the  superficial  and 
deep  reflexes  in  the  spinal  cord. 


538 


THE   EVIDENCES  OF   DISEASE 


thus  exciting  a  sudden  contraction.  There  is,  however,  good  author- 
ity for  its  true  reflex  origin.  Practically  it  makes  no  difference,  for 
according  to  either  hypothesis  a  reflex  arc  is  indispensable,  in  the 
one  case  to  enable  the  reflex,  in  the  other  to  maintain  the  muscular 
tonus.  The  more  important  deep  reflexes  are  those  of  the  jaw,  elbow, 
wrist,  knee,  and  ankle;  to  which  may  be  added  the  pupillary  and 
ciliary  reflexes. 

(a)  Method  of  Examination. — (1)  Jaw  Jerk. — Place  a  finger  upon 
the  chin,  let  the  patient  open  his  mouth,  but  not  too  Avidely,  and  de- 
liver one  or  two  strong  percussion  strokes  upon  the  finger;  or  per- 
cuss similarly  upon  a  knife  blade  or  paper  cutter  laid  upon  the  lower 
teeth.     If  this  reflex  is  present  the  muscles  which  close  the  jaw  will 

suddenly  contract.  It  is  dependent 
upon  the  motor  nucleus  of  the  trigem- 
inus. 

(2)  Elbow  or  Triceps  Jerk. — Bring 
the  arm  out  from  the  body  and  let  it 
rest  upon  the  examiner's  hand,  which 
is  placed  in  the  crook  of  the  elbow,  in 
such  a  manner  that  the  forearm  hangs 
vertically  downward  at  right  angles  to 
the  upper  arm.  Then  with  the  fore- 
finger and  thumb  grasping  the  straight- 
ened middle  finger,  as  in  Fig.  196 
(which  makes  an  excellent  strong  per- 
cussor),  or  with  the  regulation  ham- 
mer, strike  just  above  the  olecranon. 
The  forearm  performs  a  movement  of  extension  because  of  the  con- 
traction of  the  triceps. 

(3)  Wrist  Jerk. — Allow  the  hand  to  hang  down  (as  in  wrist  drop) 
and  strike  the  extensor  tendons  proximal  to  the  wrist  joint.  The 
hand  will  suddenly  be  extended. 

(4)  Knee  Jerk. — The  leg  should,  if  possible,  be  allowed  to  hang 
limply  at  right  angles  to  the  thigh.  The  knees  may  be  crossed  ;  or 
if  a  chair  or  the  bed  is  sufficiently  high  so  that  the  feet  do  not  touch 
the  floor,  he  may  sit  in  such  a  Avay  that  the  legs  hang  vertically  down- 
ward over  the  edge ;  or  the  examiner  may  support  the  leg  by  placing 
his  hand  in  the  crook  of  the  knee ;  or  push  his  hand  from  the  outside 
far  enough  under  to  rest  it  upon  the  opposite  knee  of  the  patient, 
thus  letting  the  leg  swing  upon  his  forearm  ;  or,  if  the  patient  can 
not  sit  up,  the  knee  may  be  flexed  and  supported  by  the  hand.  The 
patient  should  be  directed  or  diverted  so  that  the  leg  hangs  loosely. 
A  sharp  blow  (with  edge  of  hand,  finger,  hammer)  should  be  struck 


Fig.  196. — Showing  method  of  re-en- 
forcing middle  finger  to  make  strong 
percussion. 


THE  REFLEXES  539 

upon  the  tendon  just  below  the  patella.  Under  normal  conditions 
there  follows  an  abrupt  jerk  of  the  leg  and  foot.  If  it  can  not  be 
obtained,  employ  "re-enforcement" — i.e.,  desire  the  patient  to  clinch 
his  fists  strongly ;  or  liooking  his  fingers  together,  to  pull,  one  hand 
against  the  other,  using  all  his  strength.  Either  by  lessening  cere- 
bral inhibition,  or  by  causing  an  increase  of  the  general  muscular 
tension,  re-enforcement  may  elicit  a  previously  absent  reflex.  In 
some  cases  of  exaggerated  knee  jerk  it  is  possible  to  obtain  a  knee 
clonus  equivalent  to  ankle  clonus  (see  (5)  following)  by  fully  ex- 
tending the  leg,  seizing  the  patella,  quickly  pushing  it  downward 
and  continuing  the  pressure.  As  a  result  the  quadriceps  may  con- 
tract rhythmically  for  a  considerable  period. 

(5)  Ankle  Jerk. — Extend  the  patient's  leg  and  hold  it  up  by 
grasping  the  foot,  at  the  same  time  bending  the  foot  upward  so  as 
to  stretch  the  tendo  Achillis.  Then  strike  the  tendon  sharply  and 
observe  the  resulting  contraction  of  the  muscles  of  the  calf.  Ankle 
■clonus  is  a  peculiar  rhythmic  contraction  of  the  calf  muscles. 
Partly  extend  the  leg,  and  it  is  essential  that  the  knee  be  slightly 
bent.  Let  the  heel  rest  in  the  examiner's  left  hand  while  his  right 
hand  seizes  the  front  part  of  the  foot  and  abruptly  pushes  up  or 
dorsiflexes  it  upon  the  leg.  The  calf  muscles  contract,  forcing  the 
foot  downward  against  the  examiner's  hand,  and  if  the  latter  con- 
tinues to  press  steadily  on  the  sole  of  the  foot  a  rhythmic,  clonic 
movement  of  the  foot  will  begin  and  continue.  Some  notion  of  the 
readiness  with  which  the  clonus  develops  may  be  obtained  by  ascer- 
taining the  degree  of  dorsiflexion  of  the  foot  at  which  the  rhythmic 
movements  begin.  In  some  cases  a  very  small  amount  of  flexion  and 
pressure  will  produce  it.  True  ankle  clonus  must  be  distinguished 
from  the  few  clonic  movements,  rapidly  ceasing,  which  may  be 
observed  as  a  result  of  similar  manipulations  in  cases  of  neuras- 
thenia and  hysteria. 

"  Paradoxical  contraction "  is  sometimes  observed  while  testing 
for  ankle  clonus  in  a  leg  the  muscles  of  which  are  extremely  spastic. 
It  consists  of  a  tonic  contraction  of  the  anterior  tibial  muscles  pro- 
duced by  the  abrupt  dorsiflexion  of  the  foot. 

(6)  The  light  reflex  (q.  v.)  and  the  ciliary  reflex  (q.  v.)  have  been 
elsewhere  considered. 

{b)  Diagnostic  Significance  of  the  Deep  Reflexes. — Of  the  deep 
reflexes  the  knee  jerk  or  patellar  reflex  is  the  most  important.  It  is 
almost  invariably  present  in  health.  Fig.  195  shows  the  spinal  local- 
ization of  the  deep  reflexes ;  Fig.  197  their  mechanism. 

(1)  Absence  of  the  knee  Jerk  is  caused  by  a  lesion  affecting  any 
part  of  the  reflex  arc.     Like  the  other  reflexes,  its  presence  implies 


640 


THE  EVIDENCES  OF  DISEASE 


a  healthy  condition  of  the  tendon,  the  afferent  (sensory)  nerve,  the^ 
posterior  roots  and  anterior  horn  of  the  spinal  cord,  the  efferent 


i 


INHIBITING  FIBRES) 

FROM 

CEREBRUM. 

DISEASE  AFFECTING 

THESE  ALLOWS 


fCORTlCAL 

LESIONS. 

I    SPASTIC 

[PARALYSIS 


EXAGGERATED  REFLEXES 


DISEASE  OF 

MOTOR 
END-PLATES 


SHOWING  THE  MECHANISM  OF  THE  DEEP 
REFLEXES  AND  EXAMPLES  OF  THE  LESIONS 
WHICH  MAY  INCREASE  OR  ABOLISH  THEM 
AS  ILLUSTRATED  BY  THE  KNEE-JERK. 

DOTTED  CIRCLES  =  LESIONS  ABOLISHING 
THE  REFLEXES. 

BLACK  CIRCLES=  LESIONS  EXAGGERATING 
THE  REFLEXES. 


Fig.  197. — Showing  mechanism  of  deep  reflexes;  also  the- 
two  main  types  (spastic  and  flaccid)  of  paralysis. 


(motor)  nerve  and  the  muscle  itself.     If  the  function  of  any  portion^, 
or  element  of  this  circuit  is  in  abeyance  the  reflex  is  abolished^ 


THE  REFLEXES  541 

Consequently  loss  of  the  knee  jerk  is  a  symptom  of  disease  affecting 
either  the  motor  or  sensory  fibres  or  both — neuritis ;  diseases  of  the 
posterior  roots  and  columns — locomotor  ataxia  and  Friedreich's  dis- 
ease ;  diseases  of  the  anterior  horns — anterior  poliomyelitis  (acute  or 
chronic)  and  Landry's  paralysis ;  and  transverse  myelitis,  if  affecting 
the  second  and  third  lumbar  segments  in  which  the  reflex  is  local- 
ized. It  is  absent  in  apoplexy  immediately  after  the  shock,  in 
epilepsy  immediately  after  the  convulsion,  in  injuries  to  the  cord 
immediately  after  the  accident,  and  in  spinal  meningitis.  It  is  fre- 
quently lacking  in  the  toxaemias  of  diphtheria,  diabetes  mellitus 
(sometimes  also  insipidus)  and  chorea. 

(2)  Exaggeration  of  the  knee  jerk  shows  that  the  reflex  arc  is 
intact,  but  that  either  the  normal  restraining  influence  of  the  upper 
(cerebral)  motor  neurones  is  destroyed  by  lesions  affecting  the  cells, 
or  their  fibres  which  run  down  in  the  lateral  pyramidal  columns ;  or 
that  the  irritability  of  the  spinal  cord  as  a  reflex  centre  has  been 
increased.  Consequently,  taking  the  intracranial  causes  first,  the 
patellar  reflex  is  exaggerated  in  the  hemiplegia  of  apoplexy  on  the 
affected  side  shortly,  but  not  immediately,  after  the  attack ;  in  the 
cerebral  paralysis  of  children ;  in  hereditary  cerebellar  ataxia ;  and 
in  general  paralysis  of  the  insane.  The  lesions  affecting  the  func- 
tion of  the  lateral  columns  are  lateral  sclerosis,  and  amyotrophic 
lateral  sclerosis.  Transverse  myelitis,  injuries  to  the  spinal  cord 
(after  the  immediate  effects  of  the  traumatism  have  passed),  pressure 
on  the  spinal  cord,  and  unilateral  lesion  of  the  spinal  cord,  if  situ- 
ated above  the  level  of  the  second  and  third  lumbar  segments,  will, 
by  cutting  off  the  inhibiting  cerebral  impulses,  cause  exaggeration 
of  the  knee  and  ankle  jerk.  If  the  lesion  is  unilateral  the  exagger- 
ated reflex  will  be  on  the  same  (paralyzed)  side.  The  patellar  reflex 
may  also  be  exaggerated  as  a  symptom  of  hysteria,  neurasthenia, 
rheumatoid  arthritis,  tetanus,  and  strychnine  poisoning. 

(3)  The  ankle  jerk  is  usually  present  in  health ;  ankle  clonus  is 
always  abnormal.  Absence  of  the  ankle  jerk  has  the  same,  although 
less  important,  significance  as  absent  knee  jerk ;  exaggerated  ankle 
jerk  and  the  presence  of  the  ankle  clonus  are  of  equivalent  value  to 
exaggerated  knee  jerk,  the  clonus  being  found  especially  in  lateral 
amyotrophic  and  disseminated  sclerosis.  A  brief  abortive  or  false 
clonus  has  already  been  mentioned  as  occurring  in  neurasthenia  and 
hysteria. 

(4)  The  deep  reflexes  of  the  upper  extremity  are  of  much  less 
diagnostic  value  than  those  of  the  lower  extremities  because  they 
are  frequently  absent  in  health.  The  jaw  jerk  is  never  found  under 
normal  circumstances.     The  presence  or  exaggeration  of  jaw,  elbow. 


542 


THE  EVIDENCES  OF   DISEASE 


or  wrist  jerk  is  therefore  of  more  importance  than  a  failure  to  elicit 
them,  and  their  diagnostic  significance,  allowing  for  the  difference  in 
localization  (Fig.  195),  is  the  same  as  that  of  the  knee  jerk. 

(c)  The  excito-motor  or  organic  reflexes  and  the  significance  of 
their  altered  functions  {q.  v.)  have  been  previously  considered,  viz., 
Defecation,  Urination,  Dysphagia,  and  Eespiration. 

ELECTRO-DIAGNOSIS  (NERVE  AND   MUSCLE) 

An  elementary  knowledge  of  the  physics  of  electricity  is  presup- 
posed. 

Apparatus  and  Technic. — Eequired  are  :  A  faradic  current 
apparatus  and  a  galvanic  current  apparatus.  These  may  run  by  dry 
cells,  wet  cells,  or  the  commercial  street  current.     If  the  latter  is 


S^ontalis. 


Facial 
{upper  branch). 

■Comigator  supercilii, 


Orbicul. palpebrarum. 
Nasal  muscles,  -j 

Zygomatic! . 


Orbicularis  oris. 


Facial  (middle  br^ch). 
Masse  ter. 

Levator  menti. 

Quadratus  menti. 

Triangularis  menti. 

Hypoglossus. 

Facial  {loioer  branch). 

Platysroa  myoides. 
Hyoid  muscles.  \ 

Omohyoid. 


Anterior  thoracic 
<Pectoralis  major). 


Region  of  tbe  centra' 
convolutions. 


Region  of   the   third 
frontal  convolution 
and  the  insula 
(speech  center;. 

Temporalis. 

Facial  (upper)   in 
front  of  ear. 

Facial  {trunk). 
Posterior  auricular. 
Facial  (middle  br'ch). 
Facial  (loioer  branch). 
Splenius. 

Sterno-cleido-mastoid. 

Spinal  accessory. 
Levator  anguli 

scapulae. 
Trapezius. 

Dorsalis  scapulae. 
Axillary  {circumflex). 

Long  thoracic  (serra- 
tus  magnusn 


Phrenic.        Supraclavicular  point. 
(Erb's  point.     Deltoid, 
biceps,  brachialis  amicus, 
and  supinator  longus.) 

Fio.  198. 


Brachial  plexus. 


employed,  guaranteed  devices  should  be  used  in  order  to  prevent 
dangerous  accidental  shocks  to  the  patient.  A  rheostat,  for  interpos- 
ing a  variable  resistance  to  the  galvanic  current,  so  that  its  strength 


ELECTRO-DIAGNOSIS 


543 


may  be  altered   at  will.     A  milliamperemeter^  for  measuring  the 
strength  of  the  galvanic  current.     A  sioitchj  for  changing  the  direc- 


Triceps  flong  head) 

Triceps  (internal  bead).  — 
Ulnar.] 


Flexor  carpi  ulnaris. 
Flexor  profundus  digitorum. 


Flexor  sublimis  digitorum 
(Hand  III). 


Flexor  sublimis  digitonmi 
■I  and  IV). 

Ulnar. 

Palmaris  brevis. 

Abductor  minimi  digiti. 

Flexor  brevis  minimi  digiti. 

Opponens  minimi  digiti. 

Lumbricales. 


Deltoid  (anterior 
half) 


Musculo-cutaneoua 
Biceps. 
Brachialis  anticus- 


Supinator  longus. 
Pronator  radii  teres. 
Flexor  carpi  radialis. 

Flexor  sublimis  digitorum. 

Flexor  longus  polUcis. 
Median. 

Abductor  poUicis. 
Opponens  pollicis. 
Flexor  brevis  pollicis. 
Adductor  pollicis. 


Fio.  199. 


tion  of  the  galvanic  current — i.  e.,  the  polarity  of  the  electrodes — at 
will.  One  (indifferent)  electrode,  2x6  inches  (5  X  15  centimetres). 
One  {.^elective  or  normal)  electrode,  1;|^  inches  in  diameter  (about  10 


544 


THE  EVIDENCES  OP  DISEASE 


square  centimetres).     A  removable  handle  for  the  small  electrode, 
furnished  with  a  button,  pressure  upon  which  closes  the  circuit. 

(1)  Begin  tcWi  the  faradic  current. — Wet  both  electrodes  with 
plain  or  slightly  salted  warm  water.     Start  with  a  weak  current,  test- 


Deltoid  (iwsterior  half). 


Radial  {musculo-spiral) 
Brachialis  anticiis 

Supinator  longus. 
Extensor  carpi  radialis  longior. 
Extensor  carpi  radialis  brevier. 

Extensor  communis  digitorum.  -^ 
Extensor  indicis. 

Extensor  ossis  metacarpi  poUieis. 
Extensor  prim!  internodii  poUicis. 


Dorsal  interossei,  I  and  II.  \ 


Triceps  (long  head). 


!•  Triceps  (external  head). 


Extensor  carpi  ulnaris. 
Supinator  brevis. 

Extensor  minimi  digitL 
Extensor  indicis. 


Extensor  secundi  internodii 
pwllicis. 


Abductor  minimi  digiti. 

(  Dorsal  interossei, 
>       III  and  IV. 


Fig.  200. 

ing  its  strength  first  upon  your  own  wrist.  Place  the  large  (indiffer- 
ent) electrode  upon  the  sternum,  or  between  the  scapulae,  or  on  the 
abdomen  of  the  patient.  Apply  the  small  (normal)  electrode  upon 
the  nerve  or  the  motor  points  (see  1st  paragraph  upon  page  547)  of 
the  muscles  to  be  examined.  If  the  current  is  not  sufficiently  strong 
to  cause  a  visible  contraction  of  the  muscle,  increase  its  strength 
until  a  contraction  is  elicited  or  the  current  becomes  too  painful  to 
be  borne.     Note  the  minimal  strength  of  current  requisite  to  obtain 


ELECTRO-DIAGNOSIS 


545 


a  contraction,  as  indicated  by  the  scale  showing  the  distance  to 
which  the  inner  and  outer  coils  overlap  (CD  =  coil  distance).  Go 
over  the  nerves  and  muscles  systematically,  comparing  each  muscle 
with  its  fellow  on  the  opposite  side  of  the  body. 

(2)  77ien  use  the  galvanic  current. — Place  electrodes  as  before. 
Turn  the  switch  so  that  the  small  electrode  is  the  negative  pole  or 
cathode.  Close  the  circuit  by  pressing  the  button  on  the  handle  of 
the  electrode,  and  let  the  current  run  for  a  moment.  It  must  be  un- 
derstood that  with  the  galvanic  current  the  contraction  of  a  muscle 
occurs  only  at  the  instant  of  closing  or  opening  the  circuit,  not  while 
the  current  is  passing.  Open  and  close  the  circuit  several  times, 
slowly  increasing  and  decreasing  the  strength  of  the  current,  until 
the  minimum  strength  of  current  is  found  which  will  cause  a  mus- 
€ular  contraction  at  the  instant  of  closing  the  circuit — the  cathode 


Crural. 

Obturator. 
Pectinens. 

Adductor  magnus. 
Adductor  loDgus. 

Crureus. 
Vastus  iuternus. 


Tensor  vagiiue  femoris. 


Sartorius. 

|_ Quadriceps  femoris 
(common  point). 

Rectus  femoris. 


>  Vastus  extemus. 


Fig.  201. 


closure  contraction  (CaCC).  Xote  the  reading  of  the  milliampere- 
meter.  Change  the  direction  of  the  current,  thus  making  the  small 
electrode  the  positive  pole  or  a7iode,  repeat  the  same  tests,  and  ascer- 


546 


THE  EVIDENCES  OF  DISEASE 


tain  the  same  facts  with  regard  to  the  anode  closure  contraction 
(AnCC).  Then,  with  the  same  strength  of  current  in  each  case,  de- 
termine whether  CaCC  is  equal  to,  stronger,  or  weaker,  than  AnCC. 
Similar  tests  (rarely  required)  may  be  made  with  the  opening  of  the 
cathodal  circuit  (cathode  opening  contraction  =  CaOC),  and  of  the 
anodal  circuit  (AnOC).  The  character  of  the  muscular  contraction 
is  of  great  importance — i.  e.,  whether  it  is  quick  and  sharp,  sluggish 
and  slow,  or  continuous  and  tetanic. 

It  is  further  to  be  borne  in  mind  that  the  testing  electrode  may 
be  placed  directly  over  the  nerve  going  to  the  muscle,  or  over  the 
body  of  the  muscle  itself  as  far  as   possible  from  the  nerve.     As  a 


Sciatic. 

Biceps  femoris  (long  head). 
Biceps  femoris  (short  head). 


Peroneal. 


Gastrocnemius  (external  head). 


Soleus. 


Flexor  longus  hallucis. 


'  Gluteus  maximus. 


Adductor  magnus. 
Semitendinosus. 
^-4 Semimembranosus. 


i Posterior  tibial. 


Gastrocnemius  (internal  head). 


Soleus. 


Flexor  longus  digitorum. 


Tibial. 


Fig.  202. 


matter  of  fact,  it  is  well-nigh  impossible  to  limit  the  action  of  the 
electric  current  to  the  muscle  alone  without  also  influencing  the 
nerve-  fibres  embedded  in  it.     In  either  case  both  the  capability  of 


ELECTRO-DIAGNOSIS 


54T 


the  nerve  as  a  conductor  and  the  preservation  of  the  contractility  of 
the  muscle  are  demonstrated  by  the  occurrence  of  visible  n^uscular 
contraction. 

Figs.  198  to  203  show  the  situation  of  the  accessible  nerve  trunks^ 
and  the  motor  points — i.  e.,  the  points  at  which  the  branches  of  the 


Tibialis  anticus 
Elxtensor  long^s  digitorum. 


Feroneus  brevis, 


Extensor  proprius  pollicis. 


Dorsal  interossei.  -j 


Peroneal. 


Gastrocnemius  (external). 
Feroneus  longus. 


VSoleus. 


Flexor  longus  hallucis. 


Extensor  brevis  digitorum. 
Abductor  minimi  dig^ti. 


Fig.  203. 


nerve  enter  the  muscles.  By  study  of  the  diagrams  in  connection 
with  the  living  subject  the  principal  nerves  and  motor  points  may 
readily  be  learned. 

Diagnostic  Indications  from  the  Electrical  Examina- 
tion.— (1)  In  health  the  behaviour  of  the  nerve  and  muscle  is  as  fol- 
lows :  A  ready  sharp  contraction  to  either  electrode  (or  pole)  upon 
closure  of  the  faradic  current^  the  contraction  continuing  while  the 
current  is  passing.  The  stronger  the  current  the  stronger  is  the 
contraction.  AVith  the  galvaiiic  cnrreuf  it  is  otherwise.  The  occur- 
rence of  a  contraction  depends  upon  the  pole  which  is  applied  to  the 
nerve,  and  whether  the  circuit  is  closed  or  open.  If  a  weak  current 
is  passed,  with  the  negative  pole  on  the  nerve,  it  will  be  found  that 


548 


THE  EVIDENCES  OF  DISEASE 


produces 

produces 

CaCC 

CaOC 

and 

AnOC 

no  contraction  occurs  while  the  current  is  passing.  But  if  the  cur- 
rent is  just  suflSciently  strong,  a  quick,  sharp  contraction  will  occur 
at  the  instant  of  closing  the  circuit  but  not  at  its  opening ;  and  if 
the  positive  pole  is  applied,  with  the  same  strength  of  current,  there 
will  be  no  contraction  at  all,  either  upon  opening  or  closing.  If  the 
test  is  continued,  using  gradually  increasing  strengths  of  current,  the 
next  contraction  appears  when  with  the  positive  pole  on  the  nerve 
the  circuit  is  opened,  then  folloAvs  one  with  the  positive  closing,  and 
finally  with  the  strongest,  perhaps  painful,  current,  a  contraction 
occurs  with  the  negative  opening.  In  other  words,  a  healthy  nerve 
and  muscle  with  the  same  strength  of  current  responds  more  readily 
to  the  negative  pole  or  cathode  than  to  the  positive  pole  or  anode. 
Letting  An  =  anode,  Ca  =  cathode,  C  =  closure,  0  =  opening,  the 
following  table  shows  the  normal  order  of  readiness  in  which  con- 
tractions appear : 

Weak  Current  Medium  Strength 


often      \ 
reversed  / 


The  symbol  <  means  greater  or  less  than,  the  apex  pointing 
toward  the  lesser  ;  thus  normally  CaCC  >  AnCC,  which  means  that 
cathode  closure  contraction  is  greater  than  anode  closure  contrac- 
tion. Using  this  symbol,  the  usual  order  of  reaction  of  a  healthy 
nerve  and  muscle  may  be  expressed  by  the  formula  CaCC  >  AnOC 
>  AnCC  >  CaOC.    Practically  it  is  suflBcient  to  test  CaCC  and  AnCC. 

(2)  In  disease  these  reactions  may  be  altered  as  follows :  The  re- 
sponse to  faradism  becomes  sluggish,  lessens,  or  disappears.  The 
response  to  galvanism  is  changed,  so  that  the  contraction  is  slow, 
sluggish,  and  wormlike ;  the  AnCC  becomes  equal  to  or  even 
greater  than  CaCC ;  and  possibly  no  contraction  can  be  obtained 
with  either  faradism  or  galvanism,  no  matter  how  strong  the  current 
may  be. 

The  variations  from  the  normal  which  have  Just  been  outlined 
constitute  the  reaction  of  degeneration  (DeR).  This  reaction 
depends  upon  the  changes  which  occur  in  a  motor  nerve  and  muscle 
which  have  been  cut  off  from  their  trophic  centre  in  the  spinal  cord 
or  medulla,  either  by  disease  of  the  centre  or  disease  of  the  nerve 
itself.  The  terminal  nerve  fibres,  their  end  plates  in  the  muscle, 
and  finally  the  muscle  itself  will  degenerate.     During  this  process 


Strong 

Very  Strong 

produces 

produces 

CaCC 

CaCC 

j  AnOC 

AnOC 

and 

AnCC 

(AnCC 

and 

CaOC 

ELECTRO-DIAGNOSIS  549 

the  electrical  reaction  progressively  alters,  affording,  according  to  its 
degree,  "  partial "  or  "  complete "  DeR.  Thus  within  3  or  4  days 
after  a  spinal  nerve  has  been  deprived  by  injury  or  disease  of  the 
trophic  influence  of  the  motor  cells  of  the  anterior  horn,  it  becomes 
less  responsive  to  either  galvanic  or  faradic  stimulation,  and  the 
faradic  response  may  soon  disappear  altogether.  In  10  days  or  2 
weeks,  however,  the  response  to  galvanism  may  increase  beyond  the 
normal.  During  this  time  the  changed  behaviour  to  the  poles  and 
the  sluggish  contraction  of  the  muscles  will  make  their  appearance  in 
varying  degrees.  Subsequently,  if  the  cause  is  permanent,  in  a  period 
varying  from  several  months  to  two  or  more  years,  the  galvanic  irri- 
tability also  becomes  nil.  If  the  lesion  is  temporary  and  removable 
the  paralyzed  muscles  begin  to  regain  their  power,  and  within  a 
short  time  the  electrical  reactions  show  improvement  and  gradually 
return  to  the  normal.  The  response  to  faradism,  which  is  composed 
of  a  number  of  excessively  short  rapid  currents,  is  the  first  to  disap- 
pear, because,  as  the  nerve  fibres  degenerate,  it  requires  a  current  of 
relatively  long  duration  to  stimulate  them — conditions  better  ful- 
filled by  the  continuous  galvanic  flow.  The  reactions  depending 
upon  the  strength  of  the  current  are  quantitative ;  those  involving 
polar  changes  and  altered  character  of  muscular  contraction  are 
qiialitative. 

The  reaction  of  degetieration  may  be  epitomized  as  presenting : 
With  faradic  current — no  response.  With  galvanic  current — slug- 
gish contraction  (by  far  the  most  important  sign)  and  as  good  or 
better  response  to  positive  than  to  negative  pole. 

(3)  As  the  peripheral  nerves  do  not  degenerate  unless  they  or 
their  cell  bodies  are  diseased  (in  other  words,  unless  there  are  lesions 
of  the  lower  motor  neurone),  if  one  finds  that  the  muscles  respond  to 
faradism,  and  that  the  galvanic  reactions  are  normal,  he  can  exclude 
diseases  of  the  anterior  horns  and  roots  and  the  peripheral  nerves, 
but  can  not  negative  even  extensive  disease  of  the  higher  (central) 
nervous  system.  If  the  reactions  of  degeneration  are  found,  he  can 
exclude  disease  of  the  brain,  functional  paralysis,  and,  because  of  the 
fact  that  DeR  occurs  very  late  in  the  disease,  primary  affections  of 
the  muscles  (dystrophies) ;  and  can  aflBnn  disease  of  the  anterior 
horns  and  roots  or  the  peripheral  nerves. 

VASOMOTOR  AND  TROPHIC   DISTURBANCES 
Vasomotor  Disturbances. — The  vasomotor  nerves  may  be 

paralyzed  or  irritated. 

Vasomotor  paralysis    {angioparalysis)   allows   the   arterioles  to 

dilate,  whereby  the  capillaries  of  the  part  supplied  become  distended 


550  THE   EVIDENCES  OF   DISEASE 

with  blood  and  the  circulation  is  increased.  The  objective  evidence 
of  vasomotor  paralysis,  therefore,  is  a  more  or  less  marked  redness 
of  the  cutaneous  surface  involved,  attended  not  only  by  a  subjective 
but  by  an  actual  increase  of  temperature. 

Vasomotor  irritation  resulting  in  a  contraction  or  spasm  [angio- 
spasm) of  the  arterioles  is  evidenced,  according  to  its  degree,  by 
pallor,  blueness  (local  asphyxia),  or  mottling  of  the  skin,  with  cold- 
ness (subjective  and  actual),  formication,  or  actual  pain.  If  the  con- 
striction of  the  vessels  is  extreme,  gangrene  may  occur,  as  in  some 
instances  of  Raynaud's  disease.  Angio-ataxia  or  vasomotor  ataxia  is 
a  condition  of  unstable  tension  in  which  there  are  more  or  less  rapid 
variations  and  irregularities  in  the  tone  of  the  vessels,  spasm  alter- 
nating with  paralysis. 

As  the  vasomotor  nerves  belong  for  the  most  part  to  the  sympa^- 
thetic  system,  and  the  latter  is  simply  a  division  of  the  peripheral 
nervous  apparatus,  receiving  its  motor  fibres  from  the  brain,  medulla, 
and  cord,  angioparalysis  or  angiospasm  may  result  from  various 
lesions  of  the  cerebrum,  medulla,  spinal  cord  or  sympathetic  nerves. 
Angio-ataxia  is  one  symptom  of  neurasthenia,  hysteria,  exophthalmic 
goitre,  the  menopause,  and  the  lesser  conditions  of  depressed  and 
irregular  nervous  action. 

Trophic  Disturbances. — Whether  or  not  there  are  nerve  cells 
and  fibres  devoted  exclusively  to  the  control  of  nutritive  influences 
is  still  an  open  question.  K^evertheless  there  are  numerous  trophic 
disturbances  Avhich  result  from  and  indicate  disease  of  the  nervous 
system.  Some  of  these  involve  also  vasomotor  irregularities.  The 
more  important  trophic  disturbances  are  the  atrophy  of  muscles 
from  disease  of  the  cranial  nuclei  or  anterior  horns  of  the  spinal 
cord,  facial  hemiatrophy,  myxoedema,  cretinism,  acromegaly,  urti- 
caria, angioneurotic  oedema,  erythema  exudativum,  acute  bedsores, 
scleroderma,  morphoea,  vitiligo,  herpes  zoster,  and  glossy  (atrophied) 
skin,  as  well  as  changes  in  the  nails  and  hair. 

CRANIAL    NERVE    FUNCTIONS 

An  important  part  of  the  examination  of  a  case  of  nervous  dis- 
ease relates  to  disturbances  of  the  functions  of  the  cranial  nerves. 
The  condition  of  each  nerve  is  indicated  by  the  manner  in  which  it 
performs  its  functions,  as  follows.  Disturbances  of  certain  cranial 
nerves  have  been  described  elsewhere. 

First  or  Olfactory  Nerve. — See  Sense  of  Smell,  page  216. 

Second  or  Optic  Nerve. — See  Vision,  page  202. 

Third  or  Oeulo-motor  Nerve. — See  Ocular  Paralyses,  page  198. 

Fourth  Nerve  or  Patheticus. — See  Ocular  Paralyses,  page  198. 


CRANIAL  NERVE  FUNCTIONS 


651 


Trigem. 


Trigem.  II 
Trigem.  Ill 


Fifth  Nerve  or  Trigeminus. — The  motor  portion  of  the  trigeminus 
supplies  the  muscles  of  mastication,  viz.,  the  two  pterygoids,  the 
temporal,  masseter,  mylohyoid,  and  anterior  belly  of  the  digastric. 

The  sensory  portion  of  the  tri- 
geminus affords  sensation  to  the 
face,  conjunctiva, nose,  frontal  and 
maxillary  sinuses,  teeth,  palate, 
tongue,  part  of  upper  pharynx, 
external  auditory  meatus,  and  the 
scalp  as  far  back  as  the  vertex 
(Fig.  204).  It  may  or  may  not 
supply  the  sense  of  taste  on  the 
anterior  two  thirds  of  the  tongue 
(Fig.  39). 

To  Test. — The  motor  functions 
of  the  trigeminus  are  tested  by  de- 
siring the  patient   to   clinch  the 
teeth  firmly,  while  the  temporal 
and  masseter  muscles  are  palpated 
in  order  to  observe  their  contrac- 
tion.    Also  desire  the  patient  to 
open  his  month.     If  the  muscles 
on  one  side  fail  to  contract,  and 
the   opened  jaw  deviates  toward 
the  paralyzed  side,  there  is  uni- 
lateral paralysis  due  to  disease  af- 
fecting at  least  the  motor  fibres 
of  the  inferior  maxillary 
division  of   the    trigemi- 
nus.   Spasm  of  these  mus- 
cles   constitutes   trismus 
or  lockjaw  («/.  v.). 

The  sensory  functiotis 
of  the  trigeminus  are  ex- 
amined in  the  ordinary  Tngem.  iii 
manner.  Whether  one 
or  all  of  its  divisions  are 
involved  may  be  deter- 
mined by  comparing  the 
areas  of  anaesthesia  found 
with  the  cuts  showing  its 

distribution.     If  there  is  complete  unilateral  anaesthesia  the  patient 
when  drinking  can  feel  the  contact  of  the  cup  or  glass  on  one  side 


Trigem. 


Trigem.  U 


FiQ.  204.- 


-Showing  sensory  supply  of  skin  of  face 
and  liead. 


552  THE  EVIDENCES  OF   DISEASE 

only,  affording  a  sensation  as  if  half  the  vessel  was  missing.  As  the 
sense  of  taste  is  partly  conducted  through  the  medium  of  the  trigem- 
inus, it  also  should  be  examined.  There  are  certain  inflammatory 
(herpes  zoster),  vasomotor  (flushing,  pallor),  and  secretory  (lachry- 
mation,  salivation)  disturbances  which  may  arise  from  disease  of  this 
nerve,  because  of  the  fact  that  it  supplies  the  lachrymal  and  salivary 
glands  with  secretory  fibres  and  is  also  the  channel  by  wliich  vaso- 
motor fibres  run. 

The  trigeminal  nerve  is  involved  in  neuralgias  and  migraine. 
Trigeminal  anaesthesia  is  seen  in  hysteria  and  in  various  forms  of 
organic  disease  involving  the  cranial  nerve  centres. 

Sixth  Nerve  or  Abducens. — See  Ocular  Paralyses,  page  198. 

Seventh  or  Facial  Nerve.— See  Facial  Paralysis,  page  169. 

Eighth  or  Auditory  Nerve. — To  Test. — Disturbance  of  the  auditory 
portion  of  the  nerve  requires  an  examination  of  the  power  of  hear- 
ing {q.  V.)  and  an  inquiry  as  to  the  presence  of  tinnitus  {q.  v.).  Dis- 
turbance of  the  space  sense  is  manifested  by  vertigo  {q.  v.). 

Ninth  or  Glossopharyngeal  Nerve. — The  glossopharyngeal  (in 
connection  with  the  vagus)  is  motor  for  the  pharyngeal  muscles  and 
the  esophagus.  Its  sensory  functions  are  to  supply  the  sense  of  taste 
to  the  posterior  third  of  the  tongue,  as  well  as  general  sensation  to 
the  upper  part  of  the  larynx,  and,  together  with  the  vagus,  to  the 
tonsils  and  pharynx. 

To  Test. — Examine  the  sense  of  taste  {q.  v.),  the  sensibility  of  the 
pharynx  {q.  v.),  and  ascertain  the  presence  of  dysphagia  {q.  v.)  and 
globus  hystericus  (q.  v.). 

Tenth  Nerve  or  Pneumogastric,  and  the  Spinal  Accessory.— (1) 
Functions  of  the  Tenth  and  Eleventh  Nerves. — The  vagus  plus  the 
accessory  part  of  the  spinal  accessory  is  motor  for  the  soft  palate, 
pharynx  and  larynx,  as  well  as  the  air  passages,  heart  and  abdomi- 
nal viscera.  The  sensory  supply  of  the  vagus  has  to  do  with  the 
sensations  from  the  pharynx,  larynx,  trachea  and  esophagus.  The 
spinal  part  of  the  spinal  accessory  is  the  motor  nerve  of  the  sterno- 
mastoid  and  upper  part  of  the  trapezius  muscles.  Physiologically  it 
is  a  motor  cervical  nerve,  while  the  accessory  portion  is  a  part  of  a 
cranial  nerve — i.  e.,  the  pneumogastric. 

(2)  To  Test. — The  yagnsjjlus  the  accessory  portion  of  the  eleventh 
nerve  is  examined  mainly  by  determining  the  condition  of  its  motor 
and  sensory  branches.  To  determine  its  motor  condition,  ascertain 
whether  the  objective  and  other  signs  of  paralysis  of  the  palate  (q.  v.), 
pharynx  {q.  v.)  and  laryngeal  muscles  (q.  v.)  are  present.  Inquire 
also  for  the  existence  of  laryngeal  spasm  (laryngismus  stridulus, 
laryngeal  crises)  or  pharyngeal  spasm  (dysphagia  from  spasm  of  the 


CEREBRAL   LOCALIZATION  653 

pharyngeal  constrictors).  Disorder  of  the  cardiac  branches  is  mani- 
fested by  altered  rhythm  and  rapidity  of  the  pulse  {q.  v.)  ;  of  the  pul- 
monary branches  by  alterations  in  the  respiratory  rhythm  {q.  v.);  of 
the  esophageal  and  gastric  branches  by  esophageal  spasm,  and  at- 
tacks of  vomiting  or  gastric  crises.  It  is  to  be  borne  in  mind  that 
the  lesion  (or  irritation)  causing  the  symptoms  just  mentioned  may 
concern  the  peripheral  portion  of  the  nerve,  but  more  commonly, 
perhaps,  involves  its  nuclei. 

The  sensory  condition  of  the  nerve  is  determined  by  ascertaining 
the  presence  of  anaesthesia  (rarely  hyperaesthesia)  of  the  larynx  {q.  v.) ; 
and  the  presence  of  unpleasant  cardiac  sensations  or  neuroses. 

The  spinal  portion  of  the  eleventh  nerve,  being  purely  motor,  is 
tested  by  ascertaining  the  presence  of  paralysis  or  spasm  (wryneck, 
q.  V.)  of  the  sterno-mastoid  muscle,  and  paralysis  of  the  upper  por- 
tion of  the  trapezius. 

Twelfth  or  Hypoglossal  Nerve. — See  Paralysis  of  Tongue. 

CEREBRAL  LOCALIZATION 

A  brief  statement  of  the  main  facts  in  regard  to  the  localization 
of  functions  in  the  brain  is  here  given.  (See  Figs.  42,  43,  and  44.) 
As  some  of  the  convolutions  have  two  or  more  synonyms,  the  indif- 
ferent use  of  which  may  cause  confusion,  a  brief  list  of  equivalent 
names  is  here  given  for  reference.  The  bracketed  terms  are  synony- 
mous. 

CONYOLUTIOKS   OR    GyRI 


First  frontal  convolution. 
Superior  frontal  convolution. 
Gyrus  frontalis  superior. 

Second  frontal  convolution. 
Middle  frontal  convolution. 
Gyrus  frontalis  medius. 

Third  frontal  convolution. 
Inferior  frontal  convolution. 


Anterior  central  convolution. 
Precentral  convolution. 
Ascending  frontal  convolution. 
Gyrus  centralis  anterior. 

r  Posterior  central  convolution. 
Postcentral  convolution. 
Ascending  parietal  convolution. 
Gyrus  centralis  posterior. 


Gyrus  frontalis  inferior.  (  First  occipital  convolution. 

Quadrate  lobule.  ^  Superior  occipital  convolution. 

Praeoimeus.  f  Second  occipital  convolution. 

Fusiform  lobe.  ^  Middle  occipital  convolution. 

Lateral  occipito-temporal  lobe,  f  Third  occipital  convolution. 

Linffual  lobe  ^  Inferior  occipital  convolution. 
Median  occipito-temporal  lobe. 


554  THE  EVIDENCES  OF   DISEASE 

Fissures  or  Sulci 
f  Fissure  of  Rolando.  f  Postcentral  fissure. 


L  Central  fissure.  t  Sulcus  retro-centralis. 

f  Interparietal  fissure.  f  First  temporal  fissure. 

[  Parietal  fissure.  [  Parallel  fissure, 

f  Second  temporal  fissure. 
[  Middle  temporal  fissure. 

Frontal  Lobes. — That  portion  of  the  frontal  lobes  lying  anterior 
to  the  precentral  convolution  probably  has  to  do  with  psychic  func- 
tions. Disease  of  this  part  of  the  brain  may  give  rise  to  irritability, 
mental  weakness,  and  loss  of  self-control. 

Central  Convolutions. — This  region  is  the  great  motor  area  of  the 
cortex  and  the  centre  for  the  cutaneous  sensations  of  the  portions  of 
the  body  whose  muscles  are  supplied  by  it — the  seiisori-motor  area. 
The  centre  for  the  leg  is  highest,  then  comes  that  for  the  arm,  and 
the  area  for  the  face  lies  lowest.  The  motor  centres  overlap  to  some 
extent,  the  sensory  areas  to  a  still  greater  extent,  thus  requiring  a 
much  more  widespread  lesion  of  this  part  of  the  cortex  to  cause 
anaesthesia  than  paralysis  of  an  extremity. 

It  is  to  be  borne  in  mind  that  while  many  muscles  are  innervated 
from  the  opposite  side  of  the  brain,  certain  groups  on  opposite  sides 
of  the  body  which  habitually  act  together  are  each  represented  in 
both  hemispheres.  These  are  the  muscles  of  respiration,  of  degluti- 
tion, of  the  vocal  cords  and  of  the  eyelids.  If  the  centre  in  one 
hemisphere  for  any  of  these  is  destroyed  the  corresponding  centre 
in  the  opposite  side  of  the  brain  is  competent  to  carry  on  the  action, 
and  paralysis  does  not  result. 

Internal  Capsule. — Through  the  capsule  pass  the  great  majority 
of  the  motor  and  sensory  fibres  connecting  the  cerebral  cortex  with 
the  periphery.  Its  functions  are  shown  in  Fig.  162.  It  will  be 
observed  that  through  the  knee  and  the  anterior  two  thirds  of  the 
posterior  limb,  or  thalamo-lenticular  portion,  pass  the  motor  fibres ; 
while  the  sensory  fibres,  including  the  visual  and  auditory,  traverse 
the  posterior  portion  of  the  thalamo-lenticular  portion  and  the  pos- 
terior third,  or  retrolenticular  portion,  of  the  posterior  limb. 

Crura. — By  way  of  the  crura  the  fibres  from  the  internal  capsule 
pass  down.  In  the  substance  of  the  crus  run  the  3d  and  4th  cranial 
nerves,  and  the  optic  tract  crosses  it. 

Pons. — The  pons  contains  the  nuclei  of  certain  cranial  nerves ; 
the  tracts  from  the  cortex  by  way  of  the  crura  pass  through  it ;  and 
its  transverse  fibres  connect  the  two  hemispheres  of  the  cerebellum. 


LOCALIZATION    OF  LESIONS  IN  BRAIN  AND  CORD  555 

Medulla. — In  the  medulla  are  the  nuclei  of  certain  cranial  nervea 
and  the  vasomotor,  secretory,  visceral,  respiratory  and  cardiac  reflex 
and  automatic  centres. 

Cerebellum. — The  cerebellum  is  so  connected  with  the  cerebrum, 
pons,  spinal  cord  and  auditory  nerve  that  it  receives  and  sends 
impulses  which  regulate  the  higher  automatic  and  reflex  actions  and 
the  maintenance  of  bodily  equilibrium. 

Special  Senses. — The  sense  of  hearing  has  its  primary  (basal) 
centre  in  the  posterior  tubercle  of  the  corpora  quadrigemina  and  the 
internal  geniculate  body ;  its  secondary  (cortical)  centre  in  the  first 
and  second  temporal  convolutions.  The  sense  of  vision  has  its 
primary  centre  in  the  posterior  portion  of  the  optic  thalamus,  the 
external  geniculate  body,  and  the  anterior  corpora  quadrigemina ;  its 
cortical  centre  in  the  cuneus  and  calcarine  fissure.  The  sense  of 
smell  has  its  primary  centre  in  the  olfactory  lobes ;  its  cortical  centre 
is  supposed  to  be  in  the  uncus  and  hippocampal  convolution.  The 
sense  of  taste  has  its  cortical  centre  in  the  hippocampal  convolution ; 
the  primary  centre  is  unknown. 

Memory  Cetitres. — These  have  been  described  in  connection  with 
aphasia  {q.  v.). 

Latent  Areas. — There  are  certain  portions  of  the  brain  which,  if 
destroyed  or  irritated  by  disease,  do  not  afford  definite  motor,  sen- 
sory, or  other  symptoms.  These  are  the  anterior  portion  of  the 
frontal  lobe,  portions  of  the  temporal  lobes,  part  of  the  inferior 
parietal  lobule,  portions  of  the  centrum  ovale,  the  corpora  striata, 
the  optic  thalami,  and  the  lateral  hemispheres  of  the  cerebellum. 

SUMMARY  OF  VARIOUS  DIAGNOSTIC  POINTS  BEAR- 
ING UPON  THE  NATURE  AND  LOCATION  OF  CERE- 
BRAL AND  SPINAL   LESIONS 

It  is  convenient  and  useful,  from  a  diagnostic  point  of  view,  to 
epitomize  some  of  the  statements  scattered  through  previous  pages 
with  regard  to  the  bearing  of  various  combinations  of  paralysis, 
anaesthesia  and  other  symptoms  upon  the  nature  and  localization  of 
lesions  of  the  brain  and  spinal  cord. 

(\)  Paralysis,  if  hemiplegic  or  at  least  unilateral,  is  almost  invariably  of 
cerebral  origin.  Light  may  be  thrown  upon  the  nature  of  the  cerebral  lesimi 
by  ascertaining  the  symptoms  preceding  and  the  mode  of  onset  of  the  paraly- 
sis, which  may  correspond  with  one  of  the  following  symptom  groups:  (a),  (ft), 
(c),  Ul),  and  (e). 

(a)  Haemorrhage,  Embolism,  or  Thrombosis. — If  due  to  these  causes  the 
paralysis  is  preceded  by  apoplectic  symptoms,  viz.,  sudden  coma  or  convul- 
sions, with  subsequent  hemiplegia,  accompanied  or  not  by  aphasia.     Hsemor- 


550  THE  EVIDENCES  OF   DISEASE 

rhage  requires  the  presence  of  arteriosclerosis  and  miliary  aneurisms;  embo- 
lism the  presence  of  left-side  heart  lesions ;  thrombosis  the  presence  of  arterio- 
sclerosis or  obliterating  sj'philitic  endarteritis. 

(b)  Brain  Tumour. — The  paralyfeis  is  preceded  by  more  or  less  prolonged  and 
progressive  general  symptoms,  viz.,  headache,  vertigo,  vomiting,  optic  neuri- 
tis, and  mental  defects. 

(c)  Syphilis  of  the  Brain.  — This  affords  a  history  of  severe  and  persistent 
headache,  with  vertigo,  nausea,  vomiting,  epileptiform  convulsions,  and  apo- 
plectiform attacks,  which  are  followed  by  various  paralyses  (hemiplegia,  paraly- 
ses of  the  cranial  nerves,  especially  the  ocular).  These  symptoms  are  usually 
due  to  a  gummatous  meningitis  affecting  the  base  of  the  brain. 

(d)  Abscess  of  the  Brain. — There  is  a  history  of  antecedent  head  injury  or 
suppurative  disease  of  ear,  nose,  or  lung,  followed  by  headache,  vomiting,  ver- 
tigo, delirium  or  mental  dulness,  optic  neuritis,  local  tenderness  and  heat  of 
scalp,  septic  symptoms  with  or  without  irregular  fever,  and  a  slow  pulse. 

(«)  Hysteria. — Peculiar  emotional  manifestations  (laughing,  crying,  globus 
hystericus),  the  presence  of  stigmata,  such  as  anjesthesias,  contraction  of  the 
visual  fields,  and  other  hysterical  manifestations,  together  with  the  age  and  sex 
of  the  patient,  may  enable  a  recognition  of  the  functional  nature  of  the  paralysis. 

(2)  Hemiplegia  is  almost  invariably  of  cerebral  origin. 

(3)  Evanescent  or  temporary  hemiplegia  may  be  due  to  embolism  or  throm- 
bosis and  premonitory  of  a  more  severe  attack ;  or  to  uraemia ;  or  occur  in  the 
extreme  weakness  of  the  final  stages  of  carcinoma  and  phthisis. 

(4)  Hemiplegia  in  young  adults  should  arouse  a  strong  suspicion  of  sy])liilis. 

(5)  Hemiplegia  which  disappears,  leaving  only  a  monoplegia,  may  be  due 
in  rare  instances  to  a  lesion  of  the  entire  motor  cortex  of  one  side. 

(6)  Ordinary  hemiplegia  (face,  arm,  and  leg  on  the  same  side)  is  most  fre- 
quently caused  by  a  lesion  of  the  posterior  limb  of  the  internal  capsule  (B  and 
G,  Fig.  191).  If  the  paralysis  is  permanent  the  motor  tract  is  destroyed  ;  if 
temporary,  the  lesion  is  slight  or  the  capsule  has  been  functionally  affected, 
perhaps  by  disease  in  its  neighbourhood.  Comjilete  hemiplegia  is  very  rarely 
of  cortical  origin,  implying  as  it  does  a  very  extensive  lesion. 

(7)  If  in  a  hemiplegia  the  arm  is  paralyzed  to  a  much  greater  extent  thau 
the  leg,  with  little  or  no  anaesthesia,  the  lesion  is  in  the  anterior  portion  of  the 
posterior  limb  of  the  internal  capsule  {G,  Fig.  191). 

(8)  If  in  a  hemiplegia  the  leg  has  lost  its  power  to  a  much  greater  extent 
than  the  arm,  and  with  it  is  found  hemianaesthesia,  hemiopia.  and  disturbances 
of  hearing,  perhaps  &\So  of  taste  and  smell,  the  lesion  is  well  back  in  the  pos- 
terior third  of  the  posterior  limb  of  the  internal  capsule  {G,  Fig.  191). 

(9)  Paralysis  of  the  face  and  leg  on  the  same  side,  the  arm  escaping,  is  a 
rare  combination,  due  to  an  irregular  linear  lesion  of  the  internal  capsule,  the 
line  of  the  lesion  curving  in  such  a  manner  as  to  pass  outside  of  the  arm  fibres. 

(10)  Hemiplegia  plus  hemiathetosis,  hemichorea  (post-hemiplegic),  or 
marked  tremor,  indicates  a  lesion  of  the  internal  capsule  involving  the  optic 
thalamus  ((?,  Fig.  191). 

(11)  Hemiplegia  of  one  side  with  paralysis  of  the  oculo-motor  nerve  on  the 
opposite  side  (crossed  or  alternating  ocular  paralysis),  perhaps  also  with  hemio- 
pia, indicates  a  lesion  of  the  crus  cerebri  ( C,  Fig.  191). 


LOCALIZATION  OP  LESIONS  IN  BRAIN  AND  CORD  557 

(12)  Hemiplegia  of  one  side  -with  paralysis  of  the  face  on  the  opposite  side 
(alternating  or  crossed  facial  paralysis)  indicates  a  lesion  of  the  lower  pons 
(/>,  Fig.  191). 

(13)  Hemiplegia  (right)  with  motor  aphasia  indicates  a  lesion  involving  the 
third  left  frontal  convolution. 

(14)  Hemiplegia  witli  speech  disturbances  (anarthria,  not  aphasia)  and  diffi- 
culty in  swallowing  indicates  a  lesion  of  the  medulla. 

(15)  Paralysis  of  the  face  and  arm  or  arm  and  leg  (associated  monoplegias) 
may  in  some  cases  be  due  to  a  lesion  of  the  cortex  involving  these  neighbour- 
ing centres.  If  the  paralysis  is  of  the  face  and  arm  on  the  right  side,  motor 
aphasia  may  also  be  present. 

(16)  Oculo-motor  paralysis  of  one  side  with  loss  of  weight  sense  and  posture 
sense  on  the  opposite  side  of  the  body  (hemiataxia )  is  suggestive  of  a  lesion  of 
the  tegmentum  of  the  crus  on  tRe  same  side  as  the  ocular  paralysis. 

(17)  If  a  paralyzed  limb  exhibits  convulsive  movements  from  time  to  time, 
or  if  a  convulsed  muscle  becomes  powerless,  it  may  indicate  a  progressive  lesion 
(tumour,  localized  meningitis,  small  haemorrhage,  or  abscess)  of  that  part  of  the 
cortex  from  which  the  limb  or  muscle  receives  its  motor  fibres. 

(18)  A  sense  of  motion,  pain,  or  tingling  preceding  a  localized  spasm  of  an 
extremity  (Jafcksonian  epilepsy)  is  a  "signal  symptom  "  indicating  the  cortical 
seat  of  the  causative  lesion. 

(19)  Paraplegia  of  the  spastic  (cerebral)  type  is  almost  invariably  due  to  a 
spinal  lesion  involving  the  motor  tracts  (F,  Fig.  191). 

Paraplegia  of  the  flaccid  (atrophic,  spinal)  type  may  be  due  to  spinal-cord 
lesions  (anterior  horns.  Fig.  197;  and  E,  Fig.  191)  or  lesions  of  the  peripheral 
nerves  (neuritis,  Fig.  197).  If  bladder  or  rectal  disturbances  are  present  the 
paraplegia  is  almost  always  caused  by  lesions  of  the  cord. 

(20)  Monoplegia,  local  and  multiple  paralysis  may  be  caused  by  either  cere- 
bral or  spinal-cord  disease,  or  disease  of  the  peripheral  nerves.  If  the  paraly- 
sis is  due  to  a  cerebral  lesion,  the  latter  is  almost  always  cortical  (A,  Fig.  191) ; 
if  to  a  spinal-cord  lesion  it  is  almost  invariably  an  affection  of  the  anterior 
horns. 

(21)  To  determine  whether  a  localized  paralysis  is  due  to  a  lesion  of  the 
spinal  cord  or  to  a  lesion  of  the  peripheral  nerves : 

(a)  If  the  paralysis  is  preceded  by  a  history  of  exposure  to  cold  or  trauma, 
it  is  probably  peripheral. 

(5)  If  the  paralyzed  muscles  and  the  associated  area  of  anaesthesia  correspond 
to  the  area  of  distribution  of  one  (or  more)  individual  cerebro-spinal  nerves, 
the  paralysis  is  due  to  disease  of  the  nerve  (or  nerves). 

(c)  If  the  paralysis  and  anaesthesia  correspond  to  tlie  segmentary  representa- 
tion in  the  cord,  the  lesion  is  in  the  latter. 

(22)  Lateral  deviation  of  the  tongue  when  protruded,  or  an  inability  to 
move  it  freely  to  the  same  side,  indicates  paralysis  of  one  hypoglossal  nerve. 

(23)  Anarthria,  dysphagia,  bilateral  atrophy  of  the  tongue,  lips,  palate  and 
throat  mu.scles  indicates  a  lesion  of  the  medulla  (bulbar  paralysis). 

(24)  Anarthria — disturbances  of  speech  involving  the  muscles  of  articula- 
tion— is  to  be  distinguished  from  aphasia  in  which  the  muscular  apparatus  is 
intact  but  the  cerebral  centres  are  affected. 


558  THE  EVIDENCES  OF   DISEASE 

(25)  A  purely  motor  aphasia  indicates  a  lesion  of  the  third  frontal  convolu- 
tioQ. 

(26)  If  the  muscles  of  mastication  are  paralyzed  it  indicates  a  lesion  of  the 
motor  (inferior  maxillary)  division  of  the  trigeminus. 

(27)  Paralysis  of  the  sterno-mastoid  and  upper  portion  of  the  trapezius  im- 
plies a  lesion  of  the  spinal  portion  of  the  spinal  accessory. 

(28)  Marked  and  more  or  less  rapid  muscular  atrophy  occurs  in  all  lesions 
of  the  lower  neurone  (anterior  horn  cells,  cranial  nuclei,  and  their  peripheral 
fibres) ;  it  does  not  occur  in  disease  of  the  motor  tract  above  the  anterior  horn 
cells  and  cranial  nuclei,  or  in  muscular  dystrophies  and  functional  paralyses. 

(29)  Hemianaesthesia  of  the  skin  and  the  special  sense  organs  is  due  to  a 
lesion  well  back  in  the  posterior  limb  of  the  internal  capsule  (G,  Fig.  191)  or, 
more  commonly,  to  hysteria. 

(30)  Partial  (limited  to  a  part  of  one  side  of  the  body)  hemianaesthesia  with 
partial  hemiplegia  on  the  opposite  side  is  found  in  unilateral  lesions  of  the 
spinal  cord. 

(31)  In  transverse  cord  lesions  the  paralysis  and  anaesthesia  below  the  lesion 
are  due  to  the  destruction  of  the  columns  or  tracts  which  should  transmit  volun- 
tary impulses  and  sensory  impressions  to  and  from  the  parts  which  have  been 
cut  off  (F,  Fig.  191). 

(32)  Disease  of  the  cervical  cord  will  cause  sensory  disturbances  in  the  fin- 
gers, hand,  and  arm ;  of  the  dorsal  cord,  in  the  back,  trunk,  and  thighs ;  of  the 
lumbar  cord,  in  the  feet  and  legs. 

(33)  In  transverse  lesions  of  the  spinal  cord  the  anaesthesia  begins  at  a  level 
three  or  four  inches  below  the  lesion  in  the  cord. 

(34)  If  paralysis  is  suspected  to  be  of  cortical  origin  the  presumption  is 
strengthened  by  the  existence  of  paraesthesias  and  vasomotor  disturbances  in 
the  paralyzed  part. 

(35)  Disturbances  of  taste  in  the  posterior  part  of  the  tongue  indicate  a 
lesion  of  the  glossopharyngeal  nerve. 

(36)  In  anaesthesia  of  cerebral  origin  the  reflexes  are  preserved  although 
the  patient  may  not  feel  the  touch  which  causes  them. 

(37)  Hemiopia  may  be  due  to  a  lesion  of  the  occipital  lobe,  the  pulvinar  of 
the  optic  thalamus,  the  anterior  corpora  quadrigemina,  or  optic  tract ;  or,  with 
associated  hemianaesthesia,  to  a  lesion  of  the  internal  capsule.     See  (8)  and  (29). 

(38)  Word  deafness  is  due  to  a  lesion  of  the  first,  and  a  part  of  the  second, 
temporal  convolution. 

(39)  The  preservation  of  the  knee  jerk  does  not  forbid  the  presence  of 
poliomyelitis,  as  the  lesion  may  lie  at  a  higher  jioint  than  the  knee-jerk 
centre. 

(40)  Ataxia  of  the  cerebellar  type,  drunken,  staggering  gait,  with  little  or 
no  ataxia  of  the  extremities  while  lying  in  bed,  with  vertigo,  vomiting,  head- 
ache, optic  neuritis,  and  forced  movements,  is  indicative  of  a  lesion  of  the  ver- 
mis or  middle  lobe  of  the  cerebellum,  usually  a  tumour. 

(41)  Ataxia  of  the  cerebellar  type  plus  ocular  paralysis,  auditory  disturb- 
ances and  paralysis  of  the  muscles  of  mastication,  points  to  a  lesion  of  the 
corpora  quadrigemina. 

(42)  In  endeavouring  to  determine  the  site  of  lesions  in  the  brain  and  spinal 


EXAMINATION  OF  THE  BLOOD  559 

cord  it  is  helpful  to  prepare  a  written  summary  of  the  signs  and  symptoms,  to 
be  compared  with  the  various  tables  referring  to  motor  and  sensory  spinal  locali- 
zation. 


SECTION  XXXVIII 
EXAMINATION   OF  THE  BLOOD 

A  PROPER  clinical  examination  of  the  blood  is  in  all  cases  useful, 
and  in  some  indispensable,  for  diagnosis.  A  full  and  scientific  ex- 
amination reveals  certain  facts,  as  yet  of  little  or  no  clinical  value, 
and  does  not  fall  within  the  scope  of  this  volume. 

THE    TECHNIC    OF    THE    CLINICAL    EXAMINATION 
OF    THE    BLOOD 

The  most  important  diagnostic  facts  to  be  obtained  by  an  exami- 
nation of  the  blood  relate  to  : 

1.  The  number  of  red  cells  (erythrocytes)  and  white  cells  (leuco- 
cytes). 

2.  The  amount  of  haemoglobin  or  (what  is  equivalent)  the  specific 
gravity  of  the  blood. 

3.  The  size  and  shape  of  the  cells,  especially  of  the  erythrocytes. 

4.  The  varieties  and  relative  number  of  each  variety  of  the  leuco- 
cytes as  revealed  by  staining  methods. 

5.  The  presence  of  parasitic  micro-organisms. 

The  haemanalysis  card  and  chart  devised  by  De  Forest  are  ex- 
tremely useful  for  purposes  of  observation  and  record  (Chart  IX). 

Counting  the  Red  Cells. — For  this  purpose  the  Thoma-Zeiss 
haemocytometer  is  to  be  used.  This  apparatus  consists  of  two  mixing 
pipettes  (one  for  the  red,  and  one  for  the  white,  cells)  and  a  count- 
ing slide  (Figs.  205,  206,  and  207). 

The  lobe  of  the  ear,  rather  than  the  finger,  should  be  chosen  as 
the  site  of  the  blood-obtaining  puncture.  As  an  invariable  prelimi- 
nary, ascertain  whether  or  not  the  patient  is  a  bleeder.  If  haemo- 
philia be  present  a  very  slight  puncture  will  suffice.  Cleanse  the 
lobe  of  the  ear  with  soap  and  water,  or  with  a  mixture  of  alcohol  and 
ether,  drying  it  with  brisk  rubbing  so  that  it  may  l)ecome  hyperaemic. 
A  3-sided  (glover's)  or  spear-pointed  needle  may  be  used.  Holding 
the  lobe  of  the  ear  firmh'  with  the  fingers  of  the  left  hand,  stab  its 
lower  border  quickly  (thus  inflicting  less  pain  than  by  a  slow  punc- 
ture) to  the  depth  of  ^  to  :^  of  an  inch.     Do  not  squeeze  the  lobe  to 


lAME 


120% 

6,000,000 

100% 

S/K>0,000 

ao% 

4,000.000 

60% 

3,000,000 

40% 

2,000,000 

20% 

1,000  X>00 

10% 

V    600 .000 

8% 

400,000 

6% 

300,000 

«% 

200,000 

2% 

100,000 

90,000 

60,000 

70,000 

60  ,000 

1% 

SO  ,000 

40,000 

30,000 

20,000 

10.000 

8.000 

6.000 

4,000 

2.000 

Chart  IX. — Blood  chart  and  hsemanalysis  card  for  recording  blood  examinations. 
560 


COUNTING  THE  RED  CELLS 


561 


cells 


make  it  bleed  (except,  perhaps,  to  start  the  flow)  as  the  blood  will 
then  be  diluted  by  lympli  from  the  surrounding  tissues  and  is  worth- 
less for  a  blood  count.  When  the  blood  issues  spontaneously  wipe 
away  the  first  3  or  4  drops.  Into  the  next  drop  insert  the  tip  of  the 
"  red  "  pipette  and  suck  up  blood  exactly  to  the  0.5  mark  ;  but  if,  as 
may  happen,  the  blood  column  slightly  overpasses  this  mark  it  may 
be  carried  down  by  gentle  blowing  or,  by  tapping  the  point  of  the 
tube  upon  a  towel  or  a  piece  of 
blotting  paper. 

It  is  now  requisite  to  dilute 
the  blood  with  the  following  so- 
lution (GowERs') : 

Sodium  sulphate.,  gr.  104 

Acetic  acid 3  v 

Distilled  water  to 

make 3  iv 

Wipe  the  pipette  clean  of 
blood,  immerse  its  tip  in  the  bot- 
tle of  solution  and  immediately  3 
suck  up  the  fluid  (meanwhile  roll-  For  white 
ing  the  pipette  between  finger 
and  thumb)  until  the  mixing 
chamber  is  filled  and  the  fluid 
reaches  the  mark  101.  The  dilu- 
tion will  be  1  :  200.  Xext  close 
the  ends  of  the  pipette  with  fin- 
ger and  thumb  and  shake  it  ac- 
tively for  one  minute  in  order  to 
thoroughly  mix  the  blood  and  the 
diluent,  the  little  glass  ball  in 
the  mixing  chamber  greatly  as- 
sisting. Then  blow  until  the 
clear  diluting  fluid  contained  in 
the  tube  below  the  mixing  chamber  is  expelled  and  3  or  4  drops  of 
the  mixed  blood  and  fluid  have  issued.  The  next  drop  may  be  placed 
upon  the  counting  slide. 

In  the  centre  of  this  slide  there  is  a  small  ruled  glass  disk,  sur- 
rounded by  a  trench  or  moat,  which  in  turn  is  bounded  by  a  wall  or 
slab  upon  which  rests  the  cover  glass  (Fig.  207).  The  relative  thick- 
ness of  the  disk  and  the  slab  is  such  that  the  distance  between  the 
upper  surface  of  the  disk  and  the  under  surface  of  the  cover  glass  is 
exactly  ^  millimetre.     Slide  and  cover  glass  must  be  thoroughly 


For  red 
cells 


Fig.  205. — Thoma-Zeiss  pipettes. 


562 


THE  EVIDENCES  OF   DISEASE 


clean  and  dry.  Upon  the  centre  of  the  disk  place  a  droplet  of  the 
diluted  blood  of  a  size  to  be  learned  by  experience.  The  usual  mis- 
take of  the  beginner  is  to  use  too  large  a  quantity.  Then  place  the 
cover  glass  in  position.  The  drop  should  almost  or  quite  cover  the 
disk,  but  if  it  spills  over  into  the  trench  the  slide  must  be  washed  and 

A.  Ruled  disk 


0.100  mm. 

4  00  ^"'• 


C .  Z  e  is  s 

Jena 


Fig.  206. — Thoma-Zeiss  counting  slide  (plan). 

a  new  drop  placed.  If  the  cover  glass  and  slide  are  quite  clean  and 
in  proper  contact  one  may  be  able  to  see  (by  looking  almost  horizon- 
tally) a  series  of  concentric  coloured  (Xewtonian)  rings  between  the 
cover  and  the  slab  upon  which  it  rests.  If  not  present  at  first,  they 
may  be  produced  by  slight  pressure  on  the  cover,  but  should  re- 
main visible  after  the  pressure  is  remitted.  Place  the  slide  upon  the 
stage  of  the  microscope  and  wait  2  or  3  minutes  for  the  corpuscles  to 
settle.  A  moderately  high  power,  with  a  rather  dim  illumination,  is 
desirable.     A  mechanical  stage,  while  not  a  necessity,  is  of  great 

,B   Cover  glass 


TW7777m-M 


w^ijjin, 


Ruled  disk  Moat 

Fig.  207. — Blood  counting  slide  (elevation). 

assistance  in  all  mechanical  work,  as  its  uniform  movement  is  less 
trying  to  the  eyes  and  therefore  tends  to  greater  accuracy. 

There  are  400  small  squares,  each  j\j  x  ^V  millimetre,  which,  by 
means  of  extra  vertical  and  horizontal  lines,  are  divided  into  16 
groups,  each  containing  16  squares  (Fig.  208).  If  the  corpuscles 
lying  in  each  of  the  16  small  squares  of  each  group  are  counted,  one 
will  have  traversed  16  X  16  ==  256  small  squares.  In  normal  blood 
diluted  in  the  proportion  here  employed  (1  :  200)  the  total  number 
of  corpuscles  counted  will  be  1,200  to  1,500,  and  the  chance  of  error 


COUNTING  THE  RED   CELLS  563 

will  not  be  over  2  to  3  per  cent  in  either  direction.  Some  haema- 
tologists  consider  a  count  of  100  small  squares  to  be  sufficient  for 
practical  purposes,  and  the  average  number  of  cells  to  each  square  is 
readily  obtained  by  placing  a  decimal  point.  The  squares  are  con- 
veniently counted  in  the  order  shown  in  Fig.  208.  Of  the  corpuscles 
which  lie  upon  the  line  between  2  small  squares,  one  should  count 
in  all  those  which  lie  upon  or  touch  the  upper  and  left-hand  lines  of 
each  square  as  indicated  in  the  same  figure. 


Fig.  208. — Showinjr  one  group  of  sixteen  small  squares,  inclosed  by  extra  vertical  and 
horizontal  lines ;  also^  by  the  dotted  angulated  arrow,  a  convenient  order  of  counting 
the  squares ;  also,  the  (shaded)  upper  and  left  lines,  cells  lying  on  which  should  be 
counted  as  in  the  square ;  also  (lower  part),  the  average  number  of  cells  to  each  square 
in  normal  blood  with  a  dilution  of  1  :  200 ;  and,  Anally,  the  method  of  measuring  the 
size  of  the  field  by  counting  the  number  (as  shown)  of  squares  in  its  horizontal  diameter, 
eacli  square  equalling  >/,o  millimetre. 

Having  ascertained  the  total  number  of  red  cells  contained  in 
256  squares,  divide  the  total  by  256,  which  gives  the  average  number 
of  cells  to  each  small  square.  In  normal  blood  this  average  is  6  or  7. 
As  the  blood  is  diluted  1  :  200  and  each  small  square  is  ^^  X  ^V  ^  sV 
mm.  =  1-4,000  cu.  millimetre,  the  average  number  is  to  be  multiplied 
by  800.000  (=  200  X  4,000),  which  gives  the  number  of  cells  in  a 
cubic  millimetre  of  blood.     To  summarize  : 

Divide  the  total  number  of  corpuscles  by  the  number  of  small 
squares  counted. 


564-  THE  EVIDENCES  OF  DISEASE 

Multiply  the  average  thus  obtained,  if,  as  presumed,  the  dilution 
is  1  :  200,  by  800,000.     If  the  dilution  is  1  :  100,  multiply  by  400,000. 

The  pipette  must  at  once  be  cleansed  by  sucking  into  and  blow- 
ing out  from  the  mixing  chamber  successively  water,  alcohol,  and 
*  ether,  and  finally  sucking  air  through  until  the  glass  ball  ceases  to 
adhere  to  any  part  of  the  wall  of  the  chamber.  If  this  precaution  is 
delayed  or  neglected  it  may  be  necessary  to  use  a  horsehair  or 
bristle  to  remove  coagulated  blood ;  or  in  bad  cases  to  dissolve  it 
away  with  strong  alkali  or  acid,  or  digest  it  out  with  a  solution  of 
pepsin. 

If  the  ruled  lines  on  the  disk  are  extremely  faint  they  may  be 
rendered  very  distinct  by  scraping  off  some  graphite  from  a  soft  lead 
pencil,  rubbing  the  powder  over  the  surface  of  the  disk,  and  then 
polishing  it  off  with  a  soft  handkerchief. 

As  a  rule  it  is  better  (in  counting  the  red  cells)  to  dilute  the 
blood  1  :  200  by  drawing  the  blood  to  the  0.5  mark,  than,  by  sucking 
blood  to  the  1  mark,  to  use  the  dilution  of  1  :  100. 

If  any*  difficulty  is  experienced  in  distinguishing  between  the  red 
and  white  cells,  the  lens  may  be  somewhat  raised  and  then  slowly 
focused  downward.  The  white  cells,  because  of  their  marked  re- 
frangibility,  will  early  become  conspicuous,  as  peculiarly  bright  and 
shining  spots.  If  it  is  desired  to  employ  a  diluting  fluid  which  will 
stain,  and  therefore  easily  differentiate,  the  leucocytes,  Toison's  solu- 
tion may  be  used.     Its  composition  is  as  follows  : 

Methyl  violet  5  B .025  grme. 

Sodium  chloride 1.000     " 

Sodium  sulphate 8.000  grmes. 

Xeutral  glycerine 30.000     " 

Distilled  water 160.000     " 

One  must  wait  8  to  10  minutes  after  mixing  to  allow  the  stain  to 
act.     The  pipette  is  cleaned  with  greater  difficulty. 

The  "  white "  pipette  may  also  be  used  for  counting  the  red 
cells  (Cabot)  by  drawing  the  blood  up  to  the  first  line  above  the  tip 
of  the  pipette  (i.  e.,  \  of  the  usual  distance)  and  then  sucking  the 
diluting  fluid  up  to  mark  11.  This  gives  a  dilution  of  1  :  100,  and 
the  calculation  must  be  made  accordingly. 

Counting  the  White  Cells. — If  the  leucocytes  are  greatly 
increased  in  number,  or  if  special  calculations  are  made,  they  may  be 
enumerated  with  the  "  red  '"  pipette.  Ordinarily  it  is  desirable  to  use 
the  "  white  "  pipette. 

The  technic  of  the  white  pipette  is  the  same  as  for  the  "  red," 
except  that,  as  its  calibre  is  greater,  a  much  larger  drop  (as  large  as 


COUNTING  THE   WHITE  CELLS  565 

will  stay  upon  the  ear  without  falling  off)  is  required ;  and  the 
pipette  must  be  kept  approximately  horizontal  or  its  contents  will 
flow  out.  Consequently  the  bottle  of  diluting  solution  must  be 
slanted  sidewise  while  the  solution  is  sucked  in.  Moreover,  a  much 
gentler  suction  is  to  be  employed  in  order  not  to  overshoot  the 
desired  mark.  In  using  the  white  pipette  the  degree  of  dilution  is 
either  1  :  20  or  1  :  10,  according  as  the  blood  is  drawn  to  the  0.5  or  1 
mark.     The  diluting  fluid  employed  in  counting  the  leucocjrtes  is  : 

Glacial  acetic  acid 0.3 

Distilled  water 100.0 

This  solution  renders  the  red  cells  almost  invisible  and  the  leuco- 
cytes more  distinct.  Some  observers  also  add  sufficient  of  an  aque- 
ous solution  of  methyl  green  to  make  the  diluting  fluid  of  a  markedly 
green  tint,  thus  causing  the  nuclei  of  the  white  cells  to  be  stained 
and  therefore  more  conspicuous. 

The  methods  and  calculations  involved  in  the  leucocyte  count  are 
somewhat  more  variable  and  confusing  than  with  the  red  cells.  Three 
of  the  most  convenient  and  serviceable  are  here  given  : 

(a)  First  Method  :  Using  the  "  White  "  Pipette. — Secure  a  dilution 

of  1 :  10  by  drawing  the  blood  up  to  the  mark  1.     Place  a  drop  upon 

the  ruled  disk  and  count  all  the  leucocytes  in  all  the  small  squares, 

of  which  there  are  400  in  the  entire  ruled  space.     Cleanse  the  slide 

and  repeat  the  count  with  a  second  drop.     Divide  the  total  number 

of  leucocytes  enumerated  by  the  number  of  squares  counted,  and 

multiply  the  quotient  by  4,000  (since  the  cubic  area  of  1  square  = 

j^j5^  cubic  millimetre),  and  this  in  turn  by  10 — i.  e,,  the  degree  of 

dilution  (1  :  10).     For  example,  suppose  the  blood  to  be  normal,  in 

which  case  about  70  leucocytes  will  have  been  found  in  each  set  of 

400  small  squares — i.  e.,  the  entire  ruled  space.     As  two  sets  of  400 

squares  have  been  gone  over  one  has 

Total  leucocvtes  140       ^_,_        j    ^-,^       .  r^r^r^ 

rr  ,  1  x."  11  ^KR  =  -175  :  and  .175  X  4,000  X  10  = 

Total  number  small  squares  800 

7,000,  the  number  of  leucocytes  in  1  cubic  millimetre  of  undiluted 
blood. 

{h)  Second  Method  :  Using  the  "  White  "  Pipette.— Another  sim- 
pler and  apparently  convenient  method  is  as  follows  (Ostheimer), 
omitting  the  mathematical  calculations  upon  which  it  is  based : 
Ascertain  the  number  of  small  squares  which  are  contained  in  the 
transverse  diameter  of  the  field  of  the  microscope  (Fig.  208),  if  neces- 
sary moving  the  sliding  tube  up  or  down  until  the  right  and  left 
edges  of  the  field  coincide  accurately  with  the  outer  boundary  lines 
of  the  two  outer  squares.  The  number  of  squares  contained  in  one 
38 


566  THE   EVIDENCES  OF   DISEASE 

diameter  of  the  field  will  of  course  vary  with  the  lenses  used  and 
the  distance  to  which  the  sliding  tube  is  drawn  out,  which  points 
must  be  noted.  Dilute  the  blood  1  :  20  (by  drawing  it  only  to  the 
0.5  mark),  as  the  figures  to  be  given  apply  only  to  this  degree  of 
dilution.  Then  count  the  leucocytes  in  2b  fields.  These  fields  may 
be  taken  in  any  part  of  the  disk,  disregarding  the  ruled  space  en- 
tirely. Having  ascertained  the  total  number  of  white  cells  contained 
in  25  fields,  multiply  it  by  one  of  the  following  factors  according  to 
the  number  of  squares  contained  in  the  diameter  of  the  field  em- 
ployed.    Thus  if  the 

Diameter  of  the  field  is  5  squares,  multiply  by  162.96 

«  "  6  "  "  113.16 

\                         «  c.  7  u  u  83.12 

"  «  8  "  "  63.54 

«  «  9  "  "  50.28 

"  ''  10  "  "  40.74 

"  «  11  "  "  33.67 

"  "  12  "  "  28.29 

For  example,  if  with  the  required  dilution  of  1  :  20  a  total  of  172 
leucocytes  has  been  obtained  from  25  fields  and  the  diameter  of  the 
field  is  10  squares,  the  desired  result  is  172  X  40.79  =  7,007. 

(c)  Third  Method  :  Using  the  "  Red  "  Pipette.— The  least  dilution 
to  be  employed  is  1  :  100 — i.  e.,  sucking  blood  up  to  the  mark  1.  It 
is  necessary  first  to  determine  the  cubic  contents  of  one  field  of  the 
microscope,  using  the  lenses  which  are  to  be  employed  for  the  count- 
ing. Ascertain  the  diameter  of  the  field  by  means  of  the  number  of 
small  squares  seen,  as  described  in  (b)  preceding.  If  it  has  been 
necessary  to  move  the  sliding  tube  of  the  instrument,  a  mark  should 
be  scratched  on  it  so  that  it  may  be  set  at  the  same  point  when  re- 
quired for  subsequent  observations.  As  the  width  (and  length)  of 
each  small  square  is  ^  millimetre,  the  exact  diameter  of  the  field  is 
known.  The  depth  of  the  cell  is  ^V  millimetre.  If  the  radius  (one 
half  the  diameter)  of  the  field  is  squared  and  multiplied  by  ■^,  and 
the  result  is  then  multiplied  by  the  factor  3.1416,  the  product  will  be 
the  cubic  contents  of  the  field.  For  instance,  the  diameter  of  the 
field  is  10  squares  =  -^g  millimetre,  the  radius  is  therefore  /^  milli- 
metre, and  ^  X  (/o)^  X  3.1416  =  .0196  cubic  millimetre  =  the  cubic 
contents  of  the  field. 

Count  the  total  number  of  leucocytes  contained  in  twenty-five 
fields.  The  fields  may  be  taken  from  any  portion  of  the  disk  with- 
out reference  to  the  ruled  space.  If  more  accuracy  is  required  fifty 
fields  may  be  counted,  using,  if  necessary,  a  second  drop  of  blood. 


EXAMINATION   OF  THE  BLOOD  567 

Then  letting  D  =  the  dilution — i.  e.,  100, 

JV=  the  number  of  leucocytes  counted, 

F  =  the  number  of  fields  counted, 

C  =  the  cubic  contents  of  one  field  (already  known), 

DX  ^ 

the  formula  -^ — ^^  =  the  number  of  leucocytes  in  each  cubic  milli- 
metre of  undiluted  blood.  For  example,  if  36  leucocytes  have  been 
counted  in  25  fields  with  a  dilution  of  1 :  100,  the  solved  equation 

will  read  -^ ^r^  =  7,578.    This  method  is  of  course  a  makeshift 

in  the  absence  of  a  "  white  "  pipette. 

Estimating  the  Volume  of  the  Cells. — It  was  anticipated 
that  the  haematocrit  of  Hedin  as  modified  by  Daland  would  supplant 
the  more  tedious  methods  of  counting  the  blood  corpuscles  which 
have  just  been  described.  But  while  its  accuracy  in  determining 
the  relative  volume  of  cells  and  plasma  is  conceded,  there  seems  to 
be  some  doubt  among  haematologists  whether  it  affords  trustworthy 
information  with  reference  to  the  number  of  cells.  The  haematocrit 
is  essentially  a  machine  whereby  a  column  of  blood  contained  in  a 
glass  tube  can  be  centrifugalized  at  a  speed  of  9,000  or  10,000  revo- 
lutions per  minute  for  2  or  3  minutes.  At  the  end  of  this  time  the 
corpuscles  are  packed  solidly  toward  one  end  of  the  tube,  the  red 
cells  nearest  the  outer  extremity  and  the  leucocytes  showing  at  the 
free  end  of  the  red  column  as  a  faint  gray  line.  The  tube  is  marked, 
each  division  being  supposed  to  represent  a  certain  number  of  cells. 
It  is  the  value  of  each  degree  of  the  scale  which  is  in  dispute,  vary- 
ing according  to  different  observers  from  99,500  to  123,000.  Until 
this  margin  of  error  can  be  eliminated  it  is  thought  best  not  to  in- 
clude the  haematocrit  as  a  blood  counter. 

Estimating'  the  Haemoglobin. — It  is  quite  as  important  to 
estimate  the  percentage  of  haemoglobin  as  to  make  a  count  of  cells. 
Either  the  haemometer  (or  haemoglobinometer)  of  v.  Fleischl  or  that 
of  Gowers  may  be  employed.  The  former  is  probably  the  more  accu- 
rate, but  it  requires  the  use  of  artificial  light  and  is  very  expensive 
as  compared  with  Gowers'.  The  latter  gives  a  sufficiently  correct 
percentage  for  clinical  use.  In  the  absence  of  both  these  pieces  of 
apparatus  the  specific  gravity  of  the  blood  may  be  utilized  (see  {c) 
following). 

{a)  V.  Fleischl's  Haemometer. — This  apparatus  comprises  a  stage 
with  a  central  opening,  in  which  is  fitted  a  short  glass-bottomed 
cylinder  divided  into  hemicylindrical  compartments  by  a  vertical 
partition  (Fig.  209).  A  small  capillary  pipette  open  at  both  ends 
and  furnished  with  a  wire  handle  accompanies  the  apparatus.     Be- 


668 


THE  EVIDENCES  OP  DISEASE 


neath  one  of  the  two  compartments  lies  a  wedge-shaped  strip  of  col- 
oured glass  held  in  a  frame,  which  is  moved  by  a  screw  so  that  any 
part  of  the  wedge  can  be  brought  under  the  compartment.  The 
colour  of  the  glass  changes  uniformly  from  clear  white  at  the  thin 
end  to  a  deep  red  at  the  base  of  the  wedge.  The  sliding  frame  is 
furnished  with  a  scale  graduated  from  0  to  120  which  is  read  through 
an  opening  in  the  stage.  Underneath  the  stage  is  a  white  disk  to 
act  as  a  light  reflector.  Artificial  light  is  essential,  but  the  following 
device  renders  it  unnecessary  to  use  a  darkened  room.  Open  a  large 
book  at  its  middle,  holding  the  leaves  smooth 
by  a  rubber  band  on  each  side.  Stand  it  on 
the  examining  table  and  place  a  small  piece  of 
lighted  candle  well  in  the  angle. 
Back  of  this  place  the  haemoglobin- 
ometer,  and  then  close  in  the  triangle 
with  a  second  book  or  a 
piece  of  cardboard.  By 
covering  in  the  top  with 
a  third  book,  a  triangu- 
lar dark  room  is  obtained, 
through  a  small  slit  at  the 
top  of  which  the  reading  is 
readily  made. 

To  use  the  in- 
strument, fill  one 
compartment  one 
quarter  full  of 
distilled  water. 
The  little  pipette 
must  be  thorough- 
ly clean  and  dry, 
an  end  readily  ob- 
tained by  drawing  through  it  a  needle  carrying  a  thread  wet  with 
alcohol  or  ether.  Puncture  the  ear,  and  keeping  the  pipette  hori- 
zontal apply  one  of  its  ends  to  the  side  of  the  drop  of  blood.  If 
the  pipette  is  dry  and  clean  it  will  immediately  fill  with  blood  by 
capillary  attraction.  Any  blood  on  the  outside  of  the  pipette  must 
be  quickly  wiped  away,  and,  after  glancing  at  the  ends  of  the 
pipette  to  be  assured  that  it  is  exactly  filled  with  blood,  plunge  it 
into  the  compartment  which  contains  the  distilled  water.  Holding 
the  wire  handle,  swish  the  pipette  rapidly  back  and  forth  until  the 
blood  is  washed  out  into  the  water.  If  any  difficulty  is  experienced 
in  doing  this,  a  medicine  dropper  may  be  filled  with  water,  its  tip 


h;emoineter. 


ESTIMATING  THE  HAEMOGLOBIN 


569 


applied  to  one  end  of  the  pipette  and  the  water  squirted  through. 
Then  with  the  handle  of  the  pipette  mix  the  blood  and  water  very 
thoroughly.  No  time  must  be  wasted  between  filling  the  pipette 
and  emptying  it  into  the  water,  as  undue  tardiness  may  allow  the 
blood  to  coagulate  in  the  tube.  Then  with  the  dropper  fill  both 
compartments  level  to  the  brim,  and  turn  the  cylinder  so  that  the 
compartment  containing  the  clear  water  lies  over  the  strip  of  coloured 
glass.  Adjust  the  white  reflecting  -disk  so  that  the  ligTit  is  thrown 
upward  through  the  cylinder,  and,  placing  the  eye  in  the  proper  posi- 
tion, turn  the  screw  back  and  forth  until  the  tint  of  the  coloured 
glass  exactly  matches  the  tint  of  the  diluted  blood.  That  figure  of 
the  scale  seen  in  the  stage  opening  will  be  the  percentage  of  haemo- 
globin contained  in  the  blood  examined. 

Certain  precautions  are  to  be  taken  (Cabot).  View  the  cylinder 
through  a  proper-sized  tube  of  black  paper;  use  as  little  light  as 
practicable ;  sit  at  one  or  other  side  of  the  instrument  so  that  the 
light  from  the  two  halves  of  the  cylinder  may  fall  on  the  right  and 
left  halves  of  the  retina,  as  the  upper  and  lower  halves  of  the  latter 
are  unequally  sensitive  to  colour ;  and  as  the  colour  sense  is  readily 
fatigued,  use  one  eye  alternately  with  the  other,  taking  snap  shots 
rather  than  a  prolonged  inspection.  The  screw  should  be  turned 
quickly  rather  than  slowly,  the  turns  becoming  shorter  and  shorter, 
the  eye  appreciating 
a  sudden  change  of 
tint  much  more  read- 
ily than  a  gradual 
shifting. 

(b)  Gowers'  HsBin- 
ometer. — This  appa- 
ratus consists  of 
two  small  test  tubes 
of  exactly  equal  size, 
a  small  platform  for 
holding  them,  and  a 
20  -  cubic  -  millimetre 
capillary  pipette  (Fig. 
210).  One  tube  is 
capped,  and  contains 
a  certain  amount  of 
coloured  fluid  as  a 
standard  of  compari- 
son. The  colour  of  the  fluid  is  that  of  normal  blood  when  diluted 
1 :  100.     The  other  tube  is  open,  and  graduated  from  0  to  120. 


Fig.  210. — Gowers'  hsemometcr ;  sliowing  standard  test  tube, 
graduated  test  tube,  bottle  for  distilled  water,  puncturing 
lancet,  and  20-cubic-ujillimetre  pipette. 


5T0  'I^HE   EVIDENCES  OF  DISEASE 

To  use  the  instrument,  place  (with  a  medicine  dropper)  2  or  3 
drops  of  distilled  water  in  the  graduated  test  tube.  Then  by  punc- 
ture secure  a  large  drop  of  blood  and  suck  it  into  the  pij)ette  up  to 
the  mark.  Wipe  the  tip  of  the  pipette,  dip  it  into  the  distilled  water 
in  the  tube,  and  expel  the  blood  by  gentle  blowing.  Add  distilled 
water  drop  by  drop  until  the  tint  of  the  mixed  blood  and  water  is 
found  by  frequent  comparison  to  correspond  to  that  of  the  fluid  in 
the  standard  tube.  When  the  tint  of  the  blood  mixture  is  the  same 
as  that  of  the  standard,  read  off  the  height  of  the  fluid  in  the  gradu- 
ated tube.  The  mark  attained — e.  g.,  70 — indicates  that  the  blood 
examined  contains  70  per  cent  of  the  normal  100  per  cent  of  haemo- 
globin. The  comparison  of  tints  should  be  made  in  good  daylight, 
the  tubes  being  placed  against  a  white  (paper)  background.  The 
standard  of  this  instrument  is  probably  set  too  high,  as  many  healthy 
persons  will  show  only  95,  or  even  90,  per  cent. 

(c)  By  Ascertaining  the  Specific  Gravity. — In  the  absence  of  the 
instruments  just  described  one  may  use  an  indirect  method  of  deter- 
mining the  percentage  of  haBmoglobin,  viz.,  ascertaining  the  specific 
gravity  of  the  blood  (Cabot).  Except  in  dropsical  cases  (in  which 
the  composition  of  the  blood  plasma  varies)  the  specific  gravity  of 
the  blood  corresponds  pretty  closely  to  the  amount  of  hsemoglobin. 
If  then  the  specific  gravity  of  the  blood  is  known  the  corresponding 
percentage  of  haemoglobin  can  be  inferred. 

The  specific  gravity  can  be  quite  readily  determined  by  the  fol- 
lowing method  (Roy-Hammerschlag).  Provide  an  accurate  urinometer 
(such  as  most  physicians  possess),  which  must  be  dry  and  clean,  a 
pipette  or  medicine  dropper,  a  glass  rod,  a  bottle  of  chloroform 
(which  is  heavier  than  blood),  and  a  bottle  of  benzol  (which  is 
lighter  than  blood).  Put  the  urinometer  in  the  footed  tube  and 
pour  in  alternately  chloroform  and  benzol  in  such  quantities  that 
the  glass  is  moderately  filled  with  a  mixture  of  the  same  specific 
gravity  as  normal  blood — i.  e.,  1059.  Remove  the  urinometer,  punc- 
ture the  ear,  take  up  some  blood  with  the  medicine  dropper  and 
expel  1  or  2  small  drops  into  the  mixture  of  chloroform  and  benzol. 
The  blood  drop  must  not  contain  air  bubbles.  The  blood  does  not 
diffuse,  but  floats  in  the  shape  of  a  small  red  globule.  If  it  rises  to 
the  top,  add  a  few  drops  of  benzol  and  stir  the  mixture  thoroughly 
with  a  glass  rod.  If  it  sinks,  add  chloroform.  Continue  thus  until 
it  neither  rises  nor  falls,  but  remains  stationary,  floating  about  mid- 
way between  top  and  bottom.  AVhen  this  is  accomplished  it  is  ob- 
vious that  the  specific  gravity  of  the  liquid  is  the  same  as  that  of 
the  suspended  blood  globule.  Use  then  the  urinometer  to  determine 
the   specific   gravity  of  the   chloroform-benzol   mixture — i.  e.,  the 


MICROSCOPICAL  EXAMINATION  OF  BLOOD 


571 


specific  gravity  of  the  blood.     The  mixture  may  be  used  indefinitely 
by  filtering  out  the  blood. 

Having  ascertained  the  specific  gravity  of  the  blood,  the  percent- 
age of  hfemoglobin  may  be  found  by  consulting  either  of  the  follow- 
ing tables,  which  are  subject  to  correction  by  further  investigations : 


Hammerschlag 
(By  the  method  described) 
Spec.  Grav.  Haemoglobin. 

1033-1035  =  25-30  per  cent. 
1035-1038  =  30-35       " 
1038-1040  =  35-40 
1040-1045  =  40-45       " 
1045-1048  =  45-55       " 
1048-1050  =  55-65       " 
1050-1053  =  65-70       " 
1053-1055  =  70-75 
1055-1057  =  75-85       " 
1057-1060  =  85-95       " 


SCHMALZ 

(By  a  direct  weighing  method) 

Spec.  Grav. 

Ilaem 

oglobin. 

1030     = 

20  per  cent 

± 

1035     = 

30 

(( 

ki. 

1038     = 

35 

(( 

u 

1041     = 

40 

(( 

(( 

1042.5  = 

45 

(( 

(( 

1045.5  = 

50 

(( 

(( 

1048     = 

55 

(( 

(( 

1049     = 

60 

(( 

u 

1051     = 

65 

C( 

u 

1052     ^ 

70 

(( 

u 

1053.5  = 

75 

(( 

u 

1056     = 

80 

(( 

u 

1057.5  = 

90 

(( 

u 

1059     = 

100 

(( 

u 

Microscopical  Examination  of  the  Blood. — In  order  to 
ascertain  the  size,  shape,  and  varieties  of  the  morphological  elements 
of  the  blood,  as  well  as  the  presence  of  parasitic  organisms,  it  is 
necessary  to  examine  both  fresh  and  dried  specimens,  the  latter 
either  stained  or  unstained.  The  microscopical  search  may  be  made 
fairly  well  with  a  good  ^  objective,  but  a  ^  immersion  lens  is  almost 
indispensable.  All  slides  and  cover  glasses  used  in  preparing  a  speci- 
men of  blood  for  examination  must  be  perfectly  clean  and  dry.  The 
complicated  methods  of  cleaning  which  have  been  recommended  are 
quite  unnecessary.  The  application  of  either  ordinary  or  green  soap 
Avith  the  fingers,  followed  by  a  thorough  washing  with  water  and  a 
subsequent  rubbing  with  a  handkerchief  fresh  from  the  laundry,  will 
afford  perfectly  clean  and  polished  slides  and  covers. 

(a)  Preparing  a  Specimen  of  Fresh  Blood. — Take  up  a  clean  cover 
glass,  holding  it  either  by  forceps,  or  (if  one  touches  the  edges  only, 
not  the  surfaces,  of  the  glass)  by  the  fingers.  Apply  its  centre  to  a 
fresh  globule  of  blood,  without  allowing  the  glass  to  touch  the  skin  of 
the  ear,  and  let  it  fall  upon  a  slide.  The  drop  of  blood  on  the  cover 
should  not  be  larger  than  a  good-sized  pinhead.     If  the  slide  and 


572  THE  EVIDENCES  OF  DISEASE 

cover  are  dry  and  clean  and  have  not  come  into  contact  with  the  skin, 
the  blood  will  at  once  spread  out  in  a  thin  layer  without  the  unde- 
sirable aid  of  pressure.  A  better  method  consists  in  painting  upon 
the  slide  with  vaseline  a  square  or  ring  corresponding  to  the  size  and 
shape  of  the  cover  glass,  and  dropping  the  latter  in  such  a  manner 
that  its  edges  coincide  with  the  narrow  band  of  vaseline.  The  thin 
layer  of  blood  is  thus  protected  from  the  air,  and  if  kept  in  a  warm 
place  neither  crenation  nor  coagulation  will  occur  for  several  hours. 

The  fresh  blood  can  be  examined  with  reference  to  the  shape  and 
size  of  the  red  cells,  their  tendency  to  form  rouleaux,  the  presence 
or  absence  of  the  Plasmodium  malaricBy  the  Filaria  sanguinis  homi- 
nis,  and  the  spirillum  of  relapsing  fever.  If  the  examiner  has  had  a 
large  experience  he  may  also  form  a  reasonably  accurate  opinion  as 
to  an  increase  of  fibrin,  a  decrease  of  hasmoglobin,  or  the  presence  of 
a  marked  anaemia  or  leucocytosis,  perhaps  of  leucaemia. 

(b)  Preparing  Blood  Films. — These  may  be  made  either  on  cover 
glasses — the  method  most  commonly  used — or  on  slides. 

(1)  Cover-glass  Films. — Provide  several  square  cover  glasses,  per- 
fectly clean  and  dry.  Lay  them  upon  a  clean  surface  in  such  a  man- 
ner, by  propping  up  or  otherwise,  that  they  can  be  readily  taken 
hold  of  with  the  fingers  by  their  opposite  edges  or  angles,  bearing  in 
mind  that  their  surfaces  are  not  to  be  touched.  Apply  the  centre  of 
one  cover  glass  to  the  tip  of  a  fresh  drop  of  blood  and  let  it  fall  upon 
a  second  cover  glass  in  such  a  relation  that  the  angles  of  the  squares 
do  not  coincide  but  lie  diagonally  to  one  another,  which  device  ren- 
ders it  practicable  to  seize  them  separately  by  their  projecting  cor- 
ners. As  soon  as  the  drop  of  blood  has  spread  between  their  sur- 
faces, which  it  should  do  immediately  if  the  covers  are  clean,  slide 
the  upper  cover  quickly  and  steadily  off  the  lower  cover,  carefully 
maintaining  their  parallelism  and  avoiding  any  separation  by  prying 
or  leverage.     Dry  quickly  by  waving  in  the  air. 

(2)  Slide  Films. — Place  upon  a  slide  a  drop  of  blood  about  half 
an  inch  from  one  end.  Take  a  second  slide  (with  ground  and  pol- 
ished edges)  and  with  one  of  its  ends,  used  like  a  plane,  push  the 
drop  along  the  slide  upon  which  it  lies.  A  thin  film  of  blood  will  be 
left  in  the  rear  of  the  pushing  slide,  much  longer  than  if  made  on 
a  cover  glass. 

(c)  Fixing  the  Blood  Films. — The  films  require  to  be  fixed — i.  e., 
the  albumin  coagulated  so  that  the  films  will  adhere  firmly.  The 
fixation  may  be  accomplished  in  various  ways,  but  the  two  methods 
about  to  be  described  are  quite  sufficient  for  clinical  work. 

(1)  Fixation  by  a  Hardening  Solution. — Immerse  the  cover  films 
in  a  mixture  of  equal  parts  of  ether  and  absolute  alcohol,  in  which 


MICROSCOPICAL  EXAMINATION  OP  BLOOD  573 

they  should  remain  for  half  an  hour  or  longer.  Even  24  hours'  sub- 
mersion will  do  no  damage.  Cover  films  may  be  placed  in  a  watch 
glass,  but  slide  films  require  to  be  plunged  in  a  wide-mouth  bottle  of 
sufficient  depth  to  entirely  cover  them.  Hardening  by  alcohol  and 
ether  is  best  adapted  for  examination  of  the  red  cells  (e.  g.,  Plasmo- 
dium malarice,  using  Plehn's  double  stain),  although  many  workers 
employ  it  for  the  differential  leucocyte  examination  as  well.  Hard- 
ening in  formalin  has  also  been  done  with  excellent  results.  The 
covers  are  placed  for  a  few  minutes  in  a  solution  made  by  diluting 
one  part  of  formalin  with  nine  times  its  volume  of  water  and  mixing 
one  part  of  the  diluted  formalin  with  nine  parts  of  absolute  alcohol. 

(2)  Fixation  by  Heat. — If  a  sterilizing  oven  is  at  hand  it  may  be 
heated  to  115°  C.  and  the  covers  or  slides  placed  in  it  for  15  to  20 
minutes.  But  ordinarily  it  is  much  more  convenient  to  heat  them 
on  a  strip  of  brass  or  copper.  This  plate  should  be  12  inches  long 
and  3  inches  wide.  Support  it  on  a  tripod  or  improvised  stand,  and 
under  its  centre  place  an  alcohol  lamp  or  Bunsen  burner.  In  a  few 
minutes  the  loss  of  heat  balances  the  gain,  and  each  point  of  the 
plate  remains  at  a  pretty  constant  temperature.  Then  with  a  medi- 
cine dropper  place  successive  drops  of  water  on  the  plate,  beginning 
at  one  end  and  going  toward  the  fiame,  until  a  point  is  reached  at 
which  the  water  just  boils.  At  or  a  little  inside  of  this  spot  the  cover 
glasses  or  slides  are  to  be  placed,  film  side  down.  Fifteen  to  20  min- 
utes is  a  sufficient  time  for  fixation,  but  they  may  be  left  2  hours  or 
more  without  detriment. 

{d )  Staining  Blood  Films  and  Fresh  Blood. — Among  the  various 
stains  and  their  modifications  the  3  following  are  all  that  are 
required  for  most  clinical  work.  Indeed,  the  first  to  be  described  is 
usually  all-sufficient.  The  stains  manufactured  by  Grubler  (Leipsic) 
alone  should  be  used.  Although  the  staining  solutions  may  be  made 
by  any  competent  pharmacist,  it  is  better  to  purchase  them  ready  for 
use  from  the  larger  firms  dealing  in  microscopical  supplies. 

The  selective  action  of  the  stains  upon  the  various  corpuscular 
elements  of  the  blood  is  dealt  with  in  subsequent  pages. 

(1)  Ehrlicli's  Triple  Stai?i. — This  is  used  especially  for  the  impor- 
tant differential  leucocyte  count,  and  consists  of 

Saturated  aqueous  solution  of  orange  G 40  c.  c. 

"  «  "  "  acid  f uchsin 45    " 

«  «  «  "  methyl  green 55    " 

Distilled  water 50    " 

Absolute  alcohol 50    " 

Glycerin 15    " 


574  THE  EVIDENCES  OF  DISEASE 

The  saturated  solutions  should  be  made  by  adding  a  small 
quantity  of  the  powder  each  day  for  a  week,  until  a  permanent 
sediment  is  formed.  After  the  various  ingredients  have  been 
mixed  the  stain  should  be  allowed  to  stand  5  or  6  weeks  before 
using,  as  it  is  not  until  then  that  its  colouring  powers  are  fully 
developed. 

To  use  Ehrlich's  triple  stain,  take  up  a  drop  of  it  on  the  end 
of  a  glass  rod  and  spread  it  over  the  blood  film.  It  should  be 
left  from  1  to  5  minutes,  and  then  washed  off  with  water.  The 
longer  the  film  has  been  soaked  in  the  ether  and  alcohol  mixture, 
or  heated  on  the  metal  strip,  the  longer  should  the  stain  be  allowed 
to  remain.  Moreover,  as  at  best  the  stains  vary  in  power,  a  few 
trials  are  requisite  to  determine  the  proper  length  of  exposure. 
The  covers  (or  slides)  are  then  dried  between  filter  paper  and 
mounted  in  balsam,  although  some  excellent  specimens  have  been 
mounted  dry. 

(2)  Plehn's  Double  Stain. — This  is  employed  particularly  in 
cases  where  the  Plasmodium  malarim  is-  to  be  sought  for,  and  is  com- 
posed of 

Concentrated  aqueous  solution  of  methylene  blue . .   60  c.  c. 
One  half  per  cent  solution  of  eosin  in  75  per  cent 

alcohol 20   " 

Distilled  water 40   " 

Twenty  per  cent  solution  of  sodium  hydrate 12  gtt. 

The  films,  which  for  this  stain  are  best  hardened  in  alcohol  and 
ether,  should  be  immersed  in  the  solution  for  5  or  6  minutes. 

(3)  Staining  Fresh  Blood. — For  ascertaining  the  presence  of  the 
Plasmodium  malar ice^  especially  its  hyaline  forms,  it  may  be  of  great 
advantage  to  stain  the  fresh  blood  as  it  flows.  A  drop  of  a  concen- 
trated solution  of  methylene  blue  made  with  six  tenths  per  cent  salt 
solution  is  placed  upon  the  lobe  of  the  ear,  and  the  puncture  made 
directly  through  the  globule  of  stain.  A  very  small  drop  of  the 
mixed  blood  and  solution  is  mounted  in  the  manner  previously 
described  for  fresh  blood. 

Order  of  Procedure  in  the  Clinical  Examination  of 
the  Blood. — Place  upon  a  table  beside  the  patient 

The  "  red  "  pipette  and  its  diluting  solution. 

The  "  white  "  pipette  and  its  diluting  solution. 

An  hfemometer  (v.  Fleischl's  or  Gowers'),  a  small  bottle  of  dis- 
tilled water,  and  a  medicine  dropper.  (In  the  absence  of  a  hsem- 
ometer  have   a  urinometer  and  its  glass,  a  glass   rod,  a   dropper, 


EXAMINATION  OP   THE  BLOOD  575 

and  a  bottle  each  of  chloroform  and  benzol,  to  take  the  specific 
gravity.) 

Two  slides  on  which  circles  or  squares  of  vaseline  have  been 
painted  of  a  size  to  fit  the  cover  glasses  used. 

One  dozen  cover  glasses  (preferably  square) ;  or,  if  slide  films  are 
to  be  made,  a  half  dozen  smooth-edged  slides. 

A  bottle  containing  equal  parts  of  ether  and  absolute  alcohol. 

A  pair  of  cover-glass  forceps. 

Some  gauze  or  absorbent  cotton. 

Two  ^inch-wide  rubber  bands. 

A  puncturing  needle. 

These  articles  having  been  conveniently  arranged,  puncture  the 
ear  and : 

Prepare  two  specimens  of  fresh  blood. 

Prepare  five  to  ten  cover  films  (or  slides),  and  lay  them  aside  to 
dry. 

Estimate  the  haemoglobin  or  find  the  specific  gravity. 

Fill  the  "red"  pipette  with  the  proper  amount  of  blood  and 
solution,  and  put  a  rubber  band  over  the  ends  to  prevent  evapora- 
tion.    May  be  kept  24  hours. 

Fill  the  "  white  "  pipette  similarly  and  band  it. 

Drop  two  of  the  films  in  the  ether  and  alcohol  mixture. 

Apparatus  and  specimens  may  be  carried  away,  and  the  blood 
count,  fixation  of  dry  films,  staining,  and  microscopical  examination 
be  done  at  the  convenience  of  the  examiner.  But  a  search  for  the 
Plasmodium  malaricB  may  be  more  successful  if  made  immediately. 

11.  THE  RESULTS  AND  DIAGNOSTIC  SIGNIFICANCE 
OF  THE  CLINICAL  EXAMINATION  OF  NORMAL  AND 
ABNORMAL    BLOOD 

Having  described  in  part  the  technic  of  blood  examination,  it 
becomes  necessary  to  study  the  results  of  the  haemoglobin  estima- 
tion, the  blood  count,  and  the  microscopical  examination,  together 
with  the  diagnostic  significance  of  the  findings.  The  items  to  be 
considered  comprise  the  red  cells  (including  the  haemoglobin),  the 
white  cells,  and  parasitic  micro-organisms. 

The  following  table  presents  an  outline  of  the  varieties  of  cellu- 
lar elements  occurring  in  normal  and  abnormal  blood.  Their  char- 
acteristics and  the  significance  of  each  are  considered  with  more 
detail  in  subsequent  pages. 


576 


THE  EVIDENCES  OP  DISEASE 


Pathological  < 


Cellular  Elements  found  in  the  Blood 
Red  Corpuscles   (Erythrocytes) 
Normal Circular,  non-medullated,  average  diameter,  7.5  ft. 

Poikilocytes,  distorted,  large  and  small. 

Microcytes^  non-nucleated,  small,  3.5  to  6  /x  in  diam- 
eter. 

Macrocytes,  non-nucleated,  large,  9.5  to  12  /a  in  diam- 
eter. 

Megalocytes,  non-nucleated,  very  large,  12  to  16  yx  in 
diameter. 

Normoblasts,  nucleated,  7.5  to  10  /*  in  diameter. 

Megalohlasts,  nucleated,  11  to  20  fi  in  diameter. 


White  Corpuscles  (Leucocytes) 

Small  lymphocytes. 
Large  lymphocytes. 
Transition  forms. 
Polymorphonuclear  neutrophiles. 
Eosinophiles. 
Mast  cells. 


Normal. 


Pathological . . .  Myelocytes. 

A.    THE    RED    CELLS  (ERYTHROCYTES) 

Haemoglobin. — The  amount  of  hasmoglobin  at  birth  is  fre- 
quently over  100  per  cent,  and  the  same  condition  exists  in  some 
grown  persons.  A  percentage  of  95,  or  even  90,  in  apparently  nor- 
mal individuals  is  quite  common.  A  notable  diminution,  however,  is 
significant  of  one  of  the  various  forms  of  ansemia. 

Normally  the  amount  of  haemoglobin  corresponds  to  the  number 
of  the  red  cells.  Thus  each  red  cell  contains  a  certain  amount  or 
percentage  of  haemoglobin,  called  variously  the  haemoglobin  value, 
valeur  glohulaire,  or  colour  index.  This  value  or  index  can  be  math- 
ematically stated  by  dividing  the  percentage  of  red  cells  into  the 
percentage  of  haemoglobin.  If  the  average  number  of  red  cells  to 
the  cubic  millimetre,  which  is  assumed  to  be  5,000,000,  is  taken  as 
100  per  cent,  and  the  haemoglobin  per  cent  is  also  100,  then  the 
colour  index  is  \%^  =  1.  So  long  as  the  haemoglobin  increases  or 
diminishes  pari  passu  with  the  number  of  red  cells  the  hsemoglobin 
value  of  the  cells  remains  1 — e.  g.,  70  per  cent  of  cells  and  70  per 
cent  of  haemoglobin  =  ^^-  =  1.     If  the  haemoglobin  is  destroyed  to  a 


EXAMINATION  OF  THE  BLOOD  577 

greater  extent  than  the  red  cells  the  valeur  glohulaire  is  less  than  1 
— e.  g.,  with  40  per  cent  of  hgemoglobin  and  80  per  cent  of  cells,  it  is 
|o  —  ^  (or  0.5)  of  the  normal.  On  the  other  hand,  if  the  cells  have 
disappeared  more  rapidly  than  the  haemoglobin,  the  haemoglobin 
value  is  greater  than  1 — e.  g.,  with  50  per  cent  of  cells  and  60  per 
cent  of  haemoglobin  it  is  %%  =  |,  or  1.2  more  than  normal.  This 
formulary  is  of  importance.  In  the  majority  of  the  anaemias  the 
haemoglobin  is  reduced  to  a  greater  extent  than  the  cells.  In  per- 
nicious anaemia,  however,  there  may  be  a  large  loss  of  cells  with  a 
smaller  loss  of  haemoglobin,  and  the  consequent  relative  increase  in 
the  richness  of  the  individual  cell  is  a  valuable  element  in  the  differ- 
ential diagnosis. 

Number  of  Red  Cells. — The  normal,  number  of  red  cells  in 
adult  men  is  5,000,000,  in  women  4,500,000,  to  the  cubic  millimetre. 

An  mcrease,  up  to  6,500,000,  in  the  number  of  eiythrocytes  {poly- 
cythwmia)  is  sometimes  observed.  It  occurs  in  diseases  or  conditions 
attended  by  the  loss  of  a  large  amount  of  fluid  from  the  body — i.  e., 
Asiatic  cholera,  dysentery,  and  severe  diarrhoea ;  in  general  cyanosis ; 
in  diabetes ;  and  in  persons  living  in  high  altitudes.  In  unusually 
strong  and  vigorous  young  men  the  red  cells  may  number  6,000,000. 

A  decrease  in  the  number  of  red  cells  (oligocythcBmia)  is  of  fre- 
quent occurrence.  Oligocythaemia  when  found  is  always  indicative 
of  one  of  the  various  forms  of  anaemia,  temporary  or  permanent. 
The  lowest  counts  are  found  in  pernicious  anaemia,  of  which  the 
oft-quoted  case  of  Quincke's  (143,000  to  the  cubic  millimetre  when 
death  was  impending)  is  a  striking  illustration.  The  average  count 
in  ordinary  anaemic  individuals  runs  from  3,000,000  to  4,000,000.  In 
the  differential  diagnosis  between  gastric  carcinoma  and  chronic 
gastritis  the  presence  of  a  marked  oligocythaemia  speaks  for  the 
former. 

When  the  red  cells  are  decreased  in  number  their  tendency  to 
rouleau  formation  diminishes  or  disappears,  and  they  may  be  obvi- 
ously fewer  in  number  in  the  field  of  the  microscope. 

Shape  of  the  Red  Cells. — The  normal  red  cell  is  not  abso- 
lutely symmetrical,  but  in  disease  extremely  irregular  shapes  (Plate 
III)  may  be  encountered.  They  may  be  ovoid,  rodlike,  or  kidney- 
shaped  ;  or  one  pole  of  the  cell  may  be  drawn  out  and  lengthened, 
making  it  resemble  a  long-necked  flask.  At  the  same  time  they  may 
be  smaller  or  larger  than  the  normal.  The  cells  are  called  poiJcilo- 
cytes,  the  condition  poihilocytosis. 

Poikilocytosis  when  found  is  indicative  of  a  high  grade  of  anae- 
mia. It  is  not  pathognomonic  of  any  special  variety  of  the  disease, 
but  is  most  marked  and  extensive  in  the  pernicious  form  ;  next  to 


578  THE  EVIDENCES  OP  DISEASE 

this  in  the  severe  chlorotic  cases  which  exhibit  thrombotic  and  em- 
bolic phenomena. 

Size  of  the  Red  Cells.  — The  average  diameter  of  the  normal 
red  cell  is  7.5  fi  (fi  =  micromillimetre  =  micron  =  ^^oir  inch),  but 
may  vary  from  6  /x  to  9  /x  without  being  considered  pathological.  In 
disease  both  abnormally  small  and  abnormally  large  cells  (Plate  III) 
may  be  found.  The  small  cells  or  microcytes  measure  from  3.5  /x  to 
6  /t ;  the  large  cells  embrace  two  sizes,  macrocytes,  which  are  from 
9.5  /A  to  12  /i  in  diameter,  and  megalocytes,  the  diameter  of  which 
runs  from  12  /x  to  16  /x.  It  is  to  be  borne  in  mind  that  abnormally 
sized  red  cells  are  apt  to  exhibit  the  variations  in  shape  (poikilocy- 
tosis)  which  have  been  previously  described. 

Microcytes  and  maorocytes  are  seen  in  the  various  anaemias. 
The  severer  the  case  the  more  abundant  they  are.  The  presence  of 
a  large  number  of  megalocytes  or  giant  red  cells  is  significant  of  per- 
nicious anaemia.     Exceptionally  they  may  be  found  in  chlorosis." 

Nucleated  Red  Cells. — Nucleated  red  cells  may  be  discovered 
in  stained  films.  In  fresh  and  unstained  specimens  it  is  rarely  pos- 
sible to  distinguish  them.     Two  varieties  are  recognised  (Plate  III)  : 

(1)  Normoblasts. — These  resemble  the  ordinary  normal  red  cells  in 
&ize,  form,  and  character,  except  in  possessing  a  nucleus,  and,  in- 
deed, are  considered  to  be  simply  young  and  immature  red  corpus- 
cles. The  nucleus  is  coloured  a  deep  blue  or  bluish  black  by  Ehr- 
lich's  triple  stain,  sometimes  presenting  one  or  more  light  spots ; 
less  commonly  its  central  portion  may  be  bluish  gray  surrounded 
by  a  narrow  rim  of  dark  blue.  The  nucleus  as  a  whole  is  clearly 
outlined  against  the  yellow  or  orange  coloured  cell  body.  The 
nucleus  usually  lies  somewhat  to  one  side,  or  even  partly  in  and 
partly  out,  of  the  cell ;  or  it  may  be  in  two  portions,  partly  or 
entirely  separated. 

Normoblasts  are  normally  found  in  the  blood  of  the  embryo,  and 
of  infants  during  the  first  two  or  three  days  of  birth ;  in  the  blood- 
making  organs — i.  e.,  the  bone  marrow  of  children  and  adults  (where 
they  may  become  very  abundant  after  a  hemorrhage),  and  in  the 
spleen.  In  these  organs  they  are  formed,  and,  after  extruding  their 
nuclei,  enter  the  general  circulation  as  ordinary  erythrocytes.  But 
if  they  are  found  in  the  blood  subsequent  to  the  second  day  after 
birth  their  presence  may  be  considered  indicative  of  one  of  the 
anaemias,  particularly  if  the  blood  condition  is  secondary  and  due  to 
cancer. 

(2)  Megaloblasts. — The  megaloblast  (or  gigantoblast)  is  an  ex- 
traordinarily large  nucleated  red  cell,  11  fi  to  20  fi  in  diameter,  and  of 
an  oval  or  slightly  irregular  outline.    Its  nucleus  is  also  large  in  pro- 


PUTE  Mi. 


qQ  ^Q 


UNSTAINED 

(8IMON> 


STAINED  WITH  ERLICH'8  TRIPLE  STAIN 

(simon)  (cabotI 


NORMAL    RED  CORPUSCLES. 


UNSTAINED  ^_X  ,.    X 


WITH  TRIPLE  STAIN 
(cabot) 

SHOWING  MICROCYTE8,  MACRCXJYTES,  AND  MEGALOCYTES 


POIKILOCYTES  (DEFORMED  CELLS) 


•  '    ons 


9 

NORMOBLASTS  MEGALOBLASTS 

STAINED  WITH  THE  TRIPLE  STAIN 
(8  AND  9  AFTER  SIMON,  THE  REMAINDER  AFTER  CABOT^ 

NUCLEATED   RED  CORPUSCLES 


RED  Corpuscles,  normal  and  Abnormal 


EXAMINATION  OP  THE  BLOOD  579 

portion  to  the  cell  body,  and  with  the  triple  stain  of  Ehrlich  takes  an 
even,  pale  green  or  greenish-blue  colour.  Xot  infrequently  the  cell 
body  or  protoplasm,  having  undergone  certain  degenerative  changes, 
stains  brown,  or  even  of  a  purplish  colour,  instead  of  yellow  or 
orange.  There  is  usually  a  narrow  white  border,  apparently  a  clear 
space,  lying  between  the  nucleus  and  the  surrounding  protoplasm. 
In  view  of  the  existence  of  atypical  varieties  of  nucleated  red  cells 
differing  in  colour,  shape,  and  relative  proportion  of  nucleus  to  cell 
body  to  an  extent  which  may  cause  great  uncertainty  in  classifica- 
tion, Cabot  has  proposed  to  restrict  the  term  normoblast  to  nucleated 
red  cells,  not  exceeding  10 /a  in  diameter,  with  a  nucleus  not  over 
half  the  diameter  of  the  cell.  This  nucleus  may  or  may  not  show 
signs  of  division,  but  must  stain  deeply.  All  other  nucleated  red 
cells  exceeding  10  fjL  in  diameter  are  megaloblasts. 

Normally  the  megaloblast  is  found  only  in  the  foetal  bone  marrow. 
When  discovered  in  the  blood  in  considerable  numbers  they  consti- 
tute an  important  symptom  of  pernicious  anaemia  and  leucaemia.  In 
small  numbers  they  may  occur  in  the  milder  forms  of  anaemia,  pri- 
mary or  secondary.     They  are  generally  associated  with  normoblasts. 

B.   THE  LEUCOCYTES 

The  diagnostic  evidence  derived  from  a  study  of  the  white  cells 
or  leucocytes  relates  not  only  to  their  total  number,  but  also  to  the 
relative  proportion  of  the  different  varieties  of  these  cells  found  in 
normal  and  diseased  conditions. 

The  Characteristics  by  -which  Leucocytes  are  Differ- 
entiated.— The  differentiation,  as  well  as  the  nomenclature,  of  the 
recognised  varieties  of  the  leucocytes  depends  upon  the  number  or 
shape  of  their  nuclei ;  the  character  of  the  protoplasm  or  substance 
of  the  cell  body,  whether  homogeneous,  finely  granular,  or  coarsely 
granular;  the  behaviour  of  the  protoplasm  to  certain  aniline  dyes 
or  stains ;  and,  finally,  upon  their  presumed  relative  age  and  birth- 
place. 

In  many  respects  the  most  important  distinction  between  the 
various  forms  of  leucocytes  is  the  manner  in  which  different  "  granu- 
lations "  exhibit  a  selective  or  chemical  affinity  for  certain  stains.  It 
should  be  borne  in  mind  that  the  granulations  are  contained  in  the 
cell  body  or  protoplasm  of  the  leucocyte,  not  in  its  nucleus ;  although 
they  may  surround  the  latter  so  completely  as  to  hide  it  from  view 
in  unstained  specimens.  Some  leucocytes  have  a  homogeneous  non- 
granular protoplasm,  while  in  others  the  granulations  are  so  fine  that 
except  with  the  highest  powers  their  appearance  is  simply  that  of  a 
diffuse  cloudiness  which  may  entirely  obscure  the  nucleus.     In  still 


580  THE  EVIDENCES  OF  DISEASE 

others  the  granulations  are  relatively  large,  coarse,  refractile,  and 
readily  seen. 

Certain  of  these  granules  will  take  up  only  acid  dyes,  others  only 
basic  dyes,  while  some  will  absorb  and  hold  both  acid  and  basic 
stains.  An  "  acid  "  stain  is  one  the  acid  element  of  which  possesses 
colouring  power ;  in  a  "  basic  "  stain  the  base  of  the  compound  is  the 
active  dyeing  agency.  Examples  of  acid  stains  are  eosin,  acid  fuch- 
sin,  and.  orange  G ;  of  basic  stains,  methyl  blue  and  methyl  green. 
Granulations  which  by  preference  take  up  acid  stains  are  spoken  of 
as  oxyphilic,  acidophilic,  or  eosinophilic ;  those  which  select  basic 
stains  as  basophilic ;  and  those  which  are  stained  both  by  acid  and 
basic  dyes  as  neutrophilic  (or  amphophilic).  The  latter  are  in  reality 
variously  oxyphilic. 

The  ClassiJB.cation  of  Leucocytes. — Concerning  the  two 
staining  solutions  recommended  as  being  sufficient  for  the  clinical 
examination  of  the  blood  the  following  facts  are  to  be  remembered  : 

Ehrlich's  triple  stain  colours  the  red  cells  yelloiv  or  orange — by 
orange  G  (acid).  Xuclei  of  red  or  white  cells  hlue — by  methyl  green 
(basic).  Large  (oxyphile,  eosinophile)  granulations  red — by  acid 
fuchsin  (acid).  Small  (neutrophile)  granulations  lilac  or  violet — by 
the  combined  action  of  acid  fuchsin  and  methyl  green  (blue  +  red). 

Plehn's  double  stain  colours  the  red  cells  red — by  eosin  (acid). 
Nuclei  of  red  or  white  cells  hlue  or  violet— hj  methylene  blue  (basic). 
Large  (oxyphile,  eosinophile)  granulations  red — by  eosin  (acid). 
The  neutrophile  granulations  are  not  stained  by  this  solution.  Ma- 
larial organisms  blue — ^by  methylene  blue. 

The  recognised  varieties  of  leucocytes  found  in  normal  blood  by 
the  triple  stain  are  as  follows.  They  are  arranged  in  what  is  sup- 
posed by  many  hsematologists  to  be  the  order  of  their  age,  the  young- 
est first.  Each  variety  is  presumed  to  represent  an  earlier  stage  in 
the  development  of  the  one  which  follows.  There  is,  however,  some 
difference  of  opinion  regarding  this  hypothesis,  its  opponents  claim- 
ing that  its  truth  has  not  yet  been  definitely  proved. 

(1)  Small  Lymphocytes.— These  are  leucocytes  not  larger  and 
often  slightly  smaller  than  a  red  cell  (Plate  IV).  Presumably  they 
are  formed  in  the  lymph  nodes,  hence  the  name.  The  lymphocyte 
is  small,  mononuclear,  and  its  single  round  nucleus,  which  stains 
very  deeply,  constitutes  the  bulk  of  the  cell.  Around  the  nucleus  is 
a  narrow  rim  of  protoplasm,  homogeneous  and  withont  granules. 

(2)  Large  Lymphocytes. — These  (often  called  large  mononuclear) 
are  considerably  larger  (13 /*  to  15 /a  in  diameter)  than  the  red  cells 
(Plate  IV).  The  nucleus  is  single,  large,  and  may  be  round,  oval, 
or  kidney-shaped.     It  stains  poorly,  its  light  bluish  tint  contrasting 


EXAMINATION  OP  THE   BLOOD  581 

with  the  darkly  dyed  nucleus  of  the  small  lymphocytes.  It  is  sur- 
rounded by  a  considerable  band  of  protoplasm,  homogeneous  and 
without  gramiles.  The  cell  as  a  whole  has  a  pale  transparent  appear- 
ance. The  large  lymphocyte  is  probably  a  later  stage  in  the  devel- 
opment of  the  small  lymphocyte,  from  which  it  differs  only  in  size, 
depth  of  staining,  and  amount  of  protoplasm.  Both  have  non-granu- 
lar protoplasm.  It  was  and  still  is  asserted  by  some  writers  that  the 
large  lymphocytes  are  formed  in  the  spleen  (hence  sometimes  called 
splenocytes)  and  bone  marrow. 

It  is  possible  that  some  diflBculty  may  arise  in  distinguishing 
between  a  nucleated  red  cell  and  a  lymphocyte,  because  of  a  certain 
similarity  in  their  appearance.  The  discrimination  may  be  made  by 
remembering  that  the  outline  of  the  latter  is  more  irregular,  its  bor- 
der of  protoplasm  is  not  so  wide,  and  its  nucleus  does  not  stain  so 
evenly  throughout  as  that  of  the  normoblast  or  megaloblast. 

(3)  Transition  Forms. — If  the  nucleus  of  the  lymphocyte  becomes 
deeply  constricted,  indented,  or  shaped  like  a  horseshoe ;  and  par- 
ticularly if  a  few  fine  neutrophilic  granules  make  their  appearance 
in  the  previously  homogeneous  protoplasm,  it  is,  and  is  so  called,  a 
transition  form  between  (2)  and 

(4)  Polymorplionuclear  (or  Polynuclear)  Neutrophiles.— These 
cells  (Plate  IV)  are  either  of  the  same  size  as  the  lymphocytes,  or  a 
little  smaller,  but  in  other  important  respects  are  very  different.  The 
nucleus  is  long,  twisted,  and  extremely  irregular  in  shape.  Its  sinu- 
osities are  such  that  portions  of  it  are  hidden  by  the  granulations  of 
the  protoplasm,  and  it  appears  to  be  broken  or  separated  into  two  or 
more  fragments.  Hence  the  name  "polynuclear,"  which  was  given 
because  of  the  impression  that  the  cell  contained  more  than  one 
nucleus.  But  the  latest  authorities  incline  to  the  opinion  that  the 
nucleus  is  "  many  shaped  "  rather  than  that  the  cell  is  "  multinucle- 
ated." The  nucleus  stains  an  irregular  dark  blue  or  greenish  blue, 
some  parts  taking  up  more  of  the  dye  than  others. 

The  special  characteristic  of  this  cell,  from  which  is  derived  the 
second  word  of  its  name,  consists  in  the  presence  of  neutrophilic 
granules  in  the  protoplasm  of  the  cell  body.  They  are  extremely 
fine  and,  as  the  cell  is  spherical,  completely  envelope  the  nucleus. 
They  do  not  stain  except  with  some  such  combination  as  the  triple 
stain  of  Ehrlich ;  by  which,  as  previously  stated,  they  are  coloured 
violet,  lilac,  or  pink.  The  polymorphonuclear  neutrophiles  are  the 
"  adult  "  or  "  ripe  "  cells,  and  constitute  the  bulk  (64  per  cent)  of  the 
leucocytes  which  are  found  in  normal  blood,  and  form  the  vast  major- 
ity of  pus  cells.  If  the  theory  of  the  relative  age  of  the  leucocytes 
holds  good,  the  neutrophiles  when  "  old  "  or  "  overripe  "  form  the 
39 


582  THE  EVIDENCES  OP  DISEASE 

(5)  Eosinophiles. — These  cells  (Plate  IV)  are  a  little  smaller  and 
more  irregular  in  shape  than  (4).  The  nucleus  is  polymorphous,  like 
that  of  the  neutrophiles,  but  stains  more  evenly  although  not  so 
darkly.  The  granules  are  large,  spherical,  refractive,  of  uniform  size, 
and  are  grouped  loosely  around  the  nucleus,  sometimes  lying  free, 
not  enveloping  it  as  do  the  fine  granulations  of  the  preceding  variety. 
They  are  stained  a  bright  pink,  red,  or  copper  colour,  by  acid  dyes 
(e.  g.,  eosin,  acid  fuchsin).  There  are  those  who  believe  that  the 
eosinophiles  originate  from  the  bone  marrow  only  and  for  that  reason 
call  them  "  myelogenic  "  leucocytes. 

(6)  Basophilic  Leucocytes  {Mast  Cells)  are  cells  usually  having  a 
polymorphous  nucleus  and  granulations  which  do  not  take  either 
Ehrlich's  triple  or  Plehn's  double  stain,  but  which  have  an  affinity 
for  dahlia,  a  basic  dye,  in  the  following  mixture  : 

Filtered  saturated  alcoholic  solution  of  dahlia. .     50.00  c.  c. 

Glacial  acetic  acid 10.00    " 

Distilled  water 100.00    " 

They  may  be  found  in  very  small  numbers  in  normal  blood.  Al- 
though they  have  been  met  with  rather  more  abundantly  in  leucae- 
mia, their  clinical  significance  is  as  yet  nil. 

The  foregoing  varieties  of  white  cells  are  normally  found  in  the 
circulating  blood,  but  there  are  certain  leucocytes  which  make  their 
appearance  in  the  blood  drops  only  in  pathological  conditions,  viz., 
the 

(7)  Myelocytes. — These  cells  belong  to  the  bone  marrow,  whence 
the  name.     Two  forms  are  recognised  (Plate  lY). 

The  first,  called  simply  a  myelocyte^  has  the  nucleus  of  a  large 
lymphocyte  and  the  granulations  of  a  polymorphonuclear  neutro- 
phile.  The  nucleus  is  spherical  or  egg-shaped,  placed  to  one  side 
(excentrically),  and  stains  an  even  pale-blue  colour.  The  cell  body  is 
filled  with  neutrophilic  granules,  and  these,  as  already  stated,  can  be 
detected  only  by  Ehrlich's  triple  stain. 

The  second  form,  the  eosinophilic  myelocyte,  resembles  the  first, 
except  that  the  granules,  instead  of  being  neutrophilic,  are  eosino- 
philic, staining  a  bright  red  or  copper  colour  with  Ehrlich's  triple 
dye.     Like  the  myelocyte,  it  inhabits  the  bone  marrow. 

Under  abnormal  conditions  certain  polynuclear  white  cells  are  met  with  in 
the  blood  which  show  granulations  with  the  triple  stain.  Like  the  mast  cells, 
their  significance  is  unknown.  Furthermore,  Neusser  claims  that  by  a  modifica- 
tion of  Ehrlich's  stain  basophilic  grannies  are  found  clustered  around  tlie  nuclei 
of  the  mononuclear  and  polymorphonuclear  leucocytes,  and  that  the  presence 
of  these  granules  is  certain  proof  of  the  uric-acid  diathesis.  The  modification 
of  the  stain  is  as  follows : 


PLATE  IV. 


SMALL   LYMPHOCYTES 


>^^'.^'^ 

^^m 

^'^■U 


mop 


LARGE   LYMPHOCYTES 


A  A     RED  CELLS 


TRANSITION    FORMS 


€ 


i^N 


POLYMORPHONUCLEAR    NEUTROPHILES 


EOSINOPHILES 


ALL  CELLS  HERE  REPRESENTED  ARE  STAINED  WITH 
THE  TRIPLE  STAIN 


THE  NUMBERED  CELLS  ARE  AFTER  SIMON 
THE  REMAINDER  AFTER  CABOT 


k^^*-: 


*  1  ' 


ORDINARY  ^NEUTROPHILIC* 


EOSINOPHILIC 


MYELOCYTES 


The  Varieties  of  Leucocytes 


EXAMINATION  OF  THE  BLOOD  583 

Saturated  aqueous  solution  of  acid  fuchsin 50  c.  c. 

"  "  "»  orange  G 70    " 

"  "  '•  methyl  green 80    " 

Distilled  water 150    " 

Absolute  alcohol 80    " 

Glycerin 20    " 

The  investigations  of  Neusser  have  been  repeated  by  Futcher  and  Simon, 
who  find  that  these  granules  exist  in  the  leucocytes  of  healthy  persons  with 
such  uniformity  that  their  absence  is  to  be  considered  pathological,  and  that 
they  are  no  more  abundant  in  gouty  persons  than  in  those  who  have  not  the 
uric-acid  diathesis. 

The  foregoing  points  and  other  questions  regarding  the  microscopical  mor- 
phology, life  historj',  and  diagnostic  significance  of  the  leucocytes  are  still  un- 
settled, and  it  is  quite  possible  that  the  views  of  to-day  may  require  more  or 
less  modification  in  the  future. 

Method  of  Differential  Counting. — To  obtain  accurate  re- 
sults in  the  colour  analysis  of  the  leucocytes  it  is  necessary  to  count 
1,000  corpuscles,  although  a  count  of  500  is  probably  trustworthy. 
If  they  are  present  in  normal  numbers  one  will  have  to  examine  2 
or  3  cover  glasses  of  the  usual  size  (^  inch)  before  the  larger  num- 
ber is  enumerated.  It  is  convenient  to  start  at  the  upper  left-hand 
portion  of  the  film,  travel  horizontally  to  the  right  upper  angle,  then 
move  downward  the  diameter  of  one  field,  travel  back  to  the  left, 
move  downward  one  field,  pass  to  the  right,  and  so  continue  until  the 
entire  film  has  been  traversed  or  the  desired  number  obtained.  A  me- 
chanical stage,  although  not  necessary,  will  greatly  facilitate  accu- 
rate covering  of  the  film  area.  As  the  leucocytes  come  into  the 
successive  fields  the  type  of  each  one  is  determined  and  recorded  in 
properly  headed  ruled  vertical  columns  by  marking  a  short  vertical 
line  in  the  proper  column.  The  adding  up  of  the  marks  is  made 
easier  by  the  well-known  device  of  grouping  the  marks  by  fives,  the  5th 
mark  in  each  group  being  drawn  diagonally  across  the  4  preceding. 

Leucocytes  in  Health. — It  is  necessary  next  to  know  the 
total  number  of  leucocytes,  and  the  percentage  of  the  various  forms. 
In  health  the  leucocytes  number  on  an  average  7,000  to  the  cubic 
millimetre,  a  proportion  of  1  white  to  700  red.  They  may  vary 
within  physiological  limits  from  5,000  to  10,000;  in  proportion  to 
the  red,  1  : 1,000  and  1 :  500.  The  percentage  of  the  different  va- 
rieties of  leucocytes  in  normal  blood  is  as  follows  : 

Small  lymphocytes 20  to  30  per  cent 

Large  lymphocytes,  young 5  to    6       " 

Transition  forms 1  per  cent 

Polymorphonuclear  neutrophiles,  adult . .   60  to  75  per  cent 
Eosinophiles,  old 2  to    4       " 


684  THE  EVIDENCES  OP  DISEASE 

Leucocytes  in  Disease. — Pathological  changes  relate  either 
to  alterations  (increase  or  diminution)  in  the  total  number  of  the 
leucocytes  (quantitative),  or  in  the  proportion  of  the  different  forms 
(qualitative).  An  increase  in  the  total  leucocyte  count  is  called 
leucocytosis  or  hyperleucocytosis.  The  latter  term  is  preferred,  per- 
haps with  greater  propriety,  by  some  writers.  A  decrease  is  termed 
leucopenia  or  hypoleucocytosis. 

(1)  Increased  Leucocyte  Count. — It  is  necessary  to  recognise  sev- 
eral forms  of  leucocytosis,  the  distinctive  differences  depending  upon 
the  presence  or  absence  of  qualitative  alterations — i.  e.,  whether  the 
relative  percentage  of  the  different  varieties  remains  unchanged,  or 
whether  one  variety  has  increased  out  of  all  proportion  to  the  nor- 
mal ratio.  The  following  subdivisions  are  clinically  convenient. 
The  first  mentioned  is  normal ;  the  others  are  pathological. 

1.  Physiological  Leucocytosis. — There  is  a  moderate  hyperleuco- 
cytosis, the  percentage  of  varieties  remaining  as  it  is  in  normal  blood, 
which  occurs  in  certain  physiological  conditions.  It  is  found  in  the 
newborn  infant  (averaging  18,000)  ;  in  pregnancy  (from  10,000  to 
16,000) ;  after  exercise  (from  11,000  to  13,000) ;  after  cold  baths  (aver- 
aging 13,000) ;  and  just  before  death.  The  leucocyte  count  also  rises 
after  taking  food  (digestive  hyperleucocytosis)  usually  to  an  average 
of  10,000,  sometimes  to  13,000  or  more.  Its  presence  within  1,  2,  or 
3  hours  after  a  hearty  meal  is  not  pathological.  The  absence  of  this 
normal  increase  is  said  to  be  a  point  in  favour  of  gastric  cancer 
(although  the  total  leucocyte  count  may  be  large)  as  against  gastric 
ulcer,  for  in  the  latter  disease  the  increase  occurs  as  usual.  It  is 
obvious  that  the  normal  digestive  leucocytosis  must  be  taken  into 
account  in  comparing  successive  examinations  on  different  days  in 
the  same  individual,  and  an  effort  made  to  take  the  blood  as  nearly  as 
possible  at  the  same  hour  before  or  after  a  meal.  It  is  always  well 
even  in  a  single  count  to  mention  its  relation  to  the  digestive  act. 

2.  Polymorphonnclear  Leucocytosis. — This  name  is  given  when 
the  hyperleucocytosis  is  due  mainly  or  alone  to  an  increase  (relative 
or  absolute)  in  the  number  of  the  polymorphonuclear  neutrophiles 
(adult  cells).  It  is  the  type  of  leucocytosis  usually  seen  in  patho- 
logical conditions.  The  total  count  may  rise  to  100,000,  but  is  most 
commonly  somewhere  under  50,000.     It  occurs  in — 

All  acute  inflammatory  diseases — e.  g.,  abscesses  of  all  varieties  in 
any  part  of  the  body;  serous  membrane  inflammations  (pleurisy, 
peritonitis,  etc.) ;  gangrenous  inflammations  (appendix,  cancrum 
oris) ;  and  many  of  the  cutaneous  inflammations. 

Certain  acute  infectious  diseases,  if  attended  by  local  inflamma- 
tory lesions  or  complications — e.  g.,  erysipelas,  pneumonia,  phthisis 


EXAMINATION  OP  THE  BLOOD  585 

(only  when  cavities  exist),  meningitis,  diphtheria,  or  pyaemia.  If 
the  infection  is  not  accompanied  by  lesions  which  give  rise  to  a  local 
reaction  there  is  no  leucocytosis — e.  g.,  typhoid  fever,  in  which,  if 
it  is  uncomplicated  by  some  localized  inflammatory  process  (pneu- 
monia, abscess),  the  leucocyte  count  is  not  increased — a  valuable 
differential  point  in  some  cases.  It  is  especially  useful  in  discrimi- 
nating between  appendicitis  and  typhoid  fever,  the  absence  of  hyper- 
leucocytosis  pretty  positively  barring  out  the  former. 

The  cachexia  of  malignant  disease,  especially  if  the  growth  is 
rapid  or  metastases  have  occurred.  The  extent  of  the  leucocytosis 
is  thought  by  some  writers  to  be  commensurate  with  the  amount  of 
local  reaction  in  the  tissues  surrounding  the  growth.  It  is  to  be 
remembered  that  the  absence  of  a  leucocytosis  does  not  forbid  malig- 
nant disease,  as  the  neoplasm  may  be  small  and  of  slow  growth,  under 
which  circumstances  (slight  local  reaction)  the  number  of  white  cells 
may  remain  normal.  In  the  differential  diagnosis  between  malignant 
and  non-malignant  disease  of  the  stomach  the  presence  of  a  leucocy- 
tosis points  toward  the  former.  Leucocytosis  of  a  moderate  degree 
occurs  in  other  secondary  anaemias  besides  that  due  to  cancerous  dis- 
ease. Subsequent  to  large  hemorrhages  there  is  a  temporary  leuco- 
cytosis (16,000-18,000)  lasting  from  one  to  several  days.  The  longer 
duration  is  in  cases  where  the  bleeding  is  due  to  traumatism. 

3.  Mononuclear  Leucocytosis  (Lymphocytosis). — In  this  form  the 
lymphocytes  are  present  in  increased  numbers.  The  increase  may 
be  absolute — i.  e.,  the  total  leucocyte  count  is  above  the  normal,  the 
lymphocytes  constituting  a  large  proportion  of  the  increase ;  or  rela- 
tive, the  total  number  of  leucocytes  being  normal  or  even  decreased, 
while  the  percentage  of  lymphocytes  is  above  the  normal.  The 
lymphocytes  may  be  either  large  or  small.  It  is  important  to  sepa- 
rate these  two  conditions,  as  their  diagnostic  significance  differs 
widely,  as  follows : 

Absolute  Lymphocytosis. — This  condition — total  number  of  leu- 
cocytes increased,  lymphocytes  in  the  majority — is  found  in  but  2 
ailments :  sarcoma  attended  with  metastases  in  the  bone  marrow,  and 
lymphatic  leucaemia.  In  view  of  the  infrequency  of  the  former  dis- 
ease, an  absolute  lymphocytosis  is  almost  invariably  significant  of 
lymphatic  leucaemia,  and  the  lymphocyte  may  be  considered  the 
characteristic  cell  of  this  disease. 

Relative  Lymphocytosis. — This  condition — total  number  of  leuco- 
cytes normal  or  less,  percentage  (relative  number)  of  lymphocytes 
increased — is  found  in  healthy  infants  and  in  various  diseases  of  the 
earliest  years  of  life.  It  also  occurs  in  pernicious  anaemia,  chlorosis, 
typhoid  fever,   scarlet  fever,  measles,   chronic   malaria,   secondary 


586  THE  EVIDENCES  OP  DISEASE 

syphilis,  rachitis,  haemophilia,  goitre,  and  certain  cases  of  exophthal- 
mic goitre. 

4.  EosinopMlic  Leucocytosis  {Eosinophil ia). — This  is  an  increase 
in  the  percentage  of  eosinophiles.  The  total  number  of  leucocytes 
may  or  may  not  be  greater  than  normal.  A  marked  eosinophil  ia  is 
very  suggestive  of  trichinosis.  It  occurs  also  in  varying  degrees  in 
bronchial  asthma,  emphysema,  phthisis  with  cavities ;  in  disease  of  the 
bones  (sarcoma,  myelogenic  leucaemia) ;  in  some  diseases  of  the  nerv- 
ous system  (neurasthenia,  hysteria,  certain  psychoses);  chlorosis; 
diseases  of  the  skin  (eczema,  pemphigus)  ;  in  the  lithaemic  or  uric- 
acid  diathesis ;  and,  during  early  convalescence,  in  the  acute  febrile 
infections,  except  measles  and  scarlatina. 

5.  Myelocytosis. — This  term  may  be  employed  to  indicate  the 
presence  of  myelocytes,  cells  which  are  never  found  in  normal  blood. 
When  found  in  large  percentage  (20-60)  containing  either  neutro- 
philic or  eosinophilic  granules,  together  with  a  great  increase  in  the 
total  number  of  leucocytes,  they  are  extremely  characteristic  of  the 
spleno-medullary  (or  lieno-myelogenous)  form  of  leucaemia.  Like  the 
normoblast,  they  are  found  in  small  percentage  in  many  diseases,  par- 
ticularly in  pernicious  anaemia  (rarely  exceeding  9  per  cent),  chlorosis, 
and  severe  secondary  anaemias. 

(2)  Decreased  Leucocyte  Count. — The  absence  of  an  increase,  per- 
haps even  a  diminution  (leucopenia,  hypoleucocytosis),  in  the  number 
of  leucocytes  is  of  much  value  in  certain  differential  diagnoses. 
Thus,  if  it  becomes  a  question  whether  a  given  case  is  one  of  appendi- 
citis or  of  uncomplicated  enteric  fever,  the  presence  of  an  increased 
number  of  leucocytes  speaks  against  the  latter,  as  it  is  one  of  the 
infections  in  which  a  leucocytosis  is  notably  absent. 

The  diseases  in  which  there  is  either  an  absence  of  leucocytosis, 
the  number  of  white  cells  remaining  within  normal  limits,  or  an 
actual  leucopenia,  are  typhoid  fever,  measles,  epidemic  influenza, 
malaria,  miliary  tuberculosis,  and  tuberculous  affections  of  the 
meninges,  lungs,  pleura,  pericardium,  peritonaeum,  and  bones.  Leu- 
copenia is  found  in  pernicious  anaemia,  sometimes  in  the  secondary 
anaemias,  and,  associated  with  lymphocytosis,  in  conditions  of  malnu- 
trition and  starvation. 

There  is  little  to  be  said  concerning  a  decrease,  either  relative 
or  absolute,  in  any  one  variety  of  leucocyte.  The  eosinophiles  may 
totally  disappear  during  the  febrile  stages  of  acute  infectious  dis- 
eases, except  scarlet  fever  and  malaria,  to  return  after  the  fever  has 
subsided ;  and  are  relatively  diminished  during  digestion,  after  cas- 
tration, and  in  most  leucocytoses.  The  lymphocytes  are  relatively 
diminished  in  spleno-medullary  leucaemia. 


EXAMINATION  OF  THE  BLOOD  537 


C.    BLOOD   PLATES   AND   MULLER'S   BLOOD   DUST 

Blood  plates  are  small  rounded  bodies  frequently  agglutinated  into  bunches. 
They  number  from  200,000  to  500,000  under  normal  conditions.  As  they 
promptly  disintegrate  on  the  slightest  exposure  to  air  they  are  rarely  seen 
unless  the  blood  is  immediately  mixed  with  Hayem's  fluid,  the  composition  of 
which  is  as  follows  : 

Bichloride  of  mercury 0.5  gramme. 

Sodium  sulphate 5.0  grammes. 

Sodium  chloride 2.0         " 

Distilled  water.    200.0        " 

A  drop  of  the  fluid  is  placed  upon  the  lobe  of  the  ear,  a  puncture  made 
through  the  drop,  and  the  mixed  fluid  immediately  examined.  Variations  in 
the  number  of  blood  plaques  have  as  yet  so  little  clinical  significance  that  there 
is  nothing  to  be  gained  by  counting  them. 

The  "  haemoconien  ■'  or  blood  dust  of  MuUer  consists  of  round,  colourless, 
highly  refractile  granules  varying  from  J  to  1  ;t  in  diameter.  They  are  not 
motile,  but  exhibit  rapid  molecular  motion.  There  is  evidence  to  show  that 
they  are  the  extruded  granules  of  the  eosinophilic  and  neutrophilic  corpuscles. 
As  yet  they  have  no  clinical  significance. 

D.    PABASITES   IN  THE   BLOOD 

The  three  micro-organisms  of  greatest  clinical  importance  to  be 
found  in  the  circulating  blood  are  the  Plasmodium  malarice^  the  Spi- 
roclicetcB  of  relapsing  fever,  and  the  Filaria  sanguinis  hominis. 

Plasmodium  Malariae. — (1)  The  Life  History  of  the  Plasmo- 
dium.— There  are  three  forms  or  varieties  of  this  organism  :  the  ter- 
tian, quartan,  and  astii'O-autumnal.  The  cycle  of  the  growth  and 
development  of  each  form  taken  separately  is  briefly  as  follows : 

Tertian  Variety. — In  the  early  stage  (Plate  V)  it  is  a  small  colourless  "hya- 
line "  body,  with  somewhat  indistinct  outlines,  occupying  only  a  small  portion 
of  the  interior  of  the  red  cell  and  situated  excentrically.  If  living,  it  exhibits 
distinct  and  rapid  amoeboid  movements.  The  hyaline  body  rapidly  increases 
in  size,  small  groups  of  actively  moving  pigment  granules  appear  within  it, 
and  the  containing  red  cell  becomes  pale  and  swollen.  When  the  parasite  has 
attained  its  full  growth  the  outlines  of  the  red  cell  are  hardly  distinguishable  ; 
the  activity  of  the  amoeboid  movements  of  the  organism  diminishes,  and  the 
pigment  tends  to  collect  along  the  circumference.  The  final  stage  of  develop- 
ment then  begins.  Signs  of  segmentation  are  visible  around  the  periphery  of 
the  parasite,  the  pigment  granules  pass  inward  to  be  collected  in  the  centre, 
and  finally,  when  the  division  is  complete,  a  "rosette"  is  formed  by  the  sym- 
metrical arrangement  of  the  segments  (10  to  20)  radiating  from  the  central 
rounded  mass  of  pigment.  These  segments  lose  their  regular  arrangement  and 
form  a  confused  group  or  are  held  loosely  together  by  an  apparent  envelope. 
The  tertian  parasite  passes  through  these  various  stages  in  48  hours. 


588 


THE  EVIDENCES  OP   DISEASE 


Qua/rtan  Variety. — The  descriptiou  of  the  tertian  cycle  just  given  answers 
also  for  the  quartan  form  of  the  organism  (Plate  V),  except  that  the  latter  is 
smaller,  its  outlines  are  more  sharply  defined,  its  amoeboid  movement  is  less 
active,  its  pigment  is  coarser,  darker  and  less  motile  ;  the  segments  number 
from  5  to  12,  and  the  rosette  arrangement  is  more  perfect  and  symmetrical. 
It  requires  72  hours  for  its  development.  The  containing  red  cell  becomes 
shrunken  rather  than  swollen,  and  brassy  rather  than  pale  in  colour. 

^stivo-autumTial  Variety. — This  variety  begins,  as  do  the  tertian  and  quar- 
tan forms,  with  a  "hyaline  "  body  (Plate  V)  which  is  actively  amoeboid  and 
develops  in  a  similar  manner,  but  the  organism  is  much  smaller  and  the  pig- 
ment granules  are  scanty  and  motionless.  The  segmenting  forms  are  rarely 
seen  in  the  blood  obtained  from  puncture  of  the  ear  or  finger,  as  this  stage  in 
its  development  takes  place  in  the  internal  organs,  particularly  in  the  spleen 
and  bone  marrow.  The  erythrocyte  host  is  shrunken  and  brassy  like  that  of 
the  quartan  parasite.  The  aestivo-autumnal  form  requires  from  24  to  48  hours 
for  its  development.  Finally,  if  the  disease  has  lasted  for  at  least  a  week,  pig- 
mented crescents  and  spherical  or  oval  bodies  may  be  found  which  appear  to 
be  pathognomonic  of  this  variety  of  the  organism.  The  crescent  contains  pig- 
ment, and  the  remains  of  the 
red  corpuscle  are  frequently  seen 
clinging  to  some  portion  of  its 
border. 

It  is  seen  that  all  three  varie- 
ties begin  as  a  hyaline  body, 
which  becomes  pigmented  and 
proceeds  to  segmentation,  but 
that  each  form  presents  certain 
peculiarities  in  development  and 
morphology  which  enable  the  ex- 
pert, but  not  the  occasional  ex- 
aminer, to  distinguish  one  from 
the  other.  Furthermore,  each 
variety  may  give  rise  to  extra- 
cellular, vacuolated,  and  flagel- 
late bodies.  Some  of  the  tertian 
and  quartan  organisms,  instead 
of  undergoing  segmentation,  dis- 
charge themselves  from  the  con- 
taining red  cell,  thus  lying  free 
in  the  blood,  and  increase  con- 
siderably in  size  while  the  pig- 
ment granules  exhibit  active 
movements.  From  any  one  of 
these  free  bodies,  and  also  from  the  crescents  and  spherical  or  oval  bodies  of 
the  aestivo-autumnal  organism,  slender  actively  moving  flagellae  may  be  put 
forth.  The  flagellse  may  break  off  and  move  about  independently  for  a  time. 
The  flagellate  organisms  of  the  tertian  variety  are  larger  than  those  of  the 
quartan  and  aestivo-autumnal  forms.  , 


Anopheles,  the 

carrier   of    the 
Plasmodium 


CULEX 


Fig.  211. — Kesting  attitudes  of  culex  and  anopheles. 


PLATE  V. 


THE    PARASITE   OF  TERTIAN    FEVER 


NORMAL 


CELL 


HYALINE  BODIES 


V  '1 


BECOMING  PIGMENTED 


^ 
%- 


^ 


^        /i 


UNDERGOING  SEGMENTATION 


VACUOLATED         FLAGELLATED 


THE   PARASITE  OF  QUARTAN   FEVER 


HYALINE 
BODY 


BECOMING  PIGMENTED 


'M 


):^i      *? 


•«-  "-it  A 


UNDERGOING  SEGMENTATION 


» ■r\  ♦.   V 


VACUOLATED  FLAGELLATED 


THE   PARASITE  OF  /ESTIVO-AUTUMNAL  FEVER 


HYALINE 
BODIES 


y 

BECOMING  PIGMENTED 


UNDERGOING  SEGMENTATION 


^l 

© 


The  Plasmodium  Malari>£ 
Selected  and  reproduced  from  Thayer's  Plates 


EXAMINATION  OF  THE  BLOOD  589 

It  may  be  considered  as  proved  (Thayer)  that  the  malarial  parasite  passes 
through  two  cycles  of  development  :  one,  usually  asexual,  in  the  human  body, 
ending  in  segmentation  ;  the  other,  reproductive,  taking  place  in  the  mos- 
quito, in  which  the  male  elements  undergo  flagellation  and.  penetrate  the 
female  elements.  The  newly  formed  parasites  enter  the  salivary  glands  and 
are  inoculated  into  the  human  being  by  the  bite  of  the  insect.  Only  one  genus 
of  mosquito  {anopheles)  appears  to  be  the  active  agent,  the  ordinary  mosquito 
(cukx)  not  participating  in  the  work.  It  has  been  stated  that  the  attitude  of 
the  two  varieties  when  at  rest  upon  a  wall  furnishes  a  ready  method  of  recog- 
nition (Fig.  211,  reproduced  from  the  British  Medical  Journal  of  September  30, 
1899),  but  unfortunately  only  a  few  species  of  anopheles  rest  with  the  axis  of 
the  body  at  right  angles  to  the  wall,  so  that  this  method  of  identification  is 
not  trustworthy  (Sambox,  Low). 

(2)  How  to  Detect  the  Plasmodium. — In  searching  for  the  malarial 
organism  it  is  always  best  to  examine  fresh  unstained  blood,  at  the 
bedside  if  possible ;  but  if  this  is  impracticable,  warm  the  slide,  seal 
the  cover  glass  with  vaseline,  and  the  organism  will  retain  its  vitality 
for  one  or  two  hours  at  least,  in  summer  weather  perhaps  for  several 
hours.  If  a  considerable  time  must  elapse  before  examination,  one 
should  make  films,  fix  them  by  ether  and  alcohol  (not  by  heat),  and 
stain  with  Plehn's  solution,  by  which  the  malarial  organisms  are 
coloured  blue,  the  nuclei  of  the  leucocytes  blue,  and  the  red  cells 
pink  ;  or  simultaneously  obtain  and  colour  the  blood  by  puncturing 
"through  a  drop  of  staining  solution. 

As  one  of  the  two  principal  reasons  for  a  failure  to  find  the  para- 
site lies  in  having  too  thick  a  layer  of  blood,  it  is  well  for  the  observer 
to  satisfy  himself  that  the  red  cells  lie  flat  and  one  deep,  without 
excessive  overlapping  or  rouleau  formation.  This  desideratum  is 
best  assured  by  following  the  directions  already  given  relative  to  the 
use  of  a  very  small  drop  of  blood  in  preparing  the  specimen.  The 
second  reason  for  non-discovery  of  the  parasite  is  a  too  brief  search. 
At  least  half  an  hour  should  be  devoted  to  the  quest  before  the  pres- 
ence of  the  organism  is  denied.  In  well-marked  cases  one  organism 
may  be  found  in-  every  field ;  in  slighter  attacks  a  number  of  fields 
may  be  examined  before  the  search  is  rewarded.  Although  the 
examination  may  be  made  at  any  period,  it  is  probable  that  the  best 
time  for  taking  the  blood  is  from  8  to  12  hours  before  or  after  a  chill, 
as  it  is  then  that  the  parasite  is  found  most  abundantly  in  the  periph- 
eral blood.  If  quinine  has  been  given  it  may  be  impossible  to  find 
them.  The  specimen  having  been  prepared,  the  red  cells  should  be 
examined  with  a  yV-i^^h  objective,  using  a  very  moderate  illumi- 
nation. 

Look  for  :  1.  Eed  cells  containing  actively  moving  black  specks 
or  dots — i.  e.,  pigment  granules  in  the  living  organism.     2.  Unusu- 


690  THE  EVIDENCES  OF   DISEASE 

ally  pale  red  cells  containing  clear  areas,  these  areas  of  irregular  and 
changing  shape — i.  e.,  hyaline  forms  with  amcBboid  motion.  3.  Extra 
large  red  cells — i.  e,,  corpuscles  swollen  by  the  growth  of  the  parasitic 
organism.  Unless  the  slide,  cover,  and  punctured  surface  have  been 
thoroughly  cleansed,  the  particles  of  dirt  which  remain  may  be  mis- 
taken for  pigment  granules,  especially  if  the  organism  is  dead  and 
its  movements  have  ceased.  If,  under  such  circumstances,  the  dis- 
tinction can  not  be  made,  a  fresh  preparation  must  be  secured. 

After  a  little  experience  the  pigmented  organisms  are  readily 
identified.  Attention  is  directed  to  the  flagellae,  if  such  be  present, 
by  the  commotion  among  the  red  cells  caused  by  the  active  whip- 
ping movements  of  the  former.  For  the  beginner  the  hyaline  bodies 
or  youngest  forms  are  the  most  difficult  of  recognition.  This  arises 
from  the  fact  that  the  white  circles  which  are  to  be  seen  in  many  of 
the  normal  red  cells  under  varying  conditions  of  illumination  or  par- 
tial desiccation  are  likely  to  be  mistaken  for  the  hyaline  bodies. 
The  discrimination  can  usually  be  made  by  attention  to  the  follow- 
ing points.  The  apparent  but  not  real  body  (artefact)  may  be  found 
in  much  larger  numbers,  a  dozen  or  more  to  each  field,  it  lies  in  the 
centre  of  the  erythrocyte,  it  is  circular,  its  edges  are  sharply  defined, 
it  is  white  and  brilliant,  it  increases  or  diminishes  in  size  as  one 
focuses  up  or  down,  and  its  motion,  if  any,  is  wavy  and  undulating. 
On  the  other  hand,  the  hyaline  organism  is  usually  found  in  much 
less  abundance,  one  to  one  or  several  fields,  it  is  placed  excentrically, 
its  shape  is  irregular  and  branching,  its  edges  ill  defined,  it  is  pale 
with  a  slight  yellowish  tinge,  if  the  focus  is  altered  it  simply  becomes 
more  or  less  distinct,  and  finally  it  undergoes  changes  of  shape  and 
position. 

One  more  point  is  to  be  remembered,  viz.,  that  pigment-bearing 
leucocytes  may  be  encountered  in  the  blood  of  malarial  cases.  These 
leucocytes,  usually  of  the  polymorphonuclear  (neutrophilic)  variety, 
take  into  themselves  (phagocytosis)  the  masses  of  pigment  and  pig- 
mented fragments  of  the  old  segmenting  or  disintegrating  organisms. 

(3)  The  Clinical  Relations  of  the  Plasmodium. — The  relation  of 
the  events  of  the  life  history  of  the  organism  to  the  clinical  events 
of  a  malarial  paroxysm  is  of  importance.  The  segmentation  of  the 
organism  immediately  precedes  the  chill  and  the  fever,  these  latter 
phenomena  depending  perhaps  on  the  formation  or  liberation  of 
some  toxic  material  at  the  time  of  segmentation.  Consequently  the 
segmenting  forms,  if  present  in  the  peripheral  circulation,  will  be 
found  at  the  beginning  or  the  height  of  the  paroxysm,  while  the  hya- 
line forms  are  discoverable  during  or  subsequent  to  the  seizure. 

As  the  tertian  parasite  requires  48  hours  to  complete  its  cycle  of 


EXAMINATION  OP  THE  BLOOD 


591 


development,  segmentation  and  paroxysm  will  occur  every  other  day, 
provided  that  only  1  group  or  brood  of  the  parasite  is  present.  More 
commonly  2  groups  of  different  ages  exist  (double  tertian),  segment- 
ing on  alternate  days  and  causing  the  quotidian  (daily)  type  of  fever. 

The  quartan  parasite^  requiring  72  hours  to  reach  maturity,  gives 
rise  to  paroxysms  separated  by  2  days  of  apyrexia,  provided  1  brood 
only  is  present ;  if  there  are  2  broods  there  will  be  paroxysms  on  2 
successive  days  followed  by  1  free  day  (double  quartan)  ;  while  3 
groups  will  cause  daily  or  quotidian  attacks  like  the  double  ter- 
tian type. 

As  the  cBstivo-autumnal  jmrasite  has  a  variable  period  of  develop- 
ment (24  to  48  hours),  segmentation  and  fever  may  be  extremely 
irregular,  and  sometimes  continuous,  organisms  at  different  stages  of 
development  coexisting  in  the  blood. 

Owing  to  the  rapid  destruction  of  the  red  cells  and  the  trans- 
formation of  the  haemoglobin  into  pigment,  the  patient  becomes 
quickly  and  characteristically  anaemic.  If  pigmented  leucocytes  are 
found  in  the  blood  the  existence  of  malaria  is  to  be  suspected,  as  the 
only  other  conditions  in  which  they  occur  are  relapsing  fever  and 
melanotic  neoplasms.  The  periodicity  of 
the  malarial  paroxysm  is  obviously  due  to 
the  natural  history  of  the  parasite. 

SpirocheetsB  of  Relapsing  Fever. 
— The  specific  organism  of  relapsing  fever 
may  be  found  in  a  specimen  of  fresh  blood 
prepared  in  the  same  manner  as  in  the 
search  for  the  malarial  parasite.  The  spi- 
rilla or  spirochaetae  are  narrow  spiral  fila- 
ments 36  to  40  fx.  in  length  and  are  actively 
motile,  attracting  attention  by  the  move- 
ments imparted  by  them  to  the  red  cells. 
They  are  present  only  during  the  fever  and 
may  then  be  abundant,  20  or  more  appear- 
ing in  a  single  field  of  the  microscope. 
In  the  apyrexial  periods  small  glistening 
bodies,  believed  by  some  to  be  the  spores 
of  the  organism,  are  to  be  found  free  in  the 
blood. 

Filaria     Hominis    Sanguinis.  — 
There  are  several  varieties  of  this  parasite 
for  the  distinguishing  points  of  which  spe- 
cial works  should  be  consulted.     The  most  important  of  these  is  the 
Filaria  nocturna  (Fig.  212),  which  is  held  responsible  for  certain 


Fig.  212. — Filaria  alive  in  blood. 
Photomicrograph  x  400  di- 
ameters.   (Henry.) 


592  THE  EVIDENCES  OF  DISEASE 

forms  of  chyluria,  elephantiasis,  and  lymph  scrotum.  The  adult  or 
parent  organisms  are  slender  and  hairlike,  varying  from  3  to  6  inches 
in  length,  and  inhabit  exclusively  the  lymphatics  and  tissues.  The 
embryos,  of  which  the  female  adult  discharges  a  large  number,  live  in 
the  circulating  blood,  which  they  enter  by  way  of  the  lymphatic  ves- 
sels. The  average  length  of  the  embryo  is  -^j  of  an  inch  and  its  width 
about  that  of  a  red  cell.  In  this  variety  they  make  their  appearance 
in  the  peripheral  blood  only  at  night,  unless  the  habits  of  sleeping  and 
waking  are  reversed,  when  the  contrary  holds  good ;  in  another  only 
during  the  day  {F.  diurna) ;  while  a  third  variety  may  be  found  at 
any  time  {F.  perstans).  The  search  for  the  embryos  in  a  suspected 
case  should  therefore  be  made  both  in  the  daytime  and  at  night. 
They  are  to  be  sought  for  in  a  fresh  drop  of  blood,  using  a  low 
power.  As  they  move  pretty  actively  their  presence  is  usually  first 
noted  by  the  commotion  which  they  create  among  the  red  corpuscles. 
When  they  finally  come  to  rest  it  will  be  seen  that  each  embryo  is 
contained  in  a  sheath,  within  which  it  contracts  and  extends,  and 
that  its  body  is  somewhat  granular  and  transversely  striated. 

E,    SEKUM   TEST   FOR   TYPHOID    FEVEE 

The  circular  of  information  furnished  by  the  Department  of 
Health  of  the  city  of  New  York  affords  an  excellent  statement  of 
the  present  status  of  the  Widal  reaction  in  the  diagnosis  of  typhoid 
fever,  together  with  directions  for  preparing  specimens  of  serum  and 
blood,  and  is  here  reprinted.  The  slide  for  blood,  and  an  oval  shield 
with  a  central  opening,  cantharidal  plaster,  and  a  glass  tube,  bulbed 
in  its  middle,  for  the  serum,  are  furnished  free  from  culture  stations. 

Directions  for  Performing  the  Widal  Test 

"  The  serum  test  (Widal)  for  the  diagnosis  of  typhoid  fever  is  performed  in 
the  following  way :  One  part  of  typhoid  blood  or  serum,  with  or  without  a  pre- 
vious dilution  with  water,  is  added  to  one  or  more  parts  of  a  24-hour  bouillon 
culture  of  the  typhoid  bacillus.  When  the  typhoid  reaction  appears,  the  bacilli 
quickly  lose  their  motility  and  become  clumped  together  in  masses.  The  sub- 
stances which  cause  this  reaction  ar€  absent,  or  present  to  only  a  very  moderate 
extent,  in  the  blood  of  those  not  suffering  from  typhoid  fever,  while  after  the 
5th  day  the  blood  of  those  having  typhoid  fever  usually  contains  these  agglu- 
tinating substances  in  abundance — in  amounts  greatly  in  excess  of  that  found 
in  the  blood  of  those  who  have  not  or  have  not  had  typhoid  infections. 

"The  serum  test,  as  seen  from  the  above  statement,  is  quantitative  rather 
than  qualitative.  The  examination  should  therefore  not  only  determine  the 
presence  or  absence  of  agglutinating  substances,  but  their  amount.  The  results 
so  far  obtained  indicate  that  we  are  safe  in  drawing  the  following  conclusions : 

"  1st.  That  the  patient  in  all  probability  has  typhoid  fever,  or  has  had  it 
within  1  year,  in  those  cases  in  which  the  reaction  occurs  promptly  upon  the 


EXAMINATION  OP  THE  BLOOD  593 

addition  of  1  part  of  blood  or  serum  to  9  parts  of  a  bouillon  culture  of  the 
typhoid  bacillus. 

"2d.  That  if  a  marked  reaction  occurs  when  1  part  of  blood  or  serum  is 
added  to  19  or  more  parts  of  a  bouillon  culture,  the  probability  that  the  patient 
has  typhoid  fever  becomes  almost  a  certainty. 

"The  agglutinating  substances  do  not  usually  appear  in  the  blood  in  suffi- 
cient amount  to  give  the  reaction  until  the  4th  day  of  the  disease.  From  the  4th 
to  the  7th  day  of  the  disease  specimens  of  blood  or  serum  from  typhoid  patients 
give  the  reaction  in  about  70  per  cent ;  from  the  8th  to  the  14th  day  in  about  80 
per  cent ;  and  during  the  3d  and  4th  weeks  in  about  90  per  cent  of  the  cases. 

"  In  from  5  to  10  per  cent  of  the  cases  of  typhoid  fever  the  blood  does  not 
at  any  time  in  the  course  of  the  disease  give  a  prompt  and  complete  reaction, 
when  1  part  of  blood  is  added  to  10  or  more  of  the  culture.  The  absence  of 
the  reaction  in  any  individual  case  does  not,  therefore,  positively  exclude  the 
diagnosis  of  typhoid  fever. 

"Either  dried  blood  or  the  serum  obtained  from  a  blister  may  be  sent  for 
examination.  The  serum  can  be  more  accurately  tested  than  the  dried  blood, 
and,  whenever  possible,  this  should  be  furnished  for  test. 

"  Directions  for  Preparing  Specimens  of  Blood. — The  skin  covering 

the  tip  of  the  finger  is  thoroughly  cleansed  and  then  pricked  with  a  clean 
needle  deeply  enough  to  cause  several  drops  of  blood  to  exude.  Two  large 
drops  are  then  placed  on  the  glass  slide,  one  near  either  end,  and  allowed  to 
dry  without  being  spread  out  on  the  surface  of  the  slide.  After  they  have 
dried,  the  slide  is  placed  in  the  holder  and  returned  in  the  addressed  envelope 
to  a  culture  station,  or  mailed  to  the  laboratory. 

"Directions  for  Obtaining  Specimens  of  Sernm  from  Blisters.— 

The  shield  (designed  to  protect  the  blister  from  rupture)  is  stripped  from  its 
protecting  gauze  and  applied  to  the  skin  somewhere  on  the  anterior  portion  of 
the  body.  The  piece  of  canthos  plaster  is  then  fixed  within  its  centre.  After 
10  to  13  hours,  the  shield  is  removed  and  one  of  the  ends  of  the  small  glass 
tube  accompanying  the  outfit  is  introduced  into  the  blister.  The  tube,  both 
€nds  of  which  should  be  open,  should  be  held  so  that  the  end  inserted  is  higher 
than  the  other,  to  allow  the  serum  to  run  into  it.  After  the  tube  has  been 
nearly  filled,  it  is  removed  and  the  ends  sealed  by  holding  them  a  moment  in  a 
gas  flame.  Care  must  be  observed  not  to  heat  the  middle  portion  of  the  tube, 
and  thus  coagulate  the  serum.  The  tube  so  prepared  is  then  placed  in  the 
wooden  box  and  returned  in  the  addressed  envelope  to  a  culture  station,  or 
mailed  to  the  laboratory." 

The  latest  statistics  indicate  that  from  95.6  to  97  per  cent  of 
cases  of  typhoid  afford  a  positive  reaction,  while  in  non-typhoid  cases 
1.5  per  cent  may  sliow  it.  If  the  serum  is  obtained  from  a  patient 
in  articulo  mortis  the  reaction  may  be  absent. 

F.  BLOOD  TESTS  FOR  DIABETES 

Bremer's  test  is  as  follows :  Slide  films  are  made  both  of  diabetic 
and  normal  blood,  the  latter  to  serve  as  a  control.     The  spreading 


594  THE  EVIDENCES  OF   DISEASE 

process  is  interrupted  at  short  intervals  so  as  to  produce  a  wavy 
appearance  of  the  film,  and  the  bars  or  ridges  must  be  suflBciently 
thick  to  present  a  distinct  red  colour.  They  are  then  placed  in  a 
sterilizing  oven  and  heat  applied  until  the  thermometer  has  risen  to 
130°  C,  the  reserve  heat  sending  the  temperature  up  to  135°  C, 
which  is  the  required  degree.  It  must  not  fall  below  130°  nor  exceed 
140°,  as  in  such  a  case  failure  will  result.  The  oven  should  be 
allowed  to  cool  completely  before  opening  the  door.  The  slides 
after  cooling  are  placed  in  a  1-per-cent  aqueous  solution  of  Congo 
red  for  2  or  3  minutes  and  then  washed  in  water.  The  diabetic  film 
is  nearly  colourless,  the  non-diabetic  is  of  a  pronounced  red.  A  ^per- 
cent aqueous  solution  of  methyl  (not  methylene)  blue  may  also  be 
employed,  in  which  case  the  diabetic  film  is  almost  unstained,  the 
non-diabetic  film  presenting  a  deep  blue  colour. 

Williamson  has  devised  the  following  test :  Mix 

Blood 20  c.  mm.  (2  drops). 

Aqueous  methyl  blue  (1 :  6,000) 1  c.  c. 

Liquor  potassae,  60  per  cent  (sp.  g.  1.058)  .40  c.  c. 

Water 40  c.  c. 

Place  the  container  in  boiling  water  for  3  or  4  minutes.  If  the 
blood  is  from  a  diabetic  the  mixture  will  turn  yellow,  otherwise  not. 

G.    IODINE    REACTION    IN   SUPPURATION 

Make  a  mixture  as  follows  (Goldberger  and  Weiss)  : 

lodi.  sublim 1 

Potass,  iodati 3 

Aq.  dest 100 

Gummi  ad  syrupam. 

Paint  some  of  this  solution  upon  a  slide,  and  press  a  dried  cover- 
glass  film  upon  it.  If  suppuration  is  not  going  on  the  red  cells  stain 
dark  yellow,  the  white  cells  light  yellow,  and  their  nuclei  a  citron 
yellow.  If  acute  suppuration  is  in  progress  the  protoplasm  of  the 
white  cells  will  be  stained  brown,  diffusely  or  as  a  network.  The  reac- 
tion may  appear  in  pneumonia,  and  in  the  dying. 

H.    OBTAINING    BLOOD    FOE    BACTERIOLOGICAL   EXAMINATION 

Place  a  moderately  tight  ligature  around  the  upper  arm  in  order 
to  distend  the  veins  at  the  elbow.  Scrub  the  flexor  surface  of  the 
bend  of  the  elbow  first  with  soap  and  water,  then  with  bichloride 
solution,  and  finally  wash  with  alcohol  and  boiled  water.  Boil  a 
rather  large-sized  hypodermic  syringe  and  its  needle  in  plain  water. 
Push  in  the  piston,  attach  the  needle,  thrust  it  quickly  but  steadily 


EXAMINATION  OP  THE  BLOOD 


595 


into  the  most  prominent  of  the  distended  veins  (which  causes  but 
little  pain),  and  slowly  withdraw  the  piston.  When  the  syringe  is 
filled  with  blood  Avithdraw  it  and  expel  its  contents  at  once  into  the 
previously  prepared  culture  tubes.  Apply  a  sterilized  gauze  dressing 
to  the  puncture.  Bleeding  is  slight  and  healing  rapid.  The  technic 
of  the  bacteriological  examination  does  not  come  within  the  scope  of 
this  volume. 

Tabulation  of  the  Results  of  H.emanalysis  in  Certain 
Diseases  of  the  Blood 

The  following  table  presents  in  brief  compass  the  salient  features 
of  the  blood  examination  in  the  principal  diseases  of  the  blood.  It 
is  to  be  remembered  that  the  table  refers  to  the  average  or  typical 
examples,  and  that  considerable  variations  may  exist  in  the  individ- 
ual case. 

Blood  Examination  in  Special  Diseases 


Normal  blood. 
For  compari- 
son. 

Chlorosis. 

Pernicious 
anaemia. 

Secondary- 
anaemia. 

Red  Cells 

4,500,000  to 

Average  4,000,- 
000,  and  rarely 

Average  1,000,- 
000.     Micro- 

May be  1,000,- 

5,000,000. 

000  or  less. 

under  2,000,- 

cytes.    Meg- 

Small  poikilo- 

000.     Poikilo- 

alocytes. 

cytes. 

cytosis.    Many 

microcytes. 

Normoblasts 

Occasional. 

Moderately 
numerous. 

Common. 

Megaloblasts 

Rare. 

Present,  con- 

Rare, never 

stantly  pre- 

predominating 

dominating 

over  normo- 

over the  nor- 

blasts. 

moblasts. 

Haemoglobin 

90  to  95 

40  per  cent. 

Often  rela- 

Relatively low. 

per  cent. 

Always  rela- 
tively low. 

tively  high. 

■ 

White  Cells 

5,000  to 

Normal  or 

Usually 

Usually 

10,000. 

slightly  in- 
crea.sed.     Av- 
erage 8,000. 

decreased. 

increased. 

Small  lymphocytes. . 

20  to  30 
per  cent. 

Increased. 

Increased. 

Usually 
diminished. 

Large  lymphocytes. . 

5  to  6 
per  cent. 

Increased. 

Increased. 

Usually 
diminished. 

Polymorphonuclear. . 

60  to  75 
per  cent. 

Decreased. 

Decreased. 

Usually 
increased. 

Eosinophiles j 

2  to  4 
■per  cent. 

Normal. 

Normal. 

Normal. 

Myelocytes 

Rare. 

Common. 
Usually 

Rare. 

eosinophilic. 

596 


THE  EVIDENCES  OF   DISEASE 


Blood  Examination  in  Special  Diseases  {continued) 


Pathological 

Myelocytaemia 
or  spleno- 

Lymphsemia  or 
lymphatic 
leucsemia. 

Leucsemia  in  in- 

leucocytosis. 

myelogenous 
leucsemia. 

fancy  (Cabot). 

Red  Cells 

Normal  or 

3,000,000, 

3,000,000  or 

May  be  under 

decreased. 

rarely  under 
2,000,000. 

somewhat  less. 

2,000,000. 

Normoblasts 

Numerous. 

Compara- 
tivelv  rare. 

Common. 

Megaloblasts 

Moderately 
numerous. 

Compara- 
tively rare. 

Common. 

Some  gigan- 

toblasts. 

Haemoglobin 

Normal  or 
decreased. 

Normal  or 
relatively 
decreased. 

Diminished. 

Relatively  low. 

White  Cells 

Usually  not 

Average  450,- 

Average  100,- 

Usually  more 

over  50,000. 

000;  maybe 

1 :  10,  1 : 5,  or 

1 : 1  red. 

000  or  less. 

increased  than 

in  any  other 

disease. 

Small  lymphocytes. . 

Diminished, 

Diminished, 

90  per  cent, 

Usually 

Large  lymphocytes. . 

averaging 

averaging 

either  small  or 

increased. 

together 

together  about 

large  forms 

about  10 

7.5  per  cent. 

predominating. 

per  cent. 

Polymorphonuclear. . 

90  per  cent. 

49  per  cent. 

Average  only 
3  per  cent. 

Usually- 
diminished. 

Eosinophiles 

1  per  cent. 

4.5  per  cent. 

Scanty. 

Average  0.7 

per  cent. 

Myelocytes 

35  per  cent 
(characteristic). 

Scanty. 

Usually  more 

Average  0.3. 

numerous  than 

in  other 

diseases. 

SECTION  XXXIX 
MICEOSCOPICAL   EXAMINATION   OF  THE   SPUTUM 

The  evidence  to  be  derived  from  gross  or  macroscopic  inspection 
•of  the  sputum  has  already  been  considered  (page  259).  With  the 
microscope  one  searches  for  cells,  elastic  fibres,  casts,  spirals,  crystals, 
and  parasitic  organisms. 

Preparation  of  the  Sputum. — It  is  desirable  first  to  examine 
a  fresh  unstained  specimen  and  afterward  to  make  a  dried  and  stained 
cover-glass  preparation. 

(1)  A  preliminary  careful  inspection,  either  by  the  unaided  eye 
or  by  a  hand  lens,  is  useful,  and  is  most  conveniently  made  by  having 
two  pieces  of  window  glass,  one  5  or  6  inches  square,  the  other  an 


MICROSCOPICAL  EXAMINATION  OF   SPUTUM  597 

inch  or  two  less  in  size,  the  larger  piece  painted  black  upon  its 
under  surface,  or,  when  in  use,  laid  upon  a  black  ground.  A  portion 
of  the  sputum  is  placed  upon  the  larger  piece  and  covered  by  the 
smaller.  Against  the  black  background,  cheesy  particles,  casts,  elas- 
tic fibres,  and  spirals  may  be  detected.  Yellowish  particles  are  prob- 
ably caseous  or  cheesy  masses  in  which  tubercle  bacilli  and  elastic 
fibres  are  most  likely  to  be  found ;  while  grayish-yellow  spots  may  be 
elastic  tissue ;  sago-like  grains,  Curschmann's  spirals ;  and  whitish, 
yellowish-brown,  or  reddish-yellow  masses,  fibrinous  casts.  By  slid- 
ing the  upper  glass  to  one  side  particular  objects  may  be  removed 
for  identification  and  detailed  examination  by  the  microscope.  A 
microscope  slide  or  a  watch  glass  placed  upon  a  piece  of  black  paper 
will  serve  almost  as  good  a  purpose  if  the  sputum  is  thoroughly 
spread  out.  Earely  there  are  found  in  the  sputum  concretions, 
sometimes  of  considerable  size,  which  have  been  formed  in  vomicae 
and  bronchiectases,  or  consist  of  portions  of  calcified  bronchial 
glands  which  have  entered  the  lungs  and  been  expectorated. 

(2)  The  fresh  spiitum  is  examined  by  picking  out  a  promising 
particle,  placing  it  on  a  slide,  and  covering.  The  cover  glass  should 
be  moved  about  with  slight  pressure  so  as  to  flatten  out  the  specimen 
into  a  layer  of  sufficient  thinness.  Examine  first  with  a  low,  then 
with  a  high,  power. 

(3)  Dried  preparations  are  made  either  by  putting  a  suspicious- 
looking  portion  of  the  sputum  upon  a  cover  glass  and  spreading  it 
over  the  glass  by  a  needle  or  small  spatula ;  or  by  placing  the  chosen 
specimen  between  two  cover  glasses,  pressing  them  gently  together 
to  diffuse  the  material,  and  then  sliding  the  covers  apart  as  in  pre- 
paring a  blood  film  (page  572).  In  either  case  they  must  be  allowed 
to  dry  in  the  air,  after  which  it  is  usually  necessary  to  fix  the  layer  of 
sputum  by  heat,  preparatory  to  staining.  This  is  best  done  by  pass- 
ing the  cover  glass,  held  in  forceps,  three  times  through  an  alcohol 
flame,  film  side  up,  each  passage  occupying  something  less  than  a 
second,  thereby  coagulating  the  albumin  and  securing  the  adherence 
of  the  film.  Appropriate  methods  of  staining  are  described  in  con- 
nection with  the  special  end  desired. 

Methods  and  Results  of  the  Microscopic  Examination. 
—{a)  Red  Blood  Cells.— According  to  the  length  of  time  that  these 
cells  have  been  out  of  the  vessel  so  will  they  vary  in  appearance, 
from  the  normal  to  pale,  shadowy,  or  fragmentary  forms.  A  few 
red  corpuscles  are  of  no  diagnostic  significance,  as  they  may  be 
found  in  many  sputa,  particularly  if  there  is  a  catarrhal  condition  of 
the  respiratory  mucous  membrane.  Tliey  necessarily  occur  in  large 
numbers  in  haemoptysis,  but,  aside  from  this,  they  appear  constantly 
40 


598 


THE  EVIDENCES  OP  DISEASE 


and  more  or  less  abundantly  in  all  pulmonary  diseases,  especially 
phthisis.  The  green  and  yellow  sputum  of  resolving  pneumonia 
owes  its  colour  to  altered  hsemoglobin,  the  corpuscles  having  been 
destroyed  so  that  they  can  not  be  seen. 

(b)  White  Cells. — Polymorphonuclear  leucocytes  (pus  cells)  in 
various  stages  of  degeneration,  granular,  fatty,  or  pigmented,  are 
found  in  all  sputa,  especially  from  a  putrid  bronchitis,  or  a  perforat- 
ing empyema,  subphrenic  abscess,  or  other  collection  of  pus. 

Eosinophilic  leucocytes  (q.  v.)  may  be  found  in  large  numbers, 
often  associated  with  Charcot-Leyden  crystals,  in  the  expectoration 
of  bronchial  asthma. 

(c)  Epithelium. — Epithelial  cells  from  the  mouth,  tracheal  tree, 
and  alveoli  are  found  in  the  sputum,  but  their  shape  is  so  much 
altered  at  the  time  of  examination  that  no  correct  inference  as  to 
the  seat  of  the  abnormal  process  can  be  derived  from  their  charac- 
ters. A  round  pigmented  (haematoidin)  alveolar  epithelial  cell  is 
quite  characteristic  of  brown  induration  of  the  lungs  due  to  the 
chronic  pulmonary  congestion  of  cardiac  valvular  disease. 

(d)  Elastic  Fibres. — To  detect  particles  and  shreds  of  elastic 
tissue,  suspicious  lumps  in  the  sputum  may  be  mixed  with  a  10-per- 
cent solution  of  sodium  hydrate  and  a  considerable  quantity  exam- 
ined under  a  low  power; 
or  the  entire  amount  of 
sputum  may  be  boiled 
for  a  few  moments 
with  an  equal  volume 
of  the  sodium  hydrate 
solution.  The  result- 
ing gelatinous  mixture 
should  be  diluted  with 
three  or  four  times  its 
volume  of  water,  and 
either  centrifugalized 
or  allowed  to  stand  un- 
til settled.  The  elastic  fibres,  which  resist  the  alkali  except  after 
prolonged  boiling,  will  be  found  in  the  sediment.  The  fibres  are 
undulating,  double  contoured,  and  the  ends  are  usually  curled.  Not 
infrequently  they  present  an  alveolar  arrangement  (Fig.  213),  and  if 
this  is  present  it  may  be  safely  affirmed  that  they  originated  in  the 
lungs  and  are  not  derived  from  particles  of  flesh  food  in  the  sputum. 

When  elastic  fibres  are  found,  it  may  be  considered  indubitable 
proof  of  a  destructive  process  in  the  lung — e.  g.,  phthisis,  abscess,  or 
bronchiectasis.     In  many  cases  of  gangrene  of  the  lung  the  elastic 


^^^ 


Fig.  213. — Elastic  tissue  from  lung  in  sputum  of  a  case  of 
phthisis.     X  300.    (Hutchison  and  Rainy.) 


MICROSCOPICAL  EXAMINATION  OP  SPUTUM 


599 


tissue  is  destroyed  (perhaps  by  a  ferment)  so  that  its  absence  in  sus- 
pected cases  does  not  disprove  the  existence  of  a  necrotic  process. 

(e)  Fibrinous  Casts.  —  These  casts 
(Fig.  214)  vary  in  size  from  those 
which  constitute  a  mould  of  the  trachea 
and  larger  bronchi — 4  or  5  inches  in 
length  and  of  corresponding  thickness 
— to  those  which  are  formed  in  the 
bronchioles,  -^  to  1:^  inches  long  and 
of  threadlike  thickness.  "While  casts 
large  enough  to  attract  attention  in 
the  naked-eye  inspection  occur  not  in- 
frequently, the  majority  require  a  low 
power  of  the  microscope  to  render  them 
visible.  The  casts  of  macroscopic  size 
may  be  unravelled  under  water.  They 
are  found  to  branch  dichotomously ; 
the  slenderer  branches  are  solid  and 
the  larger  are  apt  to  be  hollow. 

Fibrin  casts  are  found  in  three  dis- 
eases :  the  largest  in  diphtheria,  the  me- 
dium sized  in  fibrinous  bronchitis,  and 
the  smallest  in  lobar  pneumonia,  either 
just  before  or  immediately  after  the  stage  of  resolution — i.  e.,  the 
third  to  the  ninth  day. 

(/)  Cursclimaiin's  Spirals. — These  consist  of  a  central  core  or 

thread  (perhaps  fi- 
brinous) which  has 
an  undulating 
course  (Fig.  215). 
Around  this  cen- 
tral thread  are 
coiled  in  a  spiral 
manner  fibrillary 
bands  ( probably 
tough  mucus).  En- 
tangled in  the  spi- 
rals are  eosinophiles, 
and  frequently 
also  Charcot-Leyden 
crystals. 

Curschmann's  spirals  are  found  especially  in  the  sputum  of  bron- 
chial asthma,  much  more  rarely  in  phthisis,  bronchitis,  and  lobar 


Fig.  214. — Bronchial  cast  from  a  case 
of  plastic  bronchitis.  Natural 
size.    (Hutchison  and  Kainy.) 


Fig.  215. — Curschmann's  spirals  in  sputum,     x  200,  and  natural 
size.    (Hutchison  and  Kainy.) 


600 


THE  EVIDENCES  OP   DISEASE 


Fig. 


216. — Charcot-Leyden  crystals 
(Hutchison  and  Kainy). 


pneumonia.      Their  presence  may  be   of  service  in  distinguishing 

between  bronchial  and  the  so-called  cardiac  or  renal  asthma. 

{g)  Crystals. — (1)   Charcot-Leyden  crystals  (Fig.  216)  (probably 

spermin  phosphate)  are  fine,  colourless,  sharply  pointed  octahedra  of 

varying  size,  often  requiring  a  high 
power  to  make  them  visible.  They  are 
found  for  the  most  part  in  asthma, 
usually  associated  with  the  spirals  just 
described,  but  occur  as  a  rarity  in 
bronchitis,  phthisis,  and  chronic  pneu- 
monia. 

(2)  Cholesterin  crystals  are  but  rare- 
ly seen  in  the  sputum,  occurring 
as  transparent,  colourless  rhomboidal 
plates,  with  notched  and  irregular  an- 
gles and  ends.  They  may  be  found  in 
old  purulent   sputum  from  phthisical 

or  pulmonary  abscess  cavities,  or  where  old  pus  accumulations  have 

perforated  into  the  bronchial  tubes. 

(3)  Hmmatoidin  crystals^  derived  from  haemoglobin,  occur  as 
needles  or  rhombi  of  a  red  or  brownish-yellow  colour.  They  are 
found  where  there  is  an  old  extravasation  of  blood  into  the  lungs,  or 
where  perforation  of  an  empyema  or  other  abscess  has  taken  place. 

(4)  Fatty  acid  crystals^  fine  long  needles,  generally  bunched  or 
clustered,  occur  frequently  in  putrid  bronchitis,  pulmonary  gan- 
grene, phthisis,  bronchiectasis,  old  sputum,  and  follicular  plugs  of 
the  tonsils ;  consequently  their  diagnostic  value  is  slight. 

(5)  Leucin  globules  and  ty rosin  crystals  are  found  in  the  puru- 
lent sputum  from  old  perforating  empyemas  and  putrid  bronchitis. 
Earely  crystals  of  calcium  oxalate 
and  triple  phosphates  may  be  en- 
countered. 

(Ji)  Animal  Parasites.  —  (l) 
Ecliinococcus. — In  the  comparative- 
ly rare  cases  of  hydatids  of  the 
lung  or  near-by  organs,  the  hook- 
lets  of  the  organism  (Fig.  217),  or 
more  frequently  the  fragments  of 
the  cyst  wall,  may  be  encountered 
in  the  sputum,  rupture  into  a  bron- 
chus having  occurred. 

(2)  Distoma  pulmonale. — This  worm  when  lodged  in  the  lung 
causes  pulmonary  haemorrhage  which  may  be  mistaken  for  that  of 


i 


Qs=^ 


f 


f 


Fig.  217. 


-Hooklets  from  taenia  echino- 
coccus.     X  350. 


MICROSCOPICAL  EXAMINATION  OF  SPUTUM 


601 


phthisis.  It  is  common  in  China  and  Japan,  but  is  extremely  rare 
in  this  country.  Its  presence  is  betrayed  by  the  finding  in  the  spu- 
tum of  its  ova,  which  are  brown,  oval  bodies,  0.1  millimetre  long  and 
0.05  millimetre  wide  (see  Stools,  microscopic  examination). 

(3)  Amoeba  coli. — This  organism  {q.  v.)  when  found  in  the  sputum 
(a  very  rare  occurrence)  is  proof  positive  of  the  perforation  into  the 
lung  of  an  hepatic  abscess. 

{%)  Vegetable  Parasites. — (1)  Actinomyces. — Pulmonary  actino- 
mycosis is  of  infrequent  occurrence  in  this  country.  I  have  reported 
a  case  terminating  in  recovery  under  the  use  of  oil  of  eucalyptus 
(Med.  Xews,  April  29,  1898).  The  organism  is  found  in  the  sputum 
as  sulphur-coloured  granules  from  0.5  to  2  millimetres  in  diameter. 
If  a  granule  is  placed  under  a 
cover  glass  and  slight  pressure 
applied,  it  will  flatten  and  be  seen 
under  the  microscope  to  consist 
of  club-shaped  rods  or  threads  ra- 
diating from  a  common  centre 
(Fig.  218). 

(2)  Bacillus  tuberculosis. — 
This  is  by  far  the  most  important 
organism — clinically,  at  least — to 
be  found  in  the  sputum.  To  find 
it,  a  dried  preparation  is  made, 
picking  out,  if  possible,  for  this 
purpose,  one  of  the  small  caseous 
or  cheesy  masses  usually  discov- 
ered by  careful  inspection  of  the 
mass  of  sputum  when  spread  out  against  a  black  background.  The 
dried  and  fixed  specimen  is  to  be  stained  by  one  of  the  following 
methods : 

Ziehl-Xeelsen  Method. — This  requires  the  use  of  the  following 
solutions : 

A.  Concentrated  alcoholic  solution  of  fuchsin . . . 
Five-per-cent  aqueous  solution  of  carbolic  acid 
Twenty-five-per-cent  solution  of  sulphuric  acid. 
Saturated  watery  solution  of  methylene  blue. 

A  sufficient  quantity  of  solution  A  is  put  in  a  watch  glass,  the 
coated  cover  glass  immersed  in  it,  and  gentle  heat  applied  until  steam 
rises.  It  is  best  to  remove  and  reheat  the  solution  several  times, 
taking  three  or  four  minutes  in  the  process.  A  more  convenient 
method  is  to  put  a  few  drops  of  the  stain  upon  the  cover  glass,  which 


Fig.  218. — Actinomyces  in  sputum  (Hutchi- 
son and  Eainy). 


10  c. 
90    ' 


B. 
C. 


602  THE  EVIDENCES  OF  DISEASE 

is  then  held  by  forceps  over  the  flame,  heating  and  reheating  it,  as 
with  the  watch  glass.  Wash  the  cover  glass  in  water  to  remove  the 
excess  of  staining  fluid,  and  then  place  it  in  solution  B.  The  film, 
which  has  been  stained  red,  will  be  decolourized  by  this  solution,  the 
tubercle  bacilli  alone  retaining  the  colour.  The  cover  glass  should  be 
kept  in  motion  to  facilitate  the  bleaching  process.  Wash  in  water 
or  50-per-cent  alcohol,  and  if  a  contrast  staining  (i.  e.,  of  all  elements 
except  the  bacilli)  is  desired,  the  cover  glass  should  be  immersed  for 
one  minute  in  solution  C.  Wash  again  in  water,  dry,  and  mount  in 
a  drop  of  water  for  examination.  To  preserve  permanently,  mount 
in  Canada  balsam. 

Gabbett's  Method. — This  is  perhaps  a  still  more  convenient  method 
than  that  just  described.     Two  solutions  are  required  : 

A.  Fuchsin 1  grme. 

Absolute  alcohol 10  c.  c. 

Five-per-cent  solution  of  carbolic  acid 100    " 

B.  Methylene  blue 2  grmes. 

Twenty-five-per-cent  solution  of  sulphuric  acid,  100  c.  c. 

Place  the  preparation  for  two  or  three  minutes  in  solution  A, 
after  which  it  is  to  be  passed  directly  into  solution  B,  where  it  should 
remain  for  one  minute.  It  may  then  be  washed  in  water  and  mounted 
as  in  the  preceding  method. 

In  both  these  methods  of  staining  the  bacilli  appear  as  red  rods 
against  a  blue  background. 

The  presence  of  tubercle  bacilli  in  the  sputum  is  positive  evidence 
of  pulmonary  phthisis ;  their  absence  does  not  disprove  the  existence 
of  this  disease  unless  repeated  examinations  have  given  a  negative 
result,  as  they  may  be  absent  at  one  time  and  present  at  another.  If 
the  symptoms  and  signs  point  toward  a  phthisical  process,  and  yet 
the  bacilli,  presumably  because  of  their  scanty  number,  are  not  found 
by  the  ordinary  methods,  resort  may  be  had  to  one  or  both  of  the 
following  devices :  First,  the  sputum  may  be  stirred  with  a  glass  rod 
in  a  glass  or  porcelain  capsule  until  smooth  and  diffluent,  and  one  or 
two  centrifuge  tubes  filled  by  means  of  a  medicine  dropper  with  the 
thinned  material  and  centrifugalized,  a  portion  of  the  sediment  be- 
ing prepared  and  stained  as  usual ;  or,  second^  a  considerable  quantity 
(2  or  3  ounces)  of  sputum  may  be  mingled  with  an  equal  quantity  of 
water,  to  which  6  or  8  drops  of  a  10-per-cent  sodium  hydrate  solution 
has  been  added,  and  the  resulting  mixture  boiled  until  homogeneous, 
after  which  it  may  either  be  allowed  to  settle  for  one  or  two  days,  or 
centrifugalized.  A  portion  of  the  sediment  is  then  examined  for  the 
bacilli  and  elastic  tissue. 


MICROSCOPICAL  EXAMINATION   OP  SPUTUM  603 

(3)  Influenza  bacillus. — This  organism  (Pfeiffee's)  may  be  stained 
by  Loeffler's  solution,  which  is  : 

Concentrated  alcoholic  solution  of  methylene  blue 3  c.  c. 

One-tenth-per-cent  aqueous  solution  of  potassium  hydrate,  10  c.  c. 

This  should  be  freshly  mixed  when  needed.  Stain  the  dried  and 
fixed  cover-slip  preparations  for  from  5  to  10  minutes,  wash  in  water, 
and  mount  in  water  or  balsam.  The  organisms  are  coloured  blue,  and 
appear  as  extremely  small  rods.  Their  ends  stain  more  readily  than 
the  middle  portion,  and  although  for  this  reason  they  resemble  diplo- 
cocci,  they  have  no  capsule.  They  are  found  in  great  abundance  in 
the  bronchial  secretion. 

(4)  Diplococcus  pneumonicB. — This  is  best  demonstrated  by  the 
following  modification  of  Gram's  method : 

A.  Saturated  (filtered)  alcoholic  solution  of  gen- 

tian violet 1  c.  c. 

Five-per-cent  aqueous  solution  of  carbolic  acid,      9  c.  c. 

A  should  be  prepared  when  needed. 

B.  Iodine 1  g-rme. 

Potassium  iodide 2  grmes. 

Distilled  water 300  c.  c. 

Place  the  dried  and  fixed  cover-slip  film  (made  from  a  bit  of  rusty 
sputum)  in  solution  A  for  3  or  4  minutes,  wash  in  water,  and  trans- 
fer to  solution  J5,  letting  it  remain  for  1  or  2  minutes.  Then  wash 
in  alcohol  until  the  darkly  stained  film  is  decolourized.  After  this 
put  it  first  in  absolute  alcohol,  then  in  oil  of  cloves,  and  finally 
mount  in  balsam.  The  organism  is  seen  as  a  dark  blue  or  violet 
diplococcus.  Welch's  method  is  said  to  be  the  best  for  differentiat- 
ing the  characteristic  capsule  of  the  organism.  A  few  drops  of 
glacial  acetic  acid  are  placed  upon  the  spread  and  dried  cover  slip 
and  allowed  to  remain  a  minute  or  two.  Then,  without  washing, 
the  film  is  treated  repeatedly  with  solution  J,  until  it  is  judged  that 
the  acid  is  removed,  after  which  the  specimen  is  washed  with,  and 
mounted  in,  a  2-per-cent  salt  solution. 

The  absence  of  this  coccus  in  the  sputum  negatives  the  existence 
of  a  croupous  pneumonia ;  its  presence  is  not  altogether  conclusive, 
as  it  occurs  in  the  sputum  of  a  certain  proportion  of  healthy  persons. 


604  THE  EVIDENCES  OP   DISEASE 

SECTION  XL 
EXAMINATION  OF   THE  STOMACH   CONTEXTS 

The  gross  or  macroscopic  characters  of  the  vomited  contents  of 
the  stomach  have  been  previously  considered  (page  113) ;  the  method 
of  obtaining  the  gastric  contents  by  means  of  the  stomach  tube  has 
also  been  described  in  connection  with  the  physical  examination  of 
the  stomach  (page  453). 

I.  Physiology  of  Digestion 

Prior  to  dealing  with  the  chemical  and  microscopic  examination 
of  the  stomach  contents  a  brief  statement  of  certain  facts  in  the 
physiology  of  gastric  digestion  may  be  serviceable. 

Stomach  digestion  is  carried  on  by  means  of  a  mineral  acid,  a 
proteolytic  enzyme  (or  ferment),  and  a  coagulating  enzyme — i.  e., 
hydrochloric  acid,  pepsin,  and  rennin,  which  constitute  the  active 
agents  of  the  gastric  juice.  Practically  the  gastric  juice  affects  only 
the  proteids  (e.  g.,  meat)  or  the  albuminoids  (e.  g.,  gelatin)  of  the 
food.  The  gastric  juice  is  secreted  in  small  quantities  even  when 
the  stomach  does  not  contain  food,  but  the  presence  of  food  acts  as 
a  prompt  and  effective  stimulus  to  an  abundant  formation.  Fats 
and  starches  exert  the  least,  proteids  the  greatest,  stimulant  action. 

The  formation  of  hydrochloric  acid  begins  directly  after  the  tak- 
ing of  food.  It  immediately  combines  with  the  proteids  and  mineral 
salts  of  'the  food  to  form  acid  proteids  (syntonin)  and  acid  salts. 
As  soon  as  the  chemical  affinities  of  the  original  food  proteids  and 
salts  have  been  satisfied,  uncombined — i.  e.,  free — hydrochloric  acid 
may  be  found.  Under  the  influence  of  the  free  acid  the  zymogens 
(pepsinogen  and  chymosinogen)  secreted  by  the  gastric  glands  are 
transformed  into  pepsin  and  rennin.  The  only  action  of  the  rennin 
is  to  coagulate  the  casein  of  milk.  The  hydrochloric  acid  and  pep- 
sin act  together,  changing  the  proteids  and  the  curdled  casein,  first 
into  albumoses  (proteoses),  finally  into  peptones. 

II.  The  Chemical  Examination  of  the  Gastric  Contents, 
AND  the  Determination  of  the  Motor  Power  of  the 
Stomach 

At  the  height  of  digestion  in  a  normal  stomach  analysis  will 
show  the  presence  of  free  hydrochloric  acid,  acid  salts,  pepsin,  ren- 
nin, albumoses,  and  peptones.  The  object  of  the  examination  of  the 
gastric  juice  is  to  determine  the  presence  and  in  some  cases  the 


CHEMICAL  EXAMINATION  OF  STOMACH  CONTENTS         605 

amount  of  certain  of  these  constituents ;  and,  furthermore,  to  ascer- 
tain whether  certain  other  substances  are  present  which  normally 
are  not  produced  by  the  stomach.  The  principal  substances  which 
should  not  be  found,  except  as  they  or  their  salts  have  been  intro- 
duced as  a  part  of  the  ingested  food,  are  lactic,  acetic,  and  butyric 
acids.  These  acids  are  formed  in  large  quantities  under  certain 
pathological  conditions  which  favour  fermentation  of  the  ingested 
food.  The  motor  power  of  the  stomach — i.  e.,  its  churning  power 
and  its  ability  to  expel  the  products  of  gastric  digestion  (chyme) 
through  the  pyloric  orifice — is  also  to  be  determined ;  and  some 
information  is  to  be  obtained  from  a  microscopical  examination  of 
the  material  obtained  by  the  stomach  tube. 

A.   TEST   MEALS 

The  gastric  juice  is  usually  not  secreted  in  sufficient  quantity  for 
analytical  purposes  unless  the  stomach  contains  food.  The  amount 
and  time  of  appearance  of  the  various  ingredients  of  the  secretion 
will  vary  normally  within  certain  limits  according  to  the  quantity 
and  quality  of  the  food  taken.  Consequently  for  purposes  of  analy- 
sis and  comparison  it  is  necessary  to  give  a  definite  quantity  and 
quality  of  food,  and  to  withdraw  the  contents  of  the  stomach  at  a 
definite  period  of  digestion.  Hence  the  utility  of  the  various  test 
meals  which  have  been  devised.  Of  these  the  three  following  are 
the  most  useful.     The  first  mentioned  is  usually  all-sufficient. 

Ewald's  Test  Breakfast. — This  consists  of  one  or  two  baker's 
rolls  or  one  or  two  slices  of  dry  bread  (35  to  70  grammes,  a  little  over 
1  to  2  ounces),  and  300  to  400  cubic  centimetres  (roughly,  9  to  12 
ounces)  of  water  or  weak  tea.  The  amount  of  lactic  acid  contained 
in  this  quantity  of  bread  is  so  small  that  it  does  not  vitiate  the 
examination  in  ordinary  cases.  It  is  taken  in  the  morning,  no  food 
having  been  ingested  since  the  previous  evening.  Between  an  hour 
and  an  hour  and  a  half  after  the  meal  the  contents  of  the  stomach 
are  to  be  withdrawn. 

Boas' s  Test  Breakfast. — This  meal  is  employed  in  cases  in 
which  it  is  of  great  importance  to  eliminate  any  possibility  of  the 
introduction  of  lactic-acid-forming  substances  as  part  of  the  food — 
e.  g.,  in  suspected  gastric  cancer.  It  is  necessary  to  thoroughly  wash 
out  the  stomach,  either  on  the  night  previous,  or  at  least  one  hour 
prior  to  giving  the  meal.  The  meal  consists  simply  of  oatmeal  soup 
prepared  by  adding  a  tablespoonful  of  oatmeal  to  one  quart  of  water 
and  boiling  it  down  to  one  pint.  Xothing  is  to  be  added  except  a 
little  salt.  The  gastric  contents  are  to  be  removed  an  hour  or  an 
hour  and  a  half  after. 


606  THE  EVIDENCES  OF  DISEASE 

Von  Leube  and  Kiegel  Test  Dinner. — This  comprises  400 
cubic  centimetres  (12  to  14  ounces)  of  soup,  a  slice  or  two — 50 
grammes  (about  2  ounces) — of  wheat  bread,  100  to  200  grammes  (3 
to  6  ounces)  of  chopped  or  minced  beefsteak,  and  200  cubic  centi- 
metres (6  ounces)  of  water.  The  gastric  contents  are  to  be  with- 
drawn four  hours  after. 

The  fluid  obtained  from  the  stomach  is  either  allowed  to  settle  in 
a  tall  glass  jar,  the  supernatant  portion  being  taken  as  required,  or, 
better,  is  filtered  through  paper  or  fine  muslin. 

B.  THE  CHEMICAL  TESTS  AND  THEIR  TECHNIC 

The  general  practitioner  is  often  deterred  from  a  chemical  exami- 
nation of  the  stomach  contents  by  an  exaggerated  idea  of  the  diffi- 
culties of  the  processes  and  the  elaborateness  of  the  required  appa- 
ratus. While  it  is  true  that  some  of  the  methods  which  may  be 
employed  require  certain  resources  commonly  found  only  in  a  labo- 
ratory, it  is  also  true  that  by  a  choice  of  procedures  the  necessary 
clinical  investigations  can  be  made  with  comparatively  simple  means. 

In  all  cases  of  disease  which  require  an  examination  of  the  stom- 
ach contents  the  following  questions  are  to  be  answered  : 

What  is  the  reaction  ? 

Is  free  acid  present  (qualitative)  ? 

If  present,  is  it  hydrochloric  or  lactic  acid,  or  both  (qualitative)  ? 

If  it  is  hydrochloric  acid,  how  much  (quantitative)  ? 

What  is  the  total  acidity  ? 

Has  the  gastric  juice  normal  digestive  power  ? 

Under  certain  circumstances,  to  be  presently  explained,  it  may  be 
further  necessary  to  determine  the 

Amount  of  combined  hydrochloric  acid,  organic  acids,  and  acid  salts  (quan- 
titative). 

Presence  of  acetic  acid  (qualitative). 
Presence  of  butyric  acid  (qualitative). 
Presence  of  rennin  (chymosin). 

Reaction  of  Stomach  Contents. — Test  with  litmus  paper. 
The  normal  gastric  juice  is  always  acid  because  of  the  free  hydro- 
chloric acid  which  it  contains ;  and  when  obtained  by  the  tube  it  is 
also  acid  in  the  majority  of  pathological  conditions  because  of  the 
presence  of  lactic  and  fatty  acids.  Vomited  material  may  be  neutral 
or  alkaline,  so  also  if  there  is  a  large  admixture  of  mucus,  as  in  cer- 
tain cases  of  chronic  gastritis. 

If  Acid,  is  the  acidity  due  to  free  acids,  or  combined  acids  or  acid 
salts  ? — To  determine  this  point  Congo  red  is  employed  either  in 


CHEMICAL  EXAMINATION  OF  STOMACH  CONTENTS         607 

solution  or  as  a  test  paper.  The  latter  is  less  sensitive.  The  solu- 
tion and  the  paper  are  brownish  red  in  colour.  A  drop  or  two  of  the 
solution  is  added  to  a  little  of  the  gastric  juice,  or  a  strip  of  the  paper 
is  moistened  with  the  latter.  If  free  acid  is  present  the  red  colour 
changes  in  each  instance  to  a  light  blue  or  dark  blue,  according  to 
the  quantity  of  free  acid.  Combined  acids  or  acid  salts  do  not  cause 
the  colour  change. 

If  Free  Acid  is  Present,  is  it  hydrochloric,  or  lactic  acid,  or 
both  ? — A  reaction  with  Congo  red  simply  declares  the  presence  of  a 
free  acid.  The  free  acid  may  be  hydrochloric,  lactic,  acetic,  or 
butyric  acid.  The  tests  for  the  last  two  are  described  subsequently, 
as  the  most  important  findings  are  with  reference  to  the  first  two. 

To  Test  for  Free  Hydrochloric  Acid. — A  number  of  tests  are  in 
use,  of  which  the  three  following  are  quite  sufficiently  reliable  and 
delicate : 

(1)  Resorcin  Test. — The  reagent  consists  of 

Kesorcin 5  grmes.  (75  grs.) 

Cane  sugar 3  grmes.  (45  grs.) 

Alcohol  (94  per  cent) 100  c.  c.  (3^  oz.) 

Six  or  seven  drops  of  the  reagent  are  mixed  in  a  small  porcelain 
dish  with  an  equal  quantity  of  gastric  juice,  and  gradually  evapo- 
rated to  dryness  by  a  gentle  heat.  If  free  hydrochloric  acid  is  pres- 
ent, a  rosy  or  bright-red  colour  will  appear  around  the  margin  of  the 
dried  fluid,  just  after  evaporation  is  complete.  The  colour  fades  as 
the  dish  cools. 

(2)  Phlorogluciii-vanillin  {Giinzherg^s)  Test. — The  solution  em- 
ployed is 

Phlorogluein 2  grmes.  (30  grs.) 

Vanillin 1  grme.  (15  grs.) 

Absolute  alcohol 30  c.  c.  (1  oz.) 

This  solution  is  yellow,  and,  as  the  colour  changes  on  exposure  to 
light,  it  should  be  kept  in  a  dark  bottle.  The  first  two  ingredients 
are  expensive.  It  is  to  be  employed  in  the  same  manner  as  the 
resorcin  test,  except  that  greater  care  must  be  taken  to  avoid  rapid 
heating  or  charring.  The  process  of  evaporation  should  be  slow  and 
gentle.  If  free  hydrochloric  acid  is  present,  pink  or  rose-coloured 
marginal  lines  will  be  seen  as  the  last  of  the  fluid  dries  oflf.  A 
brownish  tint  indicates  either  overheating  or  the  absence  of  free 
hydrochloric  acid. 

(3)  Dimethyl-amido-azohenzol  Test. — This  reagent  (TOpfer)  is  used 
in  a  0.5-per-cent  alcoholic  solution.     One  or  two  drops  of  this  y^ellow 


608  THE  EVIDENCES  OP  DISEASE 

solution  are  added  to  a  little  of  the  gastric  juice  in  a  test  tube  or 
small  porcelain  dish,  without  heat.  If  free  hydrochloric  acid  is  pres- 
ent a  carmine  or  cherry-red  tint  develops,  the  depth  of  the  colour 
depending  upon  the  amount  of  the  free  hydrochloric  acid  contained 
in  the  juice. 

Of  the  three  tests  just  described  the  last  is  the  most  sensitive  and 
will  perhaps  replace  the  others  (Simon). 

To  Test  for  Free  Lactic  Acid.— (1)  Uffelmann's  Test. — Place  10 
cubic  centimetres  of  the  filtered  gastric  fluid  in  a  large  test  tube  or 
a  separation  funnel  and  add  50  cubic  centimetres  of  ether.  Shake 
thoroughly  for  several  minutes  and  pour  off  the  ether.  The  sepa- 
rated ether  may  be  divided  into  two  portions,  one  to  be  tested  for 
lactic  acid,  the  other  (if  required)  to  be  subsequently  employed  for 
the  detection  of  acetic  and  butyric  acids.  The  portion  to  be  tested 
for  lactic  acid  should  be  put  in  a  test  tube  or  shallow  dish  and  set  in 
hot  water.  The  other  portion,  in  a  similar  container,  is  allowed  to 
evaporate  spontaneously. 

The  residue  of  the  first  portion  is  to  be  dissolved  in  about  5  cubic 
centimetres  of  water.  Test  this  with  Uffelmann's  reagent,  which 
should  be  freshly  made  by  placing  in  a  test  tube  3  drops  of  liquefied 
carbolic  acid  and  3  drops  of  a  saturated  aqueous  solution  of  the 
sesquichloride  of  iron.  This  is  to  be  diluted  with  water  until  a  pale 
amethyst-blue  tint  is  secured.  To  the  bluish  solution  add  a  small 
portion  of  the  ethereal  extract,  when,  if  lactic  acid  is  present,  the 
blue  tint  changes  to  a  canary  yellow. 

(2)  KeUing's  Test. — Place  in  a  test  tube  5  cubic  centimetres  of  the 
gastric  fluid  and  add  ten  times  its  bulk  of  water.  Treat  the  diluted 
fl.uid  with  1  or  2  drops  of  a  5-per-cent  watery  solution  of  the  sesqui- 
chloride of  iron.  If,  upon  looking  at  the  tube  against  a  white  back- 
ground, the  fluid  is  distinctly  green,  the  presence  of  lactic  acid  is 
assured. 

To  Determine  the  Amount  of  Free  Hydrochloric  Acid. 
— If  the  previous  tests  have  shown  that  free  hydrochloric  acid  is 
present,  its  amount  may  be  determined  in  the  following  manner : 
Fill  a  graduated  burette  with  a  decinormal  solution  of  sodium 
hydrate  (4  grammes  to  1,000  cubic  centimetres  of  water).  Take  10 
cubic  centimetres  of  the  filtered  gastric  contents  and  add  to  it  3 
or  4  drops  of  a  0.5-per-cent  solution  of  dimethyl-amido-azobenzol, 
which,  owing  to  the  presence  of  hydrochloric  acid,  will  colour  the 
solution  red.  The  decinormal  sodium  -  hydrate  solution  is  then 
allowed  to  run  in,  drop  by  drop,  until  the  red  colour  disappears  and 
is  replaced  by  a  yellow  colour,  which  shows  that  the  free  hydrochloric 
acid  has  been  neutralized.     The  number  of  cubic  centimetres  of  the 


CHEMICAL  EXAMINATION  OF  STOMACH  CONTENTS         609 

decinormal  solution  required  to  effect  the  neutralization  is  then  read 
off  from  the  burette.  One  cubic  centimetre  of  the  sodium  solution 
neutralizes,  and  is  therefore  equivalent  to,  0.00365  gramme  of  hydro- 
chloric acid.  Consequently  if  3.6  cubic  centimetres  of  the  decinor- 
mal solution  have  been  required,  the  amount  of  hydrochloric  acid  in 
the  10  cubic  centimetres  of  gastric  juice  is  0.00365  X  3.6  =  0.01314 
gramme,  and  the  percentage  amount  in  100  cubic  centimetres  would 
be  0.01314  X  10  =:  0.1314. 

To  Determine  the  Total  Acidity. — The  total  acidity  of  the 
gastric  juice  is  due  to  the  free  hydrochloric  acid,  the  hydrochloric 
acid  combined  with  the  original  proteids  of  the  food,  and  the  organic 
acids  if  present  (lactic,  acetic),  together  with  the  acid  salts.  To 
determine  the  total  acidity,  the  gastric  fluid  is  titrated  with  the  deci- 
normal soda  solution  as  described  in  the  previous  paragraph,  except 
that  a  solution  of  phenolphthalein  is  used  as  the  indicator  instead  of 
dimethyl-amido-azobenzol.  Phenolphthalein  does  not  change  colour 
in  contact  with  acids,  but  becomes  red  in  an  alkaline  solution.  It  is 
employed  in  a  1-per-cent  alcoholic  solution,  2  or  3  drops  of  which 
are  added  to  10  cubic  centimetres  of  gastric  juice  in  a  test  tube, 
the  juice  remaining  colourless  because  acid.  The  soda  solution  is 
allowed  to  run  in,  the  test  tube  being  shaken  after  each  addition, 
until  the  rose  colour  which  appears  upon  the  addition  of  each  drop 
of  the  alkaline  solution  does  not  vanish  upon  shaking,  but  becomes 
permanent.  The  titration  is  not  to  be  stopped  at  this  point.  One 
should  continue  to  add  the  soda  solution,  still  shaking  the  test  tube, 
until  the  rose  colour  deepens  into  a  dark-red  hue.  The  number  of 
cubic  centimetres  of  the  decinormal  solution  required  to  neutralize 
the  acidity  of  100  cubic  centimetres  of  the  juice  is  taken  as  a  con- 
venient indicator  of  the  total  acidity.  Thus,  if  it  requires  7  cubic 
centimetres  of  the  decinormal  solution  to  produce  a  permanent  dark- 
red  colour  in  10  cubic  centimetres  of  the  gastric  juice — i.  e.,  to  neu- 
tralize its  total  acidity  it  will  require  10  times  this  amount  of  the 
alkaline  solution  to  neutralize  100  cubic  centimetres,  namely,  7  X 
10  =  70  =  the  degree  of  acidity.  It  may  be  expressed  also  in  terms 
of  hydrochloric  acid  by  multiplying  the  number  of  cubic  centimetres 
by  0.00365,  which  in  the  present  example  will  give  0.2555  per  cent. 

To  Test  the  Digestive  Po-wer  of  the  Gastric  Juice  and 
the  Presence  or  Absence  of  Pepsin  and  its  Zymogen. — As 
a  rule,  if  free  hydrochloric  acid  is  present  pepsin  is  usually  present. 
If  hydrochloric  acid  is  present  the  power  of  digestion  may  be  tested 
by  putting  0.05  gramme  (a  little  less  than  one  grain)  of  the  white  of 
a  hard-boiled  egg  in  a  test  tube  with  25  cubic  centimetres  of  the 
filtered  gastric  juice,  and  keeping  it  at  a  temperature  of  37°-40°  C. 


610  THE  EVIDENCES  OF   DISEASE 

If  the  coagulated  albumin  has  been  completely  digested  at  the  end 
of  3  hours,  it  may  be  inferred  that  pepsin  and  hydrochloric  acid 
are  present  in  normal  proportions  and  quantity.  If  the  previous 
tests  have  shown  the  absence  of  hydrochloric  acid,  the  juice  must 
be  acidulated  by  adding  5  drops  of  the  officinal  dilute  acid  before 
attempting  to  digest  the  white  of  egg.  If  under  these  conditions 
the  albumin  is  digested,  it  shows  that  the  zymogen  of  pepsin  (pep- 
sinogen) is  present  and  has  been  converted  into  pepsin  by  the  added 
hydrochloric  acid,  for  in  the  absence  of  the  latter  the  zymogen  alone 
is  usually  found.  On  the  other  hand,  if  digestion  does  not  take 
place  after  the  acid  is  added,  it  may  be  inferred  that  neither  pepsin 
nor  its  zymogen  are  present,  and  the  digestive  power  is  nil. 

If  the  foregoing  determinations  have  been  made  and  the  findings 
correspond  to  the  standards  of  health  (see  Index,  Gastric  Juice, 
normal  findings)  no  further  examination  need  be  made.  If,  how- 
ever, any  decided  departure  from  the  normal  has  been  discovered  the 
investigation  should  be  carried  further,  as  follows  : 

Determine  the  Amount  of  the  Combined  Hydrochloric 
Acid  and  the  Organic  Acids  and  Acid  Salts. — The  gastric 
contents  are  to  be  titrated  with  the  decinormal  soda  solution  as  in 
determining  the  amount  of  free  hydrochloric  acid  {q.  v.),  except  that 
a  1-per-cent  aqueous  solution  of  alizarin  monosulphonate  of  sodium  is 
used  as  the  indicator.  The  alizarin  solution  shows  no  change  of 
colour  when  added  to  a  fluid  containing  free  acids  or  acid  salts,  but 
turns  to  a  pure  violet  tint  either  when  the  fluid  is  alkaline,  or  if, 
when  acid,  the  acidity  is  due  to  combined  acids  alone.  As,  without 
considerable  experience,  it  is  difficult  to  judge  of  the  proper  tint  at 
which  to  terminate  the  titration,  it  is  recommended  (TOpfer)  that 
to  5  cubic  centimetres  of  a  1-per-cent  solution  of  sodium  carbonate 
3  drops  of  the  alizarin  solution  be  added.  The  resulting  violet 
colour  is  taken  as  a  standard  of  comparison. 

To  make  the  test,  place  10  cubic  centimetres  of  the  gastric  con- 
tents in  a  test  tube  and  add  3  or  4  drops  of  the  alizarin  solution. 
Eun  in  the  soda  solution  until  the  desired  colour  is  obtained.  The 
appearance  of  the  pure  violet  tint  indicates  that  the  free  acids  and 
acid  salts  have  been  neutralized  by  the  alkaline  solution,  and  that 
the  remaining  acidity  of  the  gastric  juice  is  due  to  the  hydrochloric 
acid  which  is  combined  with  the  albuminous  constituents  of  the 
food. 

The  total  acidity  of  the  gastric  juice  has  already  been  ascertained, 
and  from  the  test  just  made  the  proportion  of  the  total  acidity 
due  to  free  acids  and  acid  salts  is  known.  If  this  latter  be  subtracted 
from  the  total  acidity  the  difference  will  be  the  acidity  due  to  the 


CHEMICAL  EXAMINATION  OP  STOMACH  CONTENTS         611 

combined  HCl.  For  example,  it  is  found  that  it  requires  5  cubic 
centimetres  of  the  soda  solution  to  strike  a  violet  colour  in  10  cubic 
centimetres  of  gastric  juice.  It  will  therefore  require  50  cubic  centi- 
metres for  100  cubic  centimetres,  and,  multiplying  the  number  of 
cubic  centimetres  of  soda  solution  by  the  amount  of  HCl  required  to 
neutralize  1  cubic  centimetre  of  the  soda  solution,  it  will  be  found 
that  50  X  0.00365  =  0.1825  per  cent  =  the  amount  of  acidity  (in  terms 
of  HCl)  due  to  free  acids  and  acid  salts.  If,  therefore,  the  total 
acidity  has  been  found  to  be  0.2555  per  cent,  and  from  this  is  sub- 
tracted the  percentage  of  free  acids  and  acid  salts,  one  will  have 
0.2555  —  0.1825  =  0.0730  per  cent  =  combined  hydrochloric  acid. 

Furthermore,  as  the  free  acids  include  both  the  mineral  (HCl) 
and  organic  acids,  and  the  amount  of  free  hydrochloric  acid  has  been 
determined  to  be  0.1314,  if  the  amount  of  free  HCl  is  added  to  the 
amount  of  combined  hydrochloric  acid  and  the  result  deducted  from 
the  total  acidity,  the  resulting  figures  will  be  equivalent  to  the 
amount  of  organic  (lactic,  acetic,  butyric)  acids  and  acid  salts — i.  e., 
0.0730  +  0.1314  =  0.2044,  and  0.2555  -  0.2044  =  0.0511  =  organic 
acids  and  acid  salts. 

To  recapitulate :  By  titration  the  following  data  have  been 
secured  i 

The  amount  of  free  HCl  =  0.1314  =  A 

The  total  acidity =  0.2555  =  B 

The  amount  of  free  acids 

and  acid  salts =  0.1825  =  C 

From  these  data  can  be  calculated  X  =  the  amount  of  combined 
HCl ;  and  Y  =  the  amount  of  organic  acids  plus  acid  salts,  by  the 
following  formulae : 

B  -  C  =  X  =  combined  HCl. 

B  —  ( A  +  X)  =  Y  =  organic  acids  and  acid  salts. 

The  factors  of  the  total  acidity  and  their  amounts  are,  therefore, 
in  tabular  form : 

Free  hydrochloric  acid 0.1314  per  cent 

Combined  hydrochloric  acid 0.0730        '' 

Organic  acids  plus  acid  salts 0.0511        " 

Total  acidity 0.2555 

To  Determine  the  Presence  of  Acetic  and  Butyric 
Acids. — Take  the  residue  left  by  the  slow  evaporation  of  the  second 
portion  of  the  ethereal  extract  (page  608)  and  dissolve  it  in  about  5 
cubic  centimetres  of  water.  Evaporation  without  heat  is  advisable 
in  order  to  avoid  driving  off  the  volatile  acetic  and  butyric  acids. 


^12  THE  EVIDENCES  OP  DISEASE 

(1)  Test  for  Acetic  Acid. — It  may  often  be  recognised  by  its  odour. 
To  demonstrate  its  presence,  take  a  portion  of  the  watery  solution  of 
the  residue  and  exactly  neutralize  it  with  a  little  dilute  sodium 
hydrate  solution  or  small  pinches  of  powdered  sodium  carbonate. 
The  exact  point  at  which  neutralization  is  complete  is  best  ascer- 
tained by  placing  from  time  to  time  one  drop  of  the  fluid  upon  red 
and  another  upon  blue  litmus  paper  until  no  change  of  colour  occurs 
in  either  case.  Add  to  it  2  drops  of  a  very  dilute  solution  of  per- 
chloride  of  iron.  If  acetic  acid  is  present,  a  claret  or  dark-red  colour 
results. 

(2)  Test  for  Butyric  Acid. — This  may  be  often  recognised  by  its 
rancid  odour,  but  its  presence  may  be  demonstrated  by  adding  to 
the  remaining  portion  of  the  dissolved  ethereal  residue  a  small  frag- 
ment of  calcium  chloride.  If  butyric  acid  is  present  it  will  separate 
out  in  small  oily  drops,  which  possess  the  characteristic  strong  odour. 

To  Test  for  Rennin  (Chymosin)  or  its  Zymogen. — Add  3 
drops  of  the  filtered  gastric  Juice  to  5  cubic  centimetres  of  milk  and 
keep  it  at  a  temperature  of  37°-40°  C.  If  coagulation  takes  place 
within  10  or  15  minutes,  rennin  is  present.  If  hydrochloric  acid  is 
absent,  rennin  is  usually  also  absent,  but  its  zymogen  (chymosinogen) 
may  be  present.  To  determine  this  point,  add  to  10  cubic  centime- 
tres of  the  slightly  alkaline  gastric  juice  2  or  3  cubic  centimetres  of 
a  1-per-cent  solution  of  calcium  chloride  and  keep  the  solution  warm 
as  before.  As  calcium  chloride  is  capable  of  changing  the  zymogen 
into  rennin,  the  formation  of  a  coagulum  proves  the  presence  of  the 
zymogen. 

C.    TO    TEST   THE    MOTOR    POWER    OF   THE 
STOMACH 

Probably  the  most  reliable  and  the  simplest  manner  of  ascertain- 
ing the  motor  power  of  the  stomach  is  to  give  a  Leube-Riegel  test 
dinner  (page  606),  and  7  hours  afterward  to  wash  out  the  stomach 
with  1,000  cubic  centimetres  of  water  ;  or  the  patient  is  directed  to 
eat  a  hearty  supper  and  the  stomach  is  washed  out  the  next  morning 
before  breakfast.  If  in  either  case  only  slight  traces  of  food  are 
found  the  motor  power  of  the  stomach  may  be  considered  normal — 
i.  e.,  the  stomach  is  able  to  propel  its  contents  into  the  small  intes- 
tine. With  the  Ewald  test  breakfast  the  stomach  should  be  empty  2 
hours  after  the  meal.  In  cases  of  gastric  dilatation  lumps  or  frag- 
ments may  be  found,  and  the  quantity  of  partially  digested  food 
removed  may  be  very  large,  and  include  food  taken  not  only  at  the 
test  meal  but  also  during  the  previous  2  or  3  days. 

A  less  reliable  test  consists  in  giving  1  gramme  of  salol  in  cap- 


MICROSCOPIC  EXAMINATION  OP  STOMACH  CONTENTS       613 


sules  immediately  after  a  meal.  The  patient  is  directed  to  urinate 
at  intervals  of  half  an  hour,  1  hour,  2  hours,  and  24  hours  afterward, 
preserving  each  portion  in  a  separate  vessel.  Each  portion  is  to  be 
tested  for  salicyluric  acid  by  adding  to  the  urine  a  small  quantity  of 
a  solution  of  the  sesquichloride  of  iron,  which  in  the  presence  of  the 
acid  strikes  a  violet  colour.  As  salol  is  decomposed  into  phenol  and 
salicylic  acid  only  in  an  alkaline  fluid,  the  appearance  of  the  violet 
colour  is  evidence  that  it  has  been  passed  from  the  acid  stomach  into 
the  alkaline  intestine.  If  the  motor  power  is  normal  the  reaction 
should  appear  in  about  1  hour.  A  delayed  reaction  shows  a  lack  in 
this  respect,  and  if  it  is  not  obtained  within  24  hours  stenosis  of  the 
pylorus  may  be  predicated. 

D.    THE    MICROSCOPIC    EXAMINATION    OF   THE 
STOMACH    CONTENTS 

Either  vomited  matter  or  the  stomach  contents  obtained  by  the 
tube  may  be  examined.  A  portion  of  the  sediment  after  settling,  or 
of  the  material  remaining  in  the  filter,  is  spread  upon  a  slide  and, 
with  or  without  a  cover  glass,  placed  under  the  microscope.  One 
may  find  (Fig.  219) : 

1.  Food  Particles. — Fat  drops  are  recognised  by  their  refractility ; 
muscle  fibres  by  their  transverse  striations ;  elastic  tissue  fibres  by 
their  curled  ends  and  double  contour ;  starch  granules  by  their  con- 

Oil  globules 

starch  granules 

Epithelial  cells  

Muscle  fibres 
Sarcina  ventriculi 

Saccharomyces 


Vegetable  cells 


Fig.  219. — Microscopical  view  of  vomited  matter. 

centric  strise,  and,  if  necessary,  their  blue  colour  reaction  when  a 
weak  iodine  solution  is  added ;  fatty  acids  by  their  needle-shaped 
crystals.  Vegetable  cells  are  to  be  recognised  only  by  a  previous 
acquaintance. 

2.  Vegetable  Parasites. — The  most  important  are  the  Sarcina 
ventriculi.)  small  spherical  cells  arranged  in  groups  of  squares ;  yeast 
41 


614  THE  EVIDENCES  OF   DISEASE 

fungi  (SaccJiaromt/ces),  oval  or  round  cells  about  as  large  as  the 
average  leucocyte,  in  bunches  or  chains,  staining  a  deep  brown  with 
a  dilute  iodine  solution ;  and  the  Boas-  Oppler  hacillus  (found  quite 
constantly  in  cancer  of  the  stomach),  rods  of  unusual  length,  fre- 
quently Joined  by  their  ends,  and  forming  characteristic  long,  angu- 
lated  threads,  stainable  by  methylene  blue  and  other  aniline  dyes. 

3.  Morphological  Elements. — Leucocytes,  red  cells  (see  Haematem- 
esis,  p.  122),  epithelial  and  mucous-gland  cells  may  also  be  found. 
From  a  diagnostic  point  of  view  the  most  important  discovery  is  that 
of  shreds  or  fragments  of  the  gastric  mucous  membrane  or  of  parti- 
cles of  gastric  tumours. 

III.  DiAGKOSTic  Value  of  an"  Examiistatiok  of  the  Stomach 

COKTEJfTS 

A  word  may  be  said  here  as  to  the  circumstances  under  which 
an  examination  of  the  stomach  contents  becomes  necessary.  The 
contraindications  to  the  passage  of  the  tube  have  been  stated  else- 
where (p.  455).  In  acute  gastric  disorders  an  examination  of  this  kind 
ip  rarely  required  ;  nor  is  it  in  nervous  affections  and  chronic  diseases 
of  the  stomach,  provided  that  a  reasonably  certain  diagnosis  can  be 
made  without  it,  and  that  the  patient  is  improving  under  the  treat- 
ment advised.  If,  however,  the  condition  is  chronic,  doubtful,  and 
does  not  improve,  an  examination  of  the  stomach  contents  in  con- 
junction with  a  careful  consideration  of  the  associated  symptoms  is 
always  of  great  value,  and  in  many  instances  indispensable,  for  cor- 
rect diagnosis  and  proper  therapy. 

Diagnostic  Significance  of  the  Various  Items  of  the 
Examination  of  the  Gastric  Contents.— (1)  Quantity  of  the 
Gastric  Juice. — The  normal  amount  of  filtrate  to  be  obtained  one 
hour  after  Ewald's  test  breakfast  varies  from  20  to  50  cubic  centi- 
metres. If  periodic  or  chronic  hypersecretion  (gastrosuccorrhcea)  is 
suspected  because  of  the  symptoms,  the  stomach  should  be  washed 
out  at  bedtime  and  the  tube  passed  before  breakfast  on  the  follow- 
ing morning,  no  fluid  or  food  having  been  taken  in  the  meantime. 
If  from  100  to  1,000  cubic  centimetres  of  gastric  juice  are  then 
obtained,  a  diagnosis  of  hypersecretion  can  be  made.  It  is  usually  a 
neurosis.  Total  absence  of  the  gastric  juice  (achylia  gastrica)  is 
either  a  neurosis  or,  more  commonly,  an  evidence  of  atrophy  of  the 
gastric  mucous  membrane. 

(2)  Acidity  of  the  Gastric  Juice. — The  normal  total  acidity  varies 
from  40  to  60  one  hour  after  Ewald's  breakfast.  A  high  degree  of 
acidity  (70  to  90)  is  significant  of  certain  gastric  neuroses,  and  may 
be  associated  with  hypersecretion.     Increased  acidity  is  also  found 


RESULTS  OP  EXAMINATION  OF  STOMACH  CONTENTS       615 

in  gastric  ulcer,  and  in  some  instances  of  dilatation  of  the  stomach. 
On  the  other  hand,  a  decreased  acidity  is  a  usual  concomitant  of 
gastritis,  either  acute  or  chronic,  and  of  some  neurotic  affections  of 
the  stomach. 

(3)  Presence  and  Amoiint  of  Free  Hydrocliloric  Acid.— For  the 
production  of  hydrochloric  acid  the  cells  of  the  gastric  glands  must 
be  in  good  condition,  the  blood  supply  ample  and  of  good  quality, 
and  the  innervation  competent  and  regular.  A  deficiency  in  one  or 
all  of  these  necessary  requirements  will  produce  disturbances  in  the 
formation  of  the  acid.  Aside  from  the  digestive  function  of  hydro- 
chloric acid,  it  has  been  proved  that  it  plays  a  not  unimportant  part 
as  a  germicide  and  antiseptic  in  regard  to  some  of  the  bacteria  which 
cause  either  fermentation  or  disease.  Consequently  the  conditions 
which  diminish  the  secretion  of  hydrochloric  acid  render  the  indi- 
vidual more  vulnerable  to  all  organisms  which  enter  by  way  of  the 
intestinal  tract,  either  those  which  are  pathogenic  (e.  g.,  Bacillus 
typhosus,  cholera  bacillus),  or  those  which  give  rise  to  fermentation 
and  putrefaction  (e.  g.,  the  bacteria  producing  lactic  or  acetic  acids). 
Under  normal  circumstances  the  amount  of  free  hydrochloric  acid 
found  one  hour  after  the  regular  test  breakfast  varies  from  0.1  to 
0.2  per  cent  {euclilorhydria).  Under  pathological  conditions  it  may 
be  increased  {hyperchlorhydria)^  diminished  (hypochlorhydria),  or 
absent  (anachlorhydria). 

A  normal  secretion  of  free  hydrochloric  acid  is  not  inconsistent 
with  subjective  symptoms  of  gastric  disorders,  usually  of  the  neurotic 
kind ;  but  if  euchlorhydria  is  present,  it  negatives  chronic  gastric 
catarrh.  An  increase  of -the  free  hydrochloric  acid  (more  than  0.2 
per  cent)  is  found  in  gastric  ulcer,  or  in  cancer  of  the  stomach  origi- 
nating from  an  old  ulcer.  Hyperchlorhydria  is  most  commonly  a 
symptom  of  a  neurosis  of  the  stomach,  especially  if  there  is  also  a 
continuous  hypersecretion.  Hypochlorhydria  (less  than  0.1  per  cent) 
indicates  in  general  some  condition  which  has  destroyed  to  a  notable 
extent  the  secreting  glands  or  cells  of  the  gastric  mucous  membrane. 
Consequently,  although  it  may  be  a  neurosis,  a  diminished  amount 
of  free  hydrochloric  acid  is  often  significant  of  a  more  or  less  chronic 
gastritis,  beginning  cancer,  dilatation,  and,  more  rarely,  of  certain 
cases  of  gastric  ulcer.  The  total  absence  of  free  hydrochloric  acid  is 
frequently  indicative  of  a  gastric  neurosis  in  hysteria  and  neuras- 
thenia, is  usually  one  of  the  findings  in  the  later  stages  of  chronic 
gastritis  (atrophic  or  sclerotic  form),  and  is  a  quite  characteristic 
but  not  invariable  symptom  of  gastric  cancer. 

In  the  absence  of  free  hydrochloric  acid  it  is  of  some  importance, 
mainly  with  reference  to  treatment,  to  ascertain  whether  combined 


616  THE  EVIDENCES   OF   DISEASE 

hydrochloric  acid  is  present,  and,  if  so,  its  amount.  If  no  combined 
HCl  is  found,  gastric  digestion  is  nil,  the  dietetic  management  must 
correspond,  and  the  prognosis  is  not  good.  Per  contra,  the  presence 
of  combined  HCl  shows  that  gastric  digestion  is  partly  accomplished, 
so  far  as  to  satisfy,  in  a  measure  at  least,  the  chemical  affinities  of  the 
albuminous  foods,  although  not  enough  HCl  is  secreted  to  afford  the 
normal  amount  of  the  free  acid. 

(4)  Pepsin  and  Pepsinogen. — Absence  of  pepsin — i.  e.,  failure  of 
the  artificially  obtained  gastric  juice  to  digest  egg  albumen  without 
the  addition  of  HCl — is  usual  when  free  HCl  is  lacking,  as  the  pres- 
ence of  the  latter  is  required  to  transform  the  pepsinogen  into  pep- 
sin. The  absence  of  pepsinogen — failure  to  digest  after  the  addition 
of  HCl — is  significant  of  a  grave  destruction  of  the  glandular  ele- 
ments of  the  gastric  mucous  membrane,  and  therefore  warrants  a 
diagnosis  of  an  organic  disease — e.  g.,  advanced  chronic  gastritis — 
rather  than  a  neurosis.  Simple  functional  derangements  (nervous 
or  circulatory)  rarely  have  any  influence  on  the  secretion  of  pep- 
sinogen as  compared  to  their  notable  effect  in  causing  marked  varia- 
tions in  the  formation  of  hydrochloric  acid. 

The  presence  or  absence  of  rennin  and  its  zymogen  has  practically 
the  same  significance  as  that  of  pepsin  and  its  zymogen. 

(5)  Lactic,  Acetic,  and  Butyric  Acids. — Lactic  acid,  except  as 
derived  from  the  action  of  certain  organized  ferments  upon  the 
ingested  food,  or  its  original  presence  therein  (sarco-lactic  acid  of 
meat,  lactic  acid  in  bread),  is  not  a  normal  constituent  of  the  gastric 
juice.  The  amount  contained  in  Ewald's  test  breakfast  is  not  suffi- 
cient to  give  a  reaction  to  the  tests  usually. employed,  but  if  a  possi- 
ble error  from  this  source  is  to  be  guarded  against,  the  Boas  break- 
fast should  be  used.  A  marked  lactic-acid  reaction  is  extremely 
significant,  but  not  absolutely  pathognomonic,  of  gastric  cancer,  since 
it  may  be  found  also  in  the  stagnation  of  gastric  dilatation  due  to 
non-malignant  disease,  or  when  the  glandular  elements  are  almost 
eutirely  destroyed.  The  absence  of  lactic  acid,  however,  does  not 
forbid  the  existence  of  cancer. 

The  presence  of  butyric  acid,  except  when  fats  have  formed  a  por- 
tion of  the  meal,  as  well  as  of  acetic  acid,  except  when  alcohol,  from 
which  acetic  acid  may  be  formed  by  fermentation,  has  been  ingested, 
has  essentially  the  same  diagnostic  significance  as  that  of  lactic  acid. 

(6)  Mucus. — The  persistent  finding  of  considerable  quantities  of 
mucus  in  the  gastric  contents  obtained  by  the  tube  is  good  proof  of 
the  existence  of  a  form  of  chronic  gastritis  which  is  characterized 
by  an  excessive  formation  of  this  substance.  Vomiting  of  mucus 
unmixed  with  food  will  exclude  gastric  dilatation,  and,  if  the  clinical 


GASTRIC  CONTENTS  IN  SPECIAL  DISEASES  617 

symptoms  of  gastritis  are  absent  and  it  occurs  especially  in  neuras- 
thenic women,  is  doubtless  akin  to  the  neurosis  improperly  termed 
membranous  enteritis. 

The  Results  of  an  Examination  of  the  Gastric  Con- 
tents in  Special  Diseases  or  Conditions. — It  should  be  clearly 
understood  that  a  diagnosis  can  not  be  based  solely  upon  an  exami- 
nation of  the  stomach  contents,  as  in  a  certain  proportion  of  cases 
abnormal  findings  may  coexist  with  an  absence  of  other  symptoms. 
Every  evidence  of  disease,  both  subjective  and  objective,  is  to  be 
taken  into  consideration  before  arriving  at  a  definite  conclusion. 
For  the  sake  of  comparison,  in  outlining  the  following  groupings  of 
the  results  the  normal  findings  are  first  stated.  The  statements  with 
reference  to  lactic  acid  apply  especially  to  Boas's  breakfast. 

(1)  Normal  Findings. — The  reaction  is  acid ;  free  hydrochloric 
acid  present  in  proportion  of  0.1  to  0.2  per  cent ;  total  acidity,  40  to 
60;  ferments  (pepsin,  rennin)  present;  lactic,  acetic,  and  butyric 
acids  absent ;  little,  if  any,  mucus,  and  only  traces  of  food. 

(2)  Gastric  Ulcer. — Total  acidity  usually  increased ;  free  hydro- 
chloric acid  usually  increased ;  ferments  present ;  lactic,  acetic,  and 
butyric  acids  absent ;  frequently  contains  blood  pigment. 

(3)  Cancer  of  the  Stomach. — Total  acidity  variable ;  free  hydro- 
chloric acid  greatly  diminished  or  absent,  unless  the  growth  has  as  a 
basis  an  old  gastric  ulcer ;  ferments  not  infrequently  absent ;  lactic, 
acetic,  and  butyric  acids  present  in  quantity  after  Boas's  breakfast ; 
mucus,  coffee-ground  material,  stagnant  food,  Boas-Oppler  bacillus. 

(4)  Dilatation  of  the  Stomach  not  caused  by  Malignant  Pyloric 
Stenosis. — Total  acidity  normal  or  increased  ;  free  hydrochloric  acid 
sometimes  diminished,  more  commonly  increased  ;  ferments  present ; 
lactic,  acetic,  and  butyric  acids  absent  after  Boas's,  present  after 
Ewald's,  breakfast ;  decomposed  and  undigested  food,  yeast  fungi, 
and  bacteria. 

(5)  Acute  Gastritis. — Total  acidity  decreased ;  free  hydrochloric 
acid  absent ;  ferments  diminished ;  lactic,  acetic,  and  butyric  acids 
usually  absent ;  mucus,  partly  digested  food  particles,  some  red 
blood  cells,  fluid  tinged  green  (bile  pigment). 

(6)  Chronic  Gastritis. — Total  acidity  diminished  (in  atrophic 
form  reaction  neutral  or  alkaline) ;  free  hydrochloric  acid  diminished 
or  absent,  and  in  the  atrophic  form  absent ;  lactic,  acetic,  and  butyric 
acids  absent  after  Boas's  breakfast ;  ferments  present  (in  atrophic 
form  absent) ;  partly  digested  food  present  (in  the  atrophic  form  no 
evidence  of  digestion) ;  much  mucus  indicates  the  so-called  "  mucous 
gastritis  " ;  shreds  of  mucous  membrane  (erosions)  present  except  in 
atrophic  form. 


618  THE  EVIDENCES  OP   DISEASE 

(7)  Hyper cJilorhydria. — Total  acidity,  70  to  140 ;  free  hydrochloric 
acid  much  increased ;  ferments  normal  or  increased ;  diagnosis  not 
to  be  made  unless  the  hyperacidity  is  persistent. 

(8)  Hypersecretion^  Periodic  {Gastroxynsis)  or  Chronic. — Pres- 
ence of  100  to  1,000  cubic  centimetres  of  gastric  juice  in  the  fasting 
stomach,  continuously  or  periodically. 

(9)  Achylia  Gastrica. — Total  acidity  low,  may  be  neutral ;  no 
hydrochloric  acid ;  no  ferments  ;  gastric  juice  practically  absent 
While  the  condition  usually  signifies  the  presence  of  one  of  the  dis- 
eases causing  anachlorhydria,  it  may  be  a  neurosis. 


SECTION  XLI 
MICROSCOPICAL  EXAMINATION   OF.  THE  F^CES 

The  gross  characters  of  the  faeces  have  been  previously  described, 
(p.  132).  The  microscopical  examination  involves  a  search  for  food 
particles,  morphological  elements,  crystals,  and  parasites  (animal 
or  vegetable).  The  osmic  unpleasantness  of  the  investigation  may 
be  lessened  by  putting  the  stool  in  a  glass  jar  or  deep  dish  and  over- 
laying it  with  ether,  turpentine,  or  carbolic-acid  solution. 

After  undergoing  a  naked-eye  inspection  any  suspicious  particle 
or  portion  should  be  placed  upon  a  slide  ;  by  means  of  forceps  if  the 
stool  is  solid,  or  a  pipette  if  fluid.  If  solid,  a  little  normal  (0.6-per- 
cent) salt  solution  may  be  added  and  a  cover  glass  put  on.  In  search- 
ing for  the  amoeba  the  slide  must  be  warmed,  or,  better,  a  warm  stage 
employed. 

Food,  Morphological  Elements,  and  Crystals. — Particles 
of  food  may  be  found  as  described  in  the  microscopical  examination 
of  the  stomach  contents  (page  613).  The  discovery  of  many  undi- 
gested starch  granules  or  muscle  fibres  is  evidence  of  a  catarrhal 
condition  of  the  small  intestine. 

Crystals — Charcot-Leyden,  fatty,  triple  phosphates,  cholesterin, 
and  haematoidin — may  be  found.  They  possess  little  pathological 
significance.  The  Charcot-Leyden  crystals  are  said  to  be  quite  con- 
stantly present  in  cases  of  helminthiasis. 

The  morphological  elements  found  in  the  faeces  comprise  leuco- 
cytes or  pus  cells,  red  corpuscles,  and  epithelial  cells.  The  presence 
of  a  considerable  number  of  leucocytes  is  significant  of  a  more  or  less 
severe  inflammation  of  the  intestinal  mucosa ;  large  amounts  of  pus 
occur  in  dysentery,  or  when  an  abscess  has  perforated  the  intestine. 
Red  corpuscles,  recognisable  as  such,  are  found  only  when  the  hem- 


MICROSCOPIC  EXAMINATION  OF  F^CES 


619 


orrhage-producing  process  (e.  g.,  ulceration)  is  situated  in  the  colon 
or  rectum.  If  the  blood  has  come  from  the  small  intestine  the  red 
cells  are  altered  and  represented  by  amorphous  brownish-red  masses 
of  hsmatoidin,  or  crystals  of  the  latter.  Epithelial  cells,  if  found 
in  large  quantities,  often  embedded  in  mucus,  are  indicative  of  a 


Fig.  220. — Ova  of  entozoa,  x  350  (after  Heller),  a,  Oxyuris  vermicularis ;  b,  ascaris  lum- 
brieoides;  c,  trichocephalus  dispar ;  v,  ttenia  solium ;  k,  taenia  mediocanellata ;  f,  both- 
riocephalus  latus :  o,  distoma  hepaticum  ;  h,  distoma  lanceolatum. 

catarrhal  condition  of  some  portion  of  the  intestinal  mucosa.  Micro- 
scopic particles  of  mucus,  coloured  with  bile  if  the  catarrhal  process 
is  seated  in  the  upper  portion  of  the  small  intestine,  are  found  in 
similar  conditions. 

Parasites,  Animal  and  Vegetable.— Of  the  many  varieties 
of  living  organisms  found  in  the  intestine  the  following  are  patho- 
genic, and  therefore  of  clinical  importance  : 


620 


THE  EVIDENCES  OP    DISEASE 


[a)  Animal  Organisms. — (1)  Vermes  or  Worms. — The  adult  vermes 
have  already  been  described  in  connection  with  the  naked-eye  in- 
spection of  the  faeces  (page  138).  In  the  event  of  the  non-discovery 
of  the  full-grown  organisms  the  search  for  and  finding  of  their  ova 
in  a  suspected  case  is  of  importance.  In  Fig.  220  the  ova  of  the 
worms  most  likely  to  be  encountered  are  shown  with  sufficient  dis- 
tinctness for  purposes  of  identification. 

(2)  Protozoa. — The  most  important  representative  of  the  pro- 
tozoa found  in  the  faeces  is  the  Amoeba  coli  (or  dysenterice).  This  is 
a  motile  unicellular  organism  varying  from  10  /a  to  25  /t  in  diameter. 
Its  outer  zone  or  ectosarc  is  clear  and  homogeneous ;  the  endosarc 

or  interior  portion  is  granular, 
containing  a  nucleus  of  vari- 
able distinctness,  and  one  or 
more  rather  striking  vacuoles. 
When  active,  the  contour  is 
irregular,  because  of  the  pro- 
trusion of  pseudopodia  com- 
posed mainly  of  the  translu- 
cent ectosarc.  At  rest,  the 
outline  is  circular  or  ovoid 
(Fig.  221).  When  searching 
for  the  Amoeba  coli  special  at- 
tention should  be  given  to  the 
small  masses  of  mucus  in  the 
stool.      When   found    in   the 

Fig.  221. — a,  Amoeba  dysenterise  fixed  and  stained    «  ,,  n        j^         i^ 

,n       .,       \   1.        x.   A       .  ■    ■     .   1    iseces  they  are  usually  at  rest, 

(Councilman) ;  o,  amoeba  dysentense  m  stools  -^  -^  ' 

(after  Losch,  Virchow's  Archiv,  Bd.  65).  and  are  to   be  recognised  by 

their  light  greenish  tint  and 
marked  refractility.  In  dried  cover-slip  films  they  may  be  stained 
with  methylene  blue. 

This  organism  is  the  cause  of  tropical  dysentery  and  the  liver 
abscess  which  may  complicate  the  disease.  A  not  inconsiderable 
number  of  cases  have  occurred  in  Europe  and  Xorth  America. 

The  Plasmodium  malarim  has  been  found  in  the  red  corpuscles 
contained  in  the  stools  from  a  case  of  chronic  malarial  colitis 
(SiMox). 

{b)  Vegetable  Organisms. — Of  these,  the  most  important  are  the 
Comma  bacillus.,  the  Bacillus  typhosus,  the  Bacillus  coli  communis., 
and  the  Bacillus  tuberculosis.  The  sure  recognition  of  these  bacilli, 
with  the  exception  of  the  last  mentioned,  requires  the  knowledge 
and  resources  of  the  bacteriological  expert.  It  is  somewhat  difficult 
to  differentiate  the  bacillus  of  true  cholera  from  that  of  cholera  nos- 


EVIDENCE  FROM  PHYSICAL  URINALYSIS  621 

tras ;  so  also  with  the  bacillus  of  typhoid  fever  and  the  Bacillus  coli 
communis. 

(1)  Comma  bacillus. — This  is  a  curved,  rod-shaped,  mobile  organ- 
ism, shorter  and  thicker  than  the  tubercle  bacillus.  It  is  the  specific 
cause  of  Asiatic  cholera. 

(2)  Typhoid  bacillus  (Eberth). — This  is  a  flagellated  motile  rod 
with  rounded  ends,  about  half  the  diameter  of  a  red  blood  cor- 
puscle. 

(3)  Bacillus  coli  communis. — This  organism,  which  closely  resem- 
bles Eberth's  bacillus  of  typhoid  fever,  is  constantly  present  in  nor- 
mal faeces.  It  may  become  pathogenic  and  cause  suppurative  in- 
flammation— e.  g.,  cystitis,  appendicitis,  and  perforation  peritonitis, 
pyelitis,  and  inflammation  of  the  gall  bladder. 

(4)  Bacillus  tuberculosis. — This  may  be  demonstrated  in  the 
faeces  by  making  and  staining  cover-slip  films  as  directed  for  the 
sputum  (page  601).  When  found  they  are  not  to  be  considered  in- 
dicative of  intestinal  tuberculosis  unless  the  clinical  symptoms  of 
the  latter  are  present,  as  they  may  originate  from  swallowed  sputum. 


SECTION  XLII 

DIAGNOSTIC   INFERENCES   TO    BE    DRAWN   FROM   THE 
RESULTS   OF  URINALYSIS 

In"  view  of  the  abundant  supply  of  excellent  special  treatises, 
both  large  and  small,  which  deal  with  the  technic  of  urinalysis,  it  has 
seemed  a  work  of  supererogation  to  cumber  this  work  with  neces- 
sarily abbreviated  descriptions  of  the  large  number  of  extant  meth- 
ods. This  section  therefore  deals  with  the  diagnostic  significance  of 
the  various  findings  of  the  urinalysis. 

The  physical  examination  of  the  kidney  has  been  previously 
described  (page  476) ;  so  also  have  certain  symptoms  relating  to  the 
genito-urinary  system  (page  139). 

I.    EVIDENCE    DERIVED    FROM    A    PHYSICAL 
EXAMINATION    OF   THE    URINE 

(1)  Quantity  of  the  Urine. — The  amount  of  urine  excreted 
in  24  hours  varies  considerably  under  normal  circumstances.  The 
average  total  quantity  is  stated  variously  by  different  writers,  the 
discrepancy  depending  largely  upon  the  country  in  which  their 
observations  were  made.     For  the  United  States  we  may  accept  as 


622  THE  EVIDENCES  OP  DISEASE 

normal  1,200  cubic  centimetres  (40  oz.)  for  the  adult  man,  and 
1,000  cubic  centimetres  (33  oz.)  for  the  adult  woman.  In  children 
between  2  and  12  years  of  age  the  number  of  ounces  is  approxi- 
mately equal  to  double  the  years  of  the  child's  age. 

The  total  daily  excretion  is  physiologically  increased  in  cold 
weather  and  by  the  taking  of  large  amounts  of  fluid  ;  it  is  decreased 
in  hot  weather,  by  free  perspiration,  and  by  a  diminished  consump- 
tion of  fluids.  With  reference  to  diurnal  variations,  it  may  be  re- 
membered that  from  2  to  4  times  as  much  urine  is  passed  during 
the  day  as  during  the  night. 

An  amount  less  than  500  cubic  centimetres  (17  oz.)  or  more 
than  3,000  cubic  centimetres  (99  oz.),  if  persistent,  may  be  con- 
sidered to  be  pathological ;  but  the  occasional  finding  of  such  quan- 
tities does  not  necessarily  imply  an  abnormal  condition. 

(a)  Increased  Quantity. — Polyuria  may  signify  diabetes  (mellitus 
or  insipidus)  in  which  25,000  cubic  centimetres  (825  oz.),  or  even 
more,  have  been  passed ;  and  chronic  interstitial  nephritis  (2,000  to 
4,000  cubic  centimetres,  66  to  132  oz.  or  more).  Amyloid  disease 
of  the  kidney  is  attended  with  an  increased  excretion  of  urine. 
Polyuria  also  occurs  during  the  resorption  of  large  effusions 
(pleural,  peritoneal,  pericardial,  anasarcous) ;  as  a  symptom  of  cer- 
tain functional  diseases  of  the  nervous  system,  notably  hysteria 
and  neurasthenia,  epilepsy,  chorea,  or  migraine ;  and,  usually  as  a 
favourable  sign,  during  the  defervescence  of  acute  fevers.  A  per- 
sistent polyuria  is  seen  in  some  organic  diseases  of  the  nervous 
system,  as  in  certain  cases  of  cerebellar,  bulbar,  and  spinal  tumours, 
meningitis,  and  locomotor  ataxia.  An  excessive  flow  of  urine  may 
in  rare  instances  be  a  part  of  the  condition  termed  phosphatic  dia- 
betes (see  Phosphates). 

(b)  Diminished  Quantity. — Oliguria  is  one  of  the  evidences  of  a 
low  blood  pressure,  and  is  consequently  met  with  in  cases  of  broken 
compensation  due  to  valvular  disease,  or  in  weak  heart  dependent 
upon  degeneration  of  the  cardiac  muscle  occurring  as  a  result  of 
long-continued  fevers  or  wasting  disease.  In  all  fevers  the  urine  is 
usually  scanty.  A  diminution  is  also  seen  in  acute  and  chronic 
parenchymatous  nephritis.  Interference  with  the  return  venous 
circulation  of  the  kidney — i.  e.,  an  increase  of  the  renal  intravenous 
pressure — produces  oliguria,  as  in  pressure  from  ascites  or  abdominal 
tumours,  or  a  damming  back  of  the  blood  by  thrombosis  of  the 
inferior  cava  or  renal  vein.  So  also  does  the  loss  of  a  large  amount 
of  fluid  from  the  body,  as  in  cases  of  severe  diarrhcea,  cholera,  per- 
sistent vomiting,  or  large  hemorrhages.  A  calculus  lodged  in  the 
ureter,  or  a  tumour  pressing  upon  the  latter,  may  account  for  an 


EVIDENCE  FROM  PHYSICAL  URINALYSIS  623 

oliguria.     Scanty  urine  finally  may  be  a  symptom  of  hysteria,  mel- 
ancholia, and  lead-poisoning. 

Complete  suppression  of  urine  (Anuria,  q.  v.)  has  been  described 
elsewhere. 

(2)  Colour  of  the  Urine. — Normally  the  urine  varies  from  a 
light  yellow  to  a  brownish  red.  The  more  acid  the  urine  and  the 
greater  its  specific  gravity  the  more  highly  coloured  it  is,  with  the 
exception  of  diabetic  urine,  in  which  the  colour  is  light  and  the 
specific  gravity  high. 

(«)  Pale  Urine. — This  usually  indicates  an  excess  of  water,  and 
is  found  in  the  various  conditions  enumerated  as  causing  polyuria. 
Its  presence  contraindicates  high  fever. 

{b)  Greenish-yelloio  or  Yellowish-brown  Urine. — Usually  indicates 
the  presence  of  bile  (see  Choluria),  but  may  be  due  to  the  ingestion 
of  santonin,  salol,  carbolic  acid,  guaiacol,  naphthaline,  or  resorcin. 

(c)  Red^  Orange-coloured^  Reddish-hroicn,  Smoky,  or  Brownish- 
hlack  Urine. — Generally  caused  by  the  presence  of  blood  or  its  deriv- 
atives (see  Haematuria).  Black  urine  (containing  melanin)  is,  in  rare 
instances,  due  to  the  existence  of  melanotic  cancer  in  some  part  of 
the  body.  The  administration  of  senna,  rhubarb,  and  chrysophanic 
acid  may  colour  the  urine  orange  or  brown.  A  port-wine  colour  may 
signify  the  existence  of  haematoporphyrinuria  {q.  v.). 

(d)  Milky  Urine. — Is  seen  as  an  evidence  of  chyluria,  or  lipuria, 
or  is  in  some  cases  due  to  the  presence  of  pus. 

(e)  Blue  Urine. — May  be  due  to  the  presence  of  indigo  formed 
from  an  excess  of  urinary  indican  {q.  r.),  or  occur  as  a  result  of  the 
administration  of  methylene  blue. 

(/)  Urines  which  Darken  on  Standing. — May  indicate  the  pres- 
ence of  alkapton  or  related  oxyacids ;  or  melanin  (melanotic  cancer)  ; 
or  the  ingestion  of  carbolic  and  salicylic  acids,  salol,  and  pyrocatechin. 
An  iridescent  brittle  film  composed  of  calcium  phosphate  may  form 
on  the  surface  of  standing  urine  if  the  latter  is  alkaline.  It  has  no 
clinical  significance. 

(3)  Odour  of  the  Urine. — The  normal  odour  of  the  urine  is 
variously  described  as  aromatic,  or  resembling  that  of  bouillon.  A 
so-called  "  urinous  "  or  ammoniacal  odour  is  indicative  of  decomposi- 
tion. The  taking  of  asparagus,  onions,  santonin,  or  cubebs  will 
impart  characteristic  odours.  Turpentine  affords  an  odour  of  vio- 
lets; in  diabetes  it  resembles  new-mown  hay;  in  acetonuria,  over- 
ripe apples  ;  and  a  faecal  odour  may  be  due  to  a  fistulous  communi- 
cation between  the  intestinal  and  urinary  tracts. 

(4)  Consistence  of  the  Urine. — Normally  it  is  aqueous  and 
very  slightly  viscid.    The  presence  of  large  amounts  of  bile,  albumin, 


624  THE   EVIDENCES  OF  DISEASE 

sugar,  pus,  blood,  or  blood  plasma  (fibrinuria)  renders  it  more  or  less 
viscid,  so  that  the  froth  formed  upon  shaking  may  remain  for  an 
unusually  long  time,  and  the  urine  is  filtered  with  difficulty. 

(5)  Specific  Gravity  of  the  Urine. — Xormally  the  density 
of  the  urine  varies  between  1.015  and  1.035.  The  specific  gravity 
depends  upon  the  relative  amount  of  the  fluid  and  the  solids  con- 
tained in  solution  (not  in  suspension).  It  may  under  normal  circum- 
stances temporarily  rise  above  or  descend  below  these  limits,  depend- 
ing for  the  most  part  on  the  amount  of  fluid  ingested  or  which  passes 
off  as  perspiration.  Pathologically,  as  a  general  rule  with  several 
exceptions,  an  increase  in  the  total  amount  of  urine  is  accom- 
panied by  a  lowered  specific  gravity,  while  in  oliguria  the  density 
is  increased. 

Polyuria  of  a  persistent  type,  with  a  lotv  specific  gravity,  is  signifi- 
cant of  chronic  interstitial  nephritis  or  diabetes  insipidus ;  with  a 
high  specific  gravity  (1.030  to  1.045),  of  diabetes  mellitus.  Oliguria 
with  a  low  specific  gravity  may  be  present  in  cases  where  defective 
elimination  of  solids  is  conjoined  with  a  weak  heart,  as  in  many 
chronic  diseases  or  grave  acute  ailments. 

(6)  Total  Urinary  Solids. — If  the  last  two  figures  of  the 
specific  gravity  of  the  collected  and  mixed  urine  of  24  hours 
are  multiplied  by  the  coefficient  2.33,  the  result  is  the  number  of 
grammes  of  solids  in  1,000  cubic  centimetres  of  urine.  Thus,  if 
the  specific  gravity  is  1.022  and  the  amount  passed  is  1,200  cubic 
centimetres,  22  X  2.33  =  51.2  grammes  to  1.000  cubic  centimetres,  or 
5.1  per  cent.  Two  hundred  cubic  centimetres  will  therefore  contain 
2  X  5.1  =  10.2  grammes,  which  added  to  51.2  gives  a  total  output  of 
61.4  grammes. 

Another  method  is :  Multiply  the  last  two  figures  of  the  specific 
gravity  by  the  number  of  ounces  voided  in  24  hours  and  the 
product  by  1.1 ;  e.g.,  if  the  total  amount  is  40  oz.,  and  the  specific 
gravity  is  1.022,  then  40  X  22  X  1.1  =  968  grains  (about  2  oz.). 

The  normal  average  daily  amount  of  solids  in  the  urine  varies 
from  60  to  70  grammes  (21  to  22  oz.).  A  notable  diminution  in 
this  amount  is  significant  of  a  corresponding  degree  of  renal  in- 
sufficiency. The  cause  of  the  insufficiency  must  be  determined 
by  a  consideration  of  the  associated  signs  and  symptoms  which 
may  indicate  that  the  kidneys  themselves  are  diseased,  or  that  their 
eliminative  power  is  lessened  as  a  remote  or  indirect  result  of  disease 
elsewhere. 

The  following  table  (constructed  after  Etheridge)  presents  the 
minimum  amounts  of  total  urinary  solids  which  can  be  considered 
as  normal  with  reference  to  the  weight  of  the  individual : 


EVIDE^XE  FROM  PHYSICAL  URINALYSIS  625 

Weight.  Minimum  urinary  solids. 

90  pounds 500  grains. 

100      "       570 

110      "       640 

120      "       710 

130      "       780 

140      " 850 

150      "       920 

160      "       990 

170     '"       1,060 

180      "       1,100 

Dyspepsias,  neuralgias,  nervous  irritability,  bronchitis,  headaches, 
insomnia,  and  backache  have  been  referred  to  a  deficient  elimination 
of  urinary  solids,  icitliont  existing  nephritis. 

(7)  Urinary  Deposits  {Macroscopic). — The  formation  of  a 
deposit,  visible  to  the  unaided  eye,  in  the  urine  when  the  latter  is 
allowed  to  stand,  depends  more  upon  the  reaction  of  the  fluid  than 
upon  the  amount  of  the  contained  ingredients.  Consequently  the 
existence  of  a  more  or  less  abundant  sediment  composed  of  a  certain 
substance  does  not  argue  the  presence  of  that  substance  in  abnormal 
quantity — a  question  to  be  settled  only  by  chemical  analysis. 

A  deposit  of  "  cayenne  pepper  "  grains,  brick-red  in  colour,  con- 
sists of  uric  acid,  and  may  or  may  not  indicate  an  increased  elimina- 
tion of  the  acid.  Its  occurrence  is  mainly  indicative  of  a  very  acid 
or  scanty  and  concentrated  urine,  such  as  occurs  in  fever,  gastric 
disorders,  wasting  diseases,  and  lithaemic  conditions.  If  actual  con- 
cretions (uric  acid  sand  or  gravel)  are  found,  their  presence  may 
serve  to  clear  up  the  nature  of  attacks  of  pain  previously  suspected 
to  be  of  renal  origin.  The  very  common  brick-dust  sediment  is  com- 
posed of  amorphous  urates.  It  occurs,  especially  in  cold  weather, 
under  the  same  circumstances  as  uric-acid  deposits.  An  abundant 
white  deposit  of  phosphates,  resembling  pus,  may  be  found  m  neu- 
tral or  alkaline  urines,  and  when  persistent  is  usually  associated  with 
neurasthenia  and  debility. 

It  is  perhaps  regrettable  that  there  are  no  accepted  terms  to 
express  the  clinical  conditions,  sometimes  well  characterized,  in 
which  there  is  a  persistent  naked-eye  deposit  of  certain  substances 
(urates,  phosphates),  while  the  total  output,  as  ascertained  by  chem^ 
ical  examination,  may  or  may  not  be  increased  or  diminished.  Even 
some  of  the  systematic  writers  upon  urinalysis,  after  giving  warning 
not  to  mistake  a  deposit  for  an  excess,  fall  into  the  very  error  against 
which  they  have  cautioned  their  readers. 


626  THE  EVIDENCES  OF  DISEASE 

(8)  Pneumaturia. — In  rare  instances,  in  connection  with  evi- 
dences of  cystitis,  gas  may  be  passed  at  the  end  of  micturition,  with 
or  without  an  audible  sound.  If  air  has  not  been  introduced  into 
the  bladder  during  instrumentation  (cystoscopic  examination,  irriga- 
tion of  the  bladder,  etc.),  it  is  due  either  to  a  fistulous  communica- 
tion between  the  bladder  and  some  portion  of  the  intestine,  or  to 
the  presence  of  gas-forming  organisms  which  have  entered  or  been 
carried  into  the  viscus.  The  yeast  fungus,  the  Bacillus  coli  com- 
tnunis,  and  the  Bacilhis  aerogenes  capsulatus  have  been  isolated,  and 
in  most  cases  glycosuria  is  present.  If  it  is  suspected  that  the  blad- 
der contains  air,  the  suspicion  may  be  confirmed  by  passing  a  cathe- 
ter and  keeping  its  end  under  water,  or  by  desiring  the  patient  to 
urinate  in  a  bath. 

II.    EVIDENCE    FROM    THE    CHEMICAL    EXAMINATION 
OF    THE    URINE 

(1)  Keaction  of  the  Urine. — {a)  Acidity. — formally  the  reac- 
tion of  the  collected  urine  of  24  hours  is  acid.  An  excessively  acid 
reaction  is  found  in  the  majority  of  scanty  urines,  particularly  the 
concentrated  urine  of  acute  rheumatic  fever  and  acute  febrile  dis- 
eases in  general.  It  is  also  observed  in  lithaemia,  gout,  diabetes, 
scurvy,  leucasmia,  and  chronic  nephritis.  A  persistent  high  acidity 
is  suggestive  of  possible  renal  lithiasis. 

{h)  Alkalinity. — If  the  diet  is  purely  vegetable  the  reaction  may 
be  alkaline.  It  is  also  temporarily  alkaline  after  the  ingestion  of  a 
large  meal  of  any  kind  of  food.  If  the  urine  is  alkaline  when  voided, 
and  the  alkalinity  is  due  to  the  presence  of  ainmonia,  it  may  be  in- 
ferred that  cystitis  exists.  If  the  urine  is  alkaline  when  voided,  but 
the  reaction  is  due  to  a  fixed  alJcali,  it  may  be  due  to  the  ingestion 
of  organic  acid  salts,  anaemia,  certain  neurasthenic  or  debilitated 
conditions,  and  prolonged  vomiting. 

(2)  Chlorides. — The  normal  average  daily  excretion  of  chlo- 
rides amounts  to  12  grammes,  but  varies  physiologically  from  10  to 
15  grammes,  the  variations  depending  mainly  on  the  amount  ingested 
as  a  part  of  the  food.  If  quantities  between  these  limits  are  found 
it  may  be  safely  inferred  that  the  appetite  and  digestion  are  not 
impaired  to  any  notable  extent. 

{a)  Increased  Chlorides. — A  persistent  increase  in  the  chlorides 
(15  to  30  grammes)  is  extremely  suggestive  of  diabetes  insipidus. 
An  increase  occurs  also  in  the  early  stage  of  general  paresis ;  in  pru- 
rigo ;  during  convalescence  from  certain  acute  fevers,  especially  the 
third  day  of  convalescence  from  acute  lobar  pneumonia ;  during  the 
post-convulsive  stage  of  epilepsy;  and  during  the  rapid  absorption 


EVIDENCE  FROM  CHEMICAL   URINALYSIS  627 

of  large  effusions.  In  the  latter  case  it  is  a  favourable  prognostic 
sign. 

(b)  Diminished  or  Absent  Chlorides.— In  cases  of  inanition  or 
starvation  the  excretion  of  chlorides  will  diminish  or  almost  cease, 
the  sodium  chloride,  which  constitutes  the  great  bulk  of  the  chlo- 
rides, being  retained  in  the  body  fluids  so  as  to  preserve  very  nearly 
its  normal  proportion  in  the  latter.  Pathologically  the  chlorides  are 
diminished  in  all  fevers  except  in  intermittent  malarial  fever,  which 
shows  no  diminution  or  only  a  relatively  slight  decrease.  The  most 
striking  instance  of  a  great  decrease,  or  even  a  total  disappearance,  of 
the  chlorides  is  witnessed  in  acute  lobar  pneumonia,  a  symptom 
which  may  be  of  great  value  in  the  differential  diagnosis  of  this 
form  of  pneumonia  from  pleurisy  and  empyema.  The  acute  fevers 
presenting  a  decrease,  but  not  to  such  a  marked  degree  as  in  pneu- 
monia, are  typhus  fever,  rheumatic  fever,  scarlet  fever,  small-pox, 
recurring  fever,  and  acute  yellow  atrophy  of  the  liver.  The  excre- 
tion of  only  0.05  gramme  of  chlorides  in  24  hours  indicates  a  very 
severe  form  of  disease.  The  chlorides  are  also  diminished  in  vary- 
ing degrees  in  excessive  diarrhoea,  anaemia,  rachitis,  chronic  plum- 
bism,  chorea,  melancholia  (decrease  marked),  gastric  cancer,  hyper- 
chlorhydria  and  hypersecretion  associated  with  gastric  ulcer  (chlo- 
rides may  disappear),  in  most  cases  of  albuminuria,  and  in  large 
effusions. 

(3)  Phosphates. — Under  normal  circumstances  the  daily  elimi- 
nation of  phosphoric  acid  varies  from  3  to  3  grammes  (30  to  45 
grains).  The  acid  is  excreted  in  combination  as  alkaline  and  earthy 
phosphates,  the  alkaline  salts  predominating.  It  is  derived  mainly 
from  the  food,  partly  from  the  decomposition  of  lecithin  and  nuclein. 

(a)  Decreased  Phosphates. — A  diminution  in  the  excretion  of 
phosphates  is  customary  in  typhus,  typhoid,  and  intermittent  mala- 
rial fevers,  in  pulmonary  tuberculosis  with  high  temperature,  and 
acute  febrile  diseases  in  general,  although  there  are  some  unex- 
plained exceptions  to  this  statement.  A  decreased  elimination  has 
also  been  noted  in  the  various  forms  of  nephritis,  acute  and  chronic 
rheumatism,  Addison's  disease,  hysteria,  chronic  lead-poisoning,  and 
acute  yellow  atrophy  of  the  liver. 

{b)  Increased  Phosphates, — An  excess  of  phosphates  (phospha- 
turia)  exists  in  wasting  diseases,  and  in  leucaemia  and  severe  anaemia. 
An  increased  elimination  is  said  to  be  particularly  marked  in  wasting 
diseases  of  the  nervous  system.  A  considerable  sediment  of  the 
earthy  phosphates  occurs  in  alkaline  urine  when  the  alkalinity  is 
due  to  a  fixed  alkali.  It  is  found  in  dyspeptic  and  nervously  debili- 
tated individuals.     Occasionally  the   deposition  takes  place  in  the 


628  THE   EVIDENCES  OF  DISEASE 

bladder,  and  the  few  whitish  drops  passed  at  the  end  of  urination 
may  be  mistaken  for  semen  and  cause  much  unnecessary  anxiety  on 
the  part  of  the  patient.  In  such  cases  there  is  usually,  but  not 
necessarily,  an  actual  increase,  as  determined  by  a  quantitative 
analysis.  There  is  a  condition,  perhaps  a  nosological  entity,  in 
which  with  polyuria,  thirst,  loss  of  flesh,  and  other  symptoms  of 
diabetes,  sugar  is  usually  absent  and  the  urine  is  alkaline,  but  there 
is  a  great  increase  (7  to  9  grammes)  in  the  phosphates  (phosphatic 
diabetes).  In  diabetes  mellitus  the  phosphates  may  increase  as  the 
sugar  diminishes,  and  per  contra. 

(4)  Oxalates. — Oxalic  acid,  of  which  from  0.010  to  0.020  gramme 
(i  to  \  grain)  is  excreted  daily,  exists  in  combination  as  calcium 
oxalate.  It  is  normally  held  in  solution  by  the  acid  sodium  phos- 
phate of  the  urine,  and  when  the  latter  is  deficient  the  oxalates  are 
precipitated.  The  amount  of  oxalic  acid  excreted  depends  largely 
upon  the  diet.  The  taking  of  certain  vegetables,  especially  cabbage, 
rhubarb,  and  tomatoes,  will  cause  a  considerable  increase.  Aspara- 
gus, spinach,  carrots,  string  beans,  and  celery  have  a  similar  action. 
In  estimating  the  pathological  importance  of  an  excess  of  oxalates 
allowance  must  be  made  for  the  effect  of  diet.  Oxalic  acid  may  also 
result  from  oxidation  of  uric  acid  or  an  incomplete  oxidation  of  car- 
bohydrates. In  the  latter  case  the  intermediate  product  is  oxaluric 
acid. 

A  persistent  increase  in  the  oxalates  (oxaluria)  may  be  due  to 
disorders  of  the  stomach  and  intestine.  When  associated  with  neu- 
rasthenia, hypochondria,  debility,  dyspepsia,  and  perhaps  various 
neuralgias,  oxaluria  constitutes  a  well-marked  clinical  condition,  con- 
sidered by  certain  writers  to  be  a  special  diathesis.  This  condition  is 
due  to  some  unknown  disturbance  of  metabolism.  Oxaluria  is  not 
infrequently  associated  with  transient  albuminuria,  and  occurs  in 
gout,  lithaemia,  and  spermatorrhoea.  Oxalates  may  be  deposited  in 
the  bladder  and  form  a  calculus. 

(5)  Sulphates. — The  sulphuric  acid  occurring  in  the  urine 
exists  in  two  forms :  first,  as  the  mineral  (inorganic  or  preformed) 
sulphates  in  combination  with  sodium  and  potassium ;  second,  as 
organic  (conjugate  or  ethereal)  sulphates  in  combination  with  indol, 
skatol,  and  phenol.  The  amount  of  the  former  is  to  the  latter  as 
10  to  1,  and  the  daily  total  excretion  of  both  varies,  in  health,  from 
2  to  3  grammes  (30  to  45  gi'ains).  With  the  exception  of  the  small 
amount  of  the  mineral  sulphates  ingested  as  a  part  of  the  food,  the 
sulphates  are  derived  from  the  breaking  up  of  albuminous  substances 
in  the  body. 

Consequently  an  increased  excretion  of  the  total  sulphates  has 


EVIDENCE  FROM  CHEMICAL  URINALYSIS  629 

been  observed  in  acute  febrile  diseases,  especially  pneumonia  and 
acute  myelitis,  as  well  as  in  non-febrile  wasting  maladies  such  as 
cancer  of  the  esophagus,  diabetes  (both  mellitus  and  insipidus),  and 
progressive  muscular  atrophy.  With  reference  to  the  organic  sul- 
phates, see  the  following  paragraph. 

(6)  Indican. — When  albuminous  substances  are  undergoing 
bacterial  putrefaction  in  the  intestine,  or  are  rapidly  decomposing 
in  any  part  of  the  body,  as  in  the  putrid  pus  of  septic  peritonitis  or 
in  empyema,  indol  is  formed.  When  the  indol  is  absorbed  it  is  oxi- 
dized, forming  indoxyl,  and  the  latter  unites  with  the  preformed 
potassium  sulphate  to  become  the  conjugate  potassium  indoxyl- 
sulphate,  or,  as  it  is  more  commonly  termed,  indican.  If  indican, 
which  is  itself  colourless,  is  treated  with  strong  acids  and  oxidizing 
agents,  it  is  decomposed  with  the  formation  of  indigo  blue. 

Indican  is  present  in  small  quantity  in  healthy  urines.  It  is 
increased  (indicanuria)  when  an  excessive  degree  of  intestinal  putre- 
faction is  taking  place.  According  to  Simon,  an  excessive  excretion 
of  indican  is  often  indicative  of  a  decreased  proportion  of  hydro- 
chloric acid  in  the  gastric  juice,  as  under  such  circumstances  the 
normal  restraining  influence  of  the  acid  upon  putrefactive  processes 
is  abolished.  Consequently  an  excess  of  indican  is  found  in  gastric 
diseases  attended  by  hypochlorhydria  or  anachlorhydria  [q.  v.),  not- 
ably gastric  cancer  and  the  various  forms  of  gastritis.  It  occurs 
also  in  diseases  of  the  small  intestine  which  involve  diminished  or 
absent  peristalsis,  as  in  peritonitis,  and  ileus  or  obstruction  of  this 
portion  of  the  digestive  tract ;  whereas  in  conditions  affecting  the 
colon  alone  no  increase  is  found.  As  a  rule,  indicanuria  does  not 
result  from  ordinary  constipation.  As  previously  stated,  an  excess 
of  indican  is  found  when  putrid  pus  exists  in  any  part  of  the  body. 
The  amount  of  indican  is  increased  by  the  ingestion  of  considerable 
quantities  of  red  meat,  and  diminished  by  an  exclusive  milk  diet. 

(7)  Urea. — In  health,  the  bulk  (85  per  cent)  of  the  nitrogen 
eliminated  by  the  kidneys  is  in  the  form  of  urea.  It  is  derived  in 
part  from  the  unused  proteids  of  the  food,  and  in  part  from  the  physi- 
ological waste  of  the  body  or  tissue  proteids.  It  is  probable,  although 
perhaps  not  definitely  determined,  that  the  liver  is  the  chief  seat  of 
production  of  urea.  The  daily  excretion  of  urea  in  health  varies 
from  20  to  40  grammes  (about  300  to  600  grains),  with  an  average  of 
28  grammes  (450  grains).  The  variations  depend  partly  upon  the 
amount  of  proteid  food  ingested,  partly  upon  the  body  weight. 
Under  normal  conditions  the  more  abundant  the  diet  and  the 
greater  the  weight  of  the  body  the  more  urea  is  formed.  The 
elimination  of  urea  is  absolutely  less  in  women  and  children  than 

42 


630  'J'HE  EVIDENCES  OP  DISEASE 

in  men,  but  relatively  greater  (compared  with  the  body  weight)  in 
children  than  in  adults. 

In  disease,  the  total  daily  excretion  of  urea  may  be  increased  or 
diminished. 

(a)  Increased  Urea. — The  excretion  of  urea  is  in  large  measure 
an  index  of  the  activity  of  tissue  destruction.  Its  total  daily  output 
is  therefore  increased  in  the  acute  febrile  and  inflammatory  diseases, 
particularly  in  those  which  terminate  by  crisis — e.  g.,  pneumonia. 
The  largest  output  is  found  in  diabetes,  in  which,  with  a  few  excep- 
tions, urea  is  found  in  excess,  due  partly  to  the  abnormally  great 
appetite,  but  partly  also  to  the  marked  tissue  waste  which  attends 
this  disease.  A  plus  amount  of  urea  may  occur  in  severe  leucaemia, 
pernicious  anaemia,  scurvy,  and  paralysis  agitans ;  also  after  the  use 
of  electricity,  and  poisoning  by  certain  drugs,  especially  arsenic  and 
phosphorus. 

(b)  Decreased  Urea. — A  lessened  elimination  of  urea  occurs  in 
the  various  forms  of  nephritis  and  renal  insufficiency.  While  it  can 
not  be  said  that  urea  alone  is  the  cause  of  uraemia,  yet  its  amount 
furnishes  a  fair  gauge  of  the  eliminative  ability  of  a  diseased  kidney. 
A  decrease  in  urea  is  also  observed  in  certain  diseases  of  the  liver, 
(cancer,  cirrhosis)  which  affect  its  functionating  power  and  there- 
fore cause  a  decreased  urea  formation.  Diminished  amounts  are 
noted  in  melancholia,  general  paralysis,  Addison's  disease,  chronic 
anaemias,  chronic  plumbism,  osteomalacia,  chronic  rheumatism,  and 
certain  cases  of  diabetes  in  which  there  is  a  deficient  absorption  of 
nitrogenous  materials  from  the  small  intestine. 

(8)  Uric  Acid. — The  total  daily  excretion  of  uric  acid  varies 
from  0.4  to  1  gramme  (6  to  15  grains).  Under  normal  circumstances 
the  ratio  between  the  excretion  of  uric  acid  and  urea  is  said  to  be  1 
to  50.  It  does  not  fall  within  the  scope  of  this  volume  to  discuss 
the  various  theories  which  have  been  propounded  with  reference  to 
the  uric-acid-urea  ratio  and  the  source,  mode  of  origin,  and  patho- 
logical relations  of  uric  acid.  The  results  of  experimentation  are  in 
many  respects  variable,  and  the  very  multiplicity  of  hypotheses  is 
proof  that  the  whole  question  is  still  open.  It  is  pretty  well  settled 
that  uric  acid  is  not  an  antecedent  of  urea ;  that  nuclein  is  appar- 
ently the  mother  substance  of  uric  acid,  the  latter  resulting  from 
the  former  by  a  process  of  dissociation ;  that  foods  (thymus  gland 
or  sweetbreads,  beans,  peas,  and  nuts)  or  beverages  (coffee,  beer) 
which  are  rich  in  nuclein  will  cause  an  excessive  formation  of  uric 
acid ;  and  that  the  spleen,  with  its  nuclein-containing  leucocytes,  is 
perhaps  the  main  seat  of  uric-acid  formation.  The  careful  experi- 
ments of  Taylor  throw  doubt  upon  the  commonly  accepted  opinion 


EVIDENCE  PROM  CHEMICAL   URINALYSIS  631 

that  a  heavy  meat  diet  increases  the  formation  of  uric  acid,  a  result 
which  he  claims  is  to  be  expected  because  of  the  small  nuclein  con- 
tent of  meat. 

The  clinical  relations  of  an  excess  or  a  diminution  of  uric  acid 
are  as  follows : 

(a)  Increased  Uric  Acid. — As  previously  stated,  the  uric-acid  out- 
put may  be  increased  by  special  articles  of  diet,  including  fat  and 
sugar,  and  by  muscular  exercise ;  so  also  by  Turkish  baths.  It  is 
quite  constantly  increased  in  the  acute  fevers  (e.  g.,  pneumonia, 
typhoid  fever,  acute  rheumatic  fever),  and  less  frequently  in  digestive 
disorders.  In  leucaemia,  because  of  the  large  destruction  of  the 
nuclein  contained  in  the  greatly  increased  number  of  leucocytes,  the 
daily  output  of  uric  acid  may  amount  to  4  grammes  (60  grains) ;  so 
also  with  splenic  diseases  in  general.  During  and  directly  after 
acute  gouty  attacks  uric-acid  elimination  is  increased.  In  some 
cases  of  diabetes  sugar  is  replaced  from  time  to  time  by  an  excessive 
excretion  (3  grammes,  45  grains)  of  uric  acid.  In  the  so-called  lith- 
semic  or  uric-acid  diathesis  the  output  of  uric  acid  is  increased,  but 
whether  the  uric  acid  is  the  sole  cause  of  the  "  lithgemic  "  symptoms 
is  questionable. 

{b)  Decreased  Uric  Acid.— Under  a  strict  milk  diet  the  amount  of 
uric  acid  decreases.  In  chronic  gout  the  elimination  is  low,  increas- 
ing, as  previously  stated,  during  and  after  the  acute  outbreaks.  It 
is  also  low  in  most  diabetics,  in  anaemia  and  chlorosis,  chronic  plum- 
bism,  and  chronic  interstitial  nephritis. 

It  is  hardly  necessary  to  remind  the  reader  that  a  deposit  of  uric 
acid  or  urates,  which  occurs  mainly  when  the  urine  is  highly  acid, 
does  not  necessarily  imply  an  increased  excretion. 

(9)  Albumin. — Several  albumins  may  be  met  with  in  the  urine, 
of  which  serum  albumin  and  serum  globulin  are  of  the  most  clinical 
importance.  The  term  "  albuminuria  "  is  understood  as  indicating 
the  presence  of  one  or  both,  usually  both,  in  the  urine.  Other  pro- 
teids  which  may  occur  are  albumoses  ("  peptones  "),  nucleo-albumin, 
and  fibrin,  but  these  have  relatively  little  diagnostic  value. 

Albumin  can  hardly  be  considered  under  any  circumstances  as  a 
normal  constituent  of  the  urine,  although  the  existence  of  a  "physio- 
logical "  albuminuria  is  claimed  by  some  authorities.  There  is  no 
doubt,  however,  that  an  albuminuria  occurs  very  frequently  in  which 
the  organic  changes  in  the  kidney,  if  there  be  such,  are  so  slight  and 
evanescent  as  to  be  unimportant.  This  form  of  albuminuria,  com- 
pared with  that  caused  by  serious  organic  lesions,  may  properly  be 
termed  functional,  although  not  physiological.  Probably  the  pres- 
ence of  albumin  in  the  urine  always  implies  some  interference  with 


632  THE  EVIDENCES  OF  DISEASE 

the  integrity  of  the  epithelial  cells  of  the  glomeruli  or  of  the  renal 
tubules,  which  epithelium  when  intact  prevents  the  passage  of  the 
proteids  of  the  blood  into  the  urine.  Whether  the  disturbance  is 
insignificant  and  transient  (renal  anaemia  or  hyperaemia,  irritating 
substances  in  the  blood)  or  great  and  permanent  (chronic  nephritis), 
must  be  determined  by  the  associated  signs  and  symptoms  (presence 
or  absence  of  fever,  cardiac  hypertrophy,  increased  arterial  tension) 
and  the  presence  or  absence  of  other  urinary  abnormalities  (blood, 
pus,  casts,  etc.).  The  not  uncommon  snap  judgment  that  Bright's 
disease  exists  because  albumin  is  found  in  the  urine  is  not  justified 
by  the  facts. 

Albumin,  when  found  in  the  urine,  may  vary  from  a  mere  trace 
up  to  an  amount  which  causes  the  urine  to  boil  almost  solid.  The 
actual  amounts  eliminated  in  24  hours  run  from  2  grammes  (30 
grains)  up  to  12  grammes  (180  grains).  Very  exceptionally  even 
larger  quantities  are  encountered. 

The  principal  causes  and  varieties  of  albuminuria  are  as  follows  : 

(a)  Febrile  Albuminuria. — In  any  disease  attended  by  fever  there 
may  be  a  slight  albuminuria,  unattended  by  evidences  of  acute 
nephritis.  It  becomes  manifest  at  the  height  of  the  fever  and  dis- 
appears when  the  temperature  returns  to  the  normal.  It  occurs 
particularly  in  typhoid  fever,  pneumonia,  cerebro-spinal  meningitis, 
acute  rheumatic  fever,  scarlet  fever,  diphtheria,  malaria,  and  erysipe- 
las. It  is  probably  largely  dependent  upon  the  intensity  of  the 
infective  process. 

(b)  Albuminuria  Due  to  Blood  Changes  or  the  Presence  of  Certain 
Abnormal  Substances  in  the  Circulation. — A  slight  amount  of  albu- 
min may  appear  in  the  urine  as  a  consequence  of  the  blood  changes 
in  scurvy,  purpura,  leucaemia,  severe  or  pernicious  anaemia ;  or  of 
abnormal  ingredients  in  the  circulation,  as  in  jaundice,  diabetes, 
syphilis,  poisoning  with  lead  or  mercury,  ether  or  chloroform  anaes- 
thesia, and  the  ingestion  of  various  drugs,  such  as  turpentine, 
cantharides,  carbolic  acid,  and  other  similarly  irritating  substances. 
In  certain  cases  in  which  excessive  amounts  of  uric  acid,  oxalic 
acid,  and  urea  are  eliminated,  albumin  may  also  be  present  in 
small  quantity. 

(c)  Albuminuria  Due  to  Disturbances  of  the  Circulation. — A  mod- 
erate albuminuria  may  occur  in  diseases  or  conditions  Avhich  cause  a 
passive  renal  hyperaemia — e.  g.,  cardiac  valvular  disease  or  pulmonary 
disease  giving  rise  to  an  increased  pressure  in  the  right  heart  and  a 
consequent  hindrance  to  the  flow  of  blood  from  the  kidney  by  way 
of  the  renal  veins;  or  pressure  upon  the  latter  by  a  tumour  or  a 
gravid  uterus. 


EVIDENCE   FROM  CHEMICAL  URINALYSIS  633 

(d)  Neurotic  Albuminuria. — Albumin  may  be  discovered  in  small 
quantity,  usually  not  persistent,  in  apoplexy,  tetanus,  migraine,  delir- 
ium tremens,  exophthalmic  goitre,  and  head  injuries.  It  may  be 
present  after  an  epileptic  paroxysm. 

(e)  Functional  Albuminuria. — Albumin  may  be  found,  usually 
but  not  always  in  small  quantities,  in  the  urine  of  young  persons, 
particularly  in  boys.  The  albumin  may  appear  intermittently  at 
irregular  intervals  of  days  or  weeks,  lasting  for  similar  periods ;  or 
it  may  become  manifest  at  regular  intervals  and  last  for  a  definite 
time,  as  in  the  cases  where  it  is  present  at  the  end  of  the  day  and 
absent  in  the  morning  (cyclic  albuminuria) ;  or  appear  after  a  hearty 
proteid  meal  (dietetic  albuminuria)  ;  or  following  a  cold  bath  or 
severe  exercise  (transitory  albuminuria).  A  large  proportion  of  these 
cases  recover  after  a  time,  but  in  some  the  albuminuria  becomes  per- 
sistent, the  pulse  tension  is  increased,  and  organic  changes  develop. 

(/)  Albuminuria  Due  to  Organic  Renal  Disease. — Albuminuria 
occurs  as  a  regular  symptom  in  acute  nephritis,  and  in  the  active 
hyperaemia  which  constitutes  the  early  stage  of  the  inflammatory 
changes.  The  albumin  is  usually  in  considerable  amount.  It  is 
also  constantly  present,  often  in  large  quantity,  as  an  evidence  of 
chronic  parenchymatous  nephritis.  In  chronic  interstitial  nephritis 
albumin  may  be  absent,  or  present  in  such  limited  amount  that  the 
most  delicate  methods  are  required  for  its  demonstration ;  but  in 
the  majority  of  cases  a  trace  at  least  can  be  found  by  the  ordinary 
heat  and  nitric  acid  test.  In  amyloid  and  fatty  degeneration,  par- 
ticularly the  former,  albumin  is  rarely  absent,  and  may  be  discovered 
in  considerable  quantity  ;  so  also  with  neoplasms  of  the  kidney. 
Pyelitis  or  suppurative  nephritis  may  be  responsible  for  the  presence 
of  albumin  derived  from  the  pus  which  the  urine  contains  under 
such  circumstances.  With  reference  to  the  relative  preponderance 
of  serum  albumin  and  serum  globulin  in  various  diseases  it  is  claimed 
by  Senator  that  in  amyloid  degeneration  of  the  kidney  the  serum 
globulin  may  equal  or  exceed  the  serum  albumin  in  many  cases,  and 
that  this  relation  constitutes  an  important  diagnostic  symptom.  In 
other  ailments  when  serum  albumin  is  present,  globulin  is  also  found, 
but  in  very  small  quantities. 

(g)  Extra-renal  Albuminuria. — The  urine  may  be  free  from  albu- 
min when  secreted,  but  become  mixed  with  some  albuminous  mate- 
rial (pus,  blood,  chyle,  lymph)  between  the  time  at  which  it  issues 
from  the  renal  tubules  and  the  time  at  which  it  is  voided  from  the 
bladder.  Pyelitis  may  perhaps  come  under  this  head.  Other  causes 
are,  in  both  sexes,  inflammation  of  the  ureters,  cystitis,  urethritis, 
simple  or  gonorrhoea! ;  in  men,  the  presence  of  semen  in  the  urethra ; 


634  THE   EVIDENCES  OP   DISEASE 

in  women,  menstrual  blood,  vaginal  discharges  (including  fistulous 
communication  with  an  abscess),  or  the  presence  of  semen  in  the 
vagina.  In  such  cases  only  a  trace  of  albumin  is  usually  found.  In 
order  to  determine  the  origin  of  the  albumin  under  such  circum- 
stances it  may  be  necessary  (especially  in  women)  to  obtain  a  speci- 
men of  urine  by  catheterization  of  the  bladder,  or  perhaps  of  the 
ureter. 

(h)  Albumosuria. — It  was  formerly  supposed  that  true  peptones 
occurred  in  the  urine  (peptonuria),  but  later  investigations  have 
shown  that  the  substances  found  are  propeptones  or  albumoses,  and 
the  condition  is  therefore  an  albumosuria.  The  diagnostic  value  of 
albumosuria  has  not  as  yet  been  definitely  decided.  Traces  of  albu- 
moses have  been  found  in  many  of  the  specific  infectious  fevers  in 
which  bacterial  disintegration  of  the  tissues  is  in  progress,  such  as 
lobar  pneumonia,  typhoid  fever,  scarlet  fever,  measles,  and  the  major- 
ity of  septic  inflammations.  Albumosuria  is  also  quite  constant  in 
cases  where  considerable  pus  accumulations  exist,  as  in  empyema  or 
large  abscesses  in  the  liver  or  elsewhere  ;  in  suppurative  meningitis ; 
and  chronic  suppurations  in  general.  A  large  albumosuria  is  rather 
significant  of  multiple  myelomata  of  the  bones,  and  has  been  found 
in  osteomalacia  and  some  cases  of  nephritis. 

(i)  Nucleo-albuminuria. — The  clinical  significance  of  the  presence 
of  nucleo-albumin  in  the  urine  is  probably  slight.  When  present,  it 
is  indicative  of  catarrhal  or  desquamative  processes  somewhere  in 
the  urinary  tract.  It  may  be  found  in  connection  with  functional 
albuminuria,  febrile  albuminuria,  acute  nephritis,  choluria  (bile  in 
the  urine),  and  cystitis ;  also  in  leucaemia.  Considerable  amounts 
are  occasionally  encountered  during  the  administration  of  large 
doses  of  certain  drugs,  particularly  bichloride  of  mercury,  arsenic, 
and  naphthol. 

{f )  Fibrinuria. — The  formation  of  a  reddish  or  almost  colourless 
sticky  sediment  or  coagulum,  or,  if  much  fibrin  is  present,  the  con- 
version of  the  urine  into  a  jellylike  mass  upon  standing,  is  a  very 
rare  occurrence.  It  is  due  to  the  presence  of  fibrinogen  and  a  fer- 
ment capable  of  forming  fibrin.  It  is  seen  in  certain  cases  where 
the  plasma  of  the  blood  enters  some  portion  of  the  urinary  tract,  as 
in  chyluria,  croupous  inflammation  of  the  tract,  villous  growths  in 
the  bladder,  and  occasionally  after  the  ingestion  of  cantharides. 
The  term  fibrinuria  does  not  apply  to  the  presence  of  ordinary  blood 
clots,  the  latter  coming  properly  under  the  head  of  lia^maturia. 

10.  Blood  and  its  Compounds  in  the  Urine. — Under  cer- 
tain circumstances  blood  itself  may  appear  in  the  urine  (haematuria) 
or  be  represented  by  some  form  of  blood  pigment  (haemoglobinuria). 


EVIDENCE  FROM  CHEMICAL  URINALYSIS  G35 

The  distinction  rests  mainly  upon  a  microscopic  examination.  If 
blood  as  a  whole  is  present,  red  corpuscles  will  be  found  more  or 
less  abundantly ;  but  if  the  smoky  or  reddish  colour  of  the  urine  is 
due  to  pigment,  red  corpuscles  are  absent,  or  found  in  very  small 
numbers. 

(a)  HaBmaturia. — In  slight  haematuria  the  colour  of  the  urine 
may  be  unaltered,  but  red  corpuscles  will  be  discovered  by  the  micro- 
scope. In  the  severer  grades  of  haematuria  the  urine  is  smoky,  red, 
brown,  or  even  black,  and  deposits  a  heavy  sediment  which  may  con- 
tain blood  coagula.  According  to  the  length  of  time  during  which 
the  blood  has  been  in  the  urine  the  red  cells  may  retain  a  nearly 
normal  appearance,  or,  especially  in  ammoniacal  urine,  because  of 
the  hsemoglobin  having  been  dissolved  out,  may  be  simply  colourless, 
shadowy,  or  transparent  circles.  The  blood  may  come  from  the  kid- 
neys or  their  pelves,  the  ureters,  the  bladder,  or  the  urethra. 

Renal  haematuria  is  most  commonly  due  to  acute  congestion  of 
the  kidney  or  acute  nephritis,  and  in  a  moderate  degree  to  chronic 
nephritis.  The  number  of  red  cells  found  in  the  latter  may  be  taken 
as  a  gauge  of  the  severity  of  the  disease.  It  occurs  also  in  the  malig- 
nant types  of  the  acute  specific  infections  such  as  scarlet  fever,  small- 
pox, and  malaria.  In  the  latter  disease  it  may  become  epidemic. 
Bloody  urine  may  be  voided  in  leucaemia,  haemophilia,  purpura,  and 
scurvy.  It  has  been  observed  in  filariasis  and  distomiasis,  and  in 
cancer,  tuberculosis,  and  abscess  of  the  kidney.  Aneurism  of  the 
renal  artery,  renal  infarctions,  and  thrombosis  of  the  renal  vein  are 
rare  causes ;  and  poisoning  by  such  substances  as  cantharides,  tur- 
pentine, or  carbolic  acid  is  usually  attended  by  haematuria.  A  stone 
in  the  kidney  frequently  causes  blood  in  the  urine;  so  also  does 
traumatism  (rupture)  of  the  kidney.  Trreteral  haematuria  may  be 
due  to  the  passage  of  a  calculus ;  vesical  haematuria  to  the  presence 
of  a  stone,  diphtheritic  cystitis,  ulceration  or  cancer  of  the  bladder, 
injury,  ruptured  veins,  or  the  presence  of  parasites ;  urethral  haema- 
turia to  impacted  calculus,  gonorrhoea,  or  instrumentation.  Finally, 
blood  may  appear  without  apparent  cause,  renal  "  epistaxis "  or 
"haemophilia."  These  cases  occur  in  neurasthenic  or  hysterical  indi- 
viduals, and  no  lesion  is  found  which  will  account  for  the  symptom. 

The  determination  of  the  source  of  the  blood  is  oftentimes  diffi- 
cult. In  renal  hematuria  the  blood  is  intimately  mixed  with  the 
urine,  individual  red  cells  are  usually  decolourized,  and  blood  casts 
are  found.  If  the  blood  is  from  the  pelvis  of  the  kidney,  or  the 
ureter,  coagula  corresponding  in  shape  to  the  pelvis,  or  the  ureter, 
may  be  found.  It  may  be  necessary  to  employ  ureteral  catheteriza- 
tion.    In  hemorrhage  from  the  bladder,  the  blood  and  the  urine  are 


636  THE  EVIDENCES  OP  DISEASE 

not  so  distinctly  blended,  the  clots  may  be  of  such  an  irregular  form 
and  large  size  as  to  indicate  their  origin,  and  the  individual  cells 
retain  their  normal  appearance.  The  cystoscope  may  be  required  to 
determine  this  point.  If  the  blood  is  from  the  urethra  it  ordinarily 
drips  away  spontaneously,  and  if  the  urine  is  voided  the  last  portion 
is  clear. 

{b)  Blood  Pigment  in  the  Urine. — The  blood-colouring  matters 
found  in  the  urine  are  haemoglobin,  methsemoglobin,  and  hsemato- 
porphyrin. 

HmmogloMnuria  embraces  not  only  the  presence  of  haemoglobin, 
but  also  an  oxidation  product  of  the  latter — methaemoglobin — which 
may  be  formed  in  acid  urine  after  standing  for  some  time,  and  in 
many  instances  is  present  when  the  urine  is  voided.  Haemoglo- 
binuria  is  indeed  usually  a  methaemoglobinuria.  This  condition 
was  of  old  mistakenly  called  hgematinuria.  Haemoglobinuria  occurs 
when  there  is  such  an  extensive  disintegration  of  red  cells  that  the 
liver  is  unable  to  transform  the  whole  of  the  liberated  haemoglobin 
into  bilirubin,  and  the  excess  escapes  by  way  of  the  kidneys.  There 
are  none,  or  but  few,  of  the  red  cells  to  be  found  in  the  urine. 

In  the  large  majority  of  instances  haemoglobinuria  is  due  to  some 
toxic  material  in  the  circulating  blood,  such  as  arseniuretted  or  sul- 
phuretted hydrogen,  potassium  chlorate,  carbolic  acid,  naphthol, 
muscarine,  and  carbon  monoxide ;  as  well  as  to  the  specific  toxines 
of  typhoid  fever,  scarlet  fever,  yellow  fever,  the  grave  form  of  jaun- 
dice, syphilis,  and  malarial  fever,  especially,  if  not  solely,  the  sestivo- 
autumnal  form.  Quinine  may  cause  it,  but  apparently  only  in  those 
who  are,  or  who  have  recently  been,  the  subjects  of  malarial  fever. 
It  follows  transfusion  of  blood  from  one  mammal  into  another,  and 
has  been  observed  as  a  sequence  of  severe  burns  and  sunstroke.  It 
has  been  noted  in  leucaemia  associated  with  cholgemia.  There  is  a 
rare  epidemic  haemoglobinuria  of  the  newborn  in  which  cyanosis, 
jaundice,  and  symptoms  referable  to  the  nervous  system  are  present. 

As  a  rarity  a  paroxysmal  haemoglobinuria  has  been  observed. 
Each  attack  is  preceded  by  chill  and  fever,  closely  resembling  a 
malarial  paroxysm,  followed  by  the  passage  of  urine  containing 
blood  pigment.  The  attack  lasis  from  a  few  hours  to  two  days,  and 
occurs  in  connection  with  syphilis,  Eaynaud's  disease  complicated 
with  epileptic  seizures,  exposure  to  cold,  and  muscular  overexertion. 

Hmmatoporpliyrinuria — the  presence  of  iron-free  h^matin  in  the 
urine — is  of  little  clinical  significance.  The  urine  is  of  a  port-wine 
colour  and  darkens  on  standing.  Traces  of  this  pigment  occur  in 
normal  urine,  and  may  be  found  in  large  quantities  as  a  result  of  the 
continued  taking  of  sulphonal  or  trional,  especially  in  women.     Its 


EVIDENCE  FROM  CHEMICAL  URINALYSIS  637 

appearance  is  an  indication  for  the  prompt  stoppage  of  the  drug  and 
the  administration  of  alkalies.  It  has  been  found  also  in  exophthal- 
mic goitre,  acute  rheumatism,  pleurisy  or  pericarditis  with  effusion, 
pneumonia,  pulmonary  tuberculosis,  cirrhosis  of  the  liver,  and  intes- 
tinal hemorrhages. 

11.  Alkaptonuria. — The  nrine  is  of  normal  colour  when  voided 
but  darkens  upon  standing.  It  contains  a  substance  termed  alkapton 
(glycosuric  acid  or  related  oxyacids),  which  has  no  apparent  clinical 
significance  aside  from  the  fact  that  it  may  give  the  glucose  reaction 
with  Trommer's  or  Fehling's  test. 

12.  Sugars  in  the  Urine. — The  only  sugars  of  clinical  impor- 
tance found  in  the  urine  are  ghicose,  and,  in  a  few  cases,  lactose. 
Earely  maltose,  levulose,  inosite,  and  the  pentoses  may  be  found, 
but  their  presence  has  little  if  any  significance. 

(a)  Glycosuria. — Although  the  presence  of  glucose  in  the  urine 
is  a  cardinal  symptom  of  diabetes  mellitus,  glycosuria  and  diabetes 
are  not  synonymous  terms.  Thus  glucose  may  appear  temporarily 
in  the  urine  of  any  healthy  person  after  the  ingestion  of  a  sufiiciently 
large  amount  of  sugar  or  starch,  the  power  of  assimilation  of  such 
substances  having  been  exceeded  (alimentary  or  digestive  glycosuria). 
A  temporary  glycosuria  may  occur,  especially  during  convalescence, 
in  acute  febrile  maladies,  such  as  typhoid  fever,  scarlet  fever,  measles, 
pneumonia,  acute  rheumatic  fever,  epidemic  influenza,  diphtheria, 
and  malaria;  and  in  various  injuries  and  diseases  of  the  nervous 
system.     A  transient  glycosuria  may  occur  in  stout  persons. 

Before  a  diagnosis  of  diabetes  mellitus  can  be  made  it  must  be 
determined  that  the  elimination  of  glucose  is  persistent,  covering  a 
period  of  weeks,  months,  or  years,  although  there  may  be  periods 
during  which  no  sugar  appears  in  the  urine.  If  glucose  is  absent 
in  suspected  cases  the  dietetic  test  may  be  employed.  This  con- 
sists in  giving  100  grammes  (d^  oz.)  of  pure  glucose  and  examin- 
ing the  urine  three  or  four  hours  after.  If  notable  quantities  are 
found,  a  pathological  condition  unquestionably  exists,  as  the  body  in 
health  is  able  to  assimilate  this  amount  of  carbohydrate. 

(b)  Lactosuria. — Lactose  is  not  infrequently  found  in  the  urine 
of  pregnant  women  toward  the  end  of  gestation,  or  during  the 
period  of  lactation.  Its  presence  is  due  to  the  resorption  of  lac- 
tose from  the  milk  in  the  breasts,  which  occurs  especially  when 
for  any  reason  the  formation  of  milk  is  beyond  the  demand,  or 
when  any  obstruction  exists  (mastitis)  to  its  free  outflow  through 
the  nipple.  The  finding  of  lactose  in  the  urine  has  been  considered 
presumptive  evidence  of  the  good  qualities  of  the  mother  as  a  wet 
nurse.     Two  cases  seen  by  me  several  years  ago  gave  an  impression 


^38  THE  EVIDEXCES  OF  DISEASE 

that  the  presence  of  a  considerable  amount  of  lactose  in  the  circulat- 
ing blood  may  cause  a  peculiar  nervous  unrest,  muscular  weakness, 
and  a  tendency  to  syncopal  attacks. 

13.  Acetone. — Traces  (8  to  27  milligrammes  per  day)  of  this 
substance  are  found  in  normal  urine.  In  all  probability  it  is  derived 
from  the  fats.  If  carbohydrates  are  eliminated  from  the  diet  there 
is  a  marked  increase  in  the  amount  of  acetone. 

Acetonuria  is  therefore  found  in  states  of  inanition,  and  in  fevers, 
especially  typhoid  fever,  pneumonia,  scarlet  fever,  measles,  acute 
rheumatic  fever,  acute  miliary  tuberculosis,  and  septicaemic  condi- 
tions, but  is  much  less  apt  to  occur  if  the  dietary  allows  sugar  and 
starch.  It  is  also  found  in  the  cancerous  cachexia,  especially  car- 
cinoma of  the  stomach  ;  in  certain  mental  and  nervous  diseases,  as 
in  melancholia  and  locomotor  ataxia ;  in  autointoxication  of  intes- 
tinal origin  ;  and  after  chloroform  anaesthesia.  The  acetonuria  asso- 
ciated with  diabetes  is  of  more  clinical  importance  than  in  the  con- 
ditions mentioned.  The  simultaneous  finding  of  glucose  and  acetone 
in  the  urine  is  good  proof  of  the  existence  of  diabetes,  and  the  larger 
the  amount  of  acetone  the  more  severe  is  the  disease.  In  the  treat- 
ment of  diabetes  it  has  been  suggested  that  sugar  or  starcli  should 
be  freely  given  if,  with  unpleasant  symptoms,  the  amount  of  acetone 
is  found  to  be  greatly  increased. 

14.  Diacetlc  Acid. — The  presence  of  this  substance  in  the  urine 
{diaceturia)  has  exactly  the  same  meaning  as  that  of  acetone,  as  it 
occurs  under  the  same  circumstances. 

15.  Oxy butyric  Acid. — It  is  regarded  as  probable  by  compe- 
tent observers  that  ^-oxybutyric  acid  is  the  exciting  cause  of  diabetic 
coma,  but  this  point  is  still  in  dispute.  Be  that  as  it  may,  the  find- 
ing of  yS-oxybutyric  acid  in  the  urine  of  a  case  of  diabetes  indicates  a 
grave  type  of  the  disease,  and  if  considerable  amounts  of  acetone  and 
diacetic  acid  are  also  present  it  is  probable  that  diabetic  coma  is 
impending.  Oxybutyric  acid  is  a  product  of  the  breaking  down  of 
albuminous  material. 

16.  liipaciduria. — This  is  a  condition  in  which  certain  fatty 
acids  (formic,  acetic,  butyric,  propionic)  are  found  in  the  urine.  It 
has  been  observed  in  diabetes,  leucaemia,  and  certain  fevers,  as  well 
as  in  some  diseases  of  the  hepatic  parenchyma.  Lipaciduria  has  no 
diagnostic  value. 

17.  Cystin  in  the  Urine. — This  rare  finding  has  little  clinical 
significance,  Cystinuria  is  associated  with  the  presence  of  certain 
diamines,  which,  with  the  cystin,  appear  to  be  due  to  a  special  form 
of  intestinal  putrefaction.  The  condition  is  in  some  instances  hered- 
itary, and  may  result  in  the  formation  of  a  cystin  calculus. 


EVIDENCE  FROM  MICROSCOPIC  URINALYSIS  639 

18.  The  Diazo-reaction  of  Ehrlich. — This  reaction  may  be 
found  at  times  in  pneumonia,  scarlet  fever,  malaria,  variola,  measles, 
septic  conditions,  and  advanced  malignant  disease.  There  are  two 
diseases,  however,  in  which  the  occurrence  of  the  diazo-reaction  is  of 
much  clinical  importance — in  one  for  diagnosis,  in  the  other  with 
reference  to  prognosis.  The  first  is  typhoid  fever.  If  in  a  doubtful 
case  the  reaction  is  found  between  the  fifth  and  thirteenth  day  of  the 
disease  and  not  later  than  the  twenty-second  day,  it  is  presumptive 
evidence  that  the  disease  is  typhoid  fever.  If  the  reaction  is  not 
found  in  the  second  or  third  week  of  a  supposed  case  of  typhoid 
fever,  it  is  probable  either  that  the  case  is  very  mild  or  that  the 
diagnosis  is  wrong  (Simox). 

The  second  disease  is  tuberculosis.  In  the  acute  miliary  form, 
which  is  liable  to  be  confounded  with  typhoid  fever,  the  reaction 
generally  does  not  appear  until  the  beginning  of  the  third  week  and 
continues  to  be  found  almost  to  the  end  (Simon).  In  pulmonary 
phthisis  a  persistent  diazo-reaction  is  almost  invariably  indicative  of 
a  rapidly  advancing  and  usually  incurable  condition.  I  have  verified 
the  truth  of  this  statement  in  a  number  of  instances. 

III.    EVIDENCE    FROM    THE    MICROSCOPICAL 
EXAMINATION   OF  THE   URINE 

(1)  Fat  in  the  Urine. — When  fat  is  present  in  such  quantities 
that  it  is  practicable  to  recognise  it  as  such  by  the  unaided  eye,  it  is 
termed  lipiiria.  Ordinarily  the  fat  is  present  in  minute  droplets, 
which  are  recognised  only  by  microscopical  examination.  If  outside 
contamination  (oily  containers,  oil-lubricated  catheters,  addition  of 
milk  by  malingerers)  can  be  excluded,  fat  in  the  urine  may  be  due 
to  the  ingestion  of  excessive  amounts  of  fat  (e.  g.,  fat  meat,  cod-liver 
oil),  or  oil  inunctions. 

It  may  be  found  in  cases  of  fracture  involving  the  bone  marrow 
and  causing  fat  embolism;  in  the  fatty  degeneration  of  phosphorus 
poisoning;  in  long-continued  suppurative  processes  (py8emia,phthisis) ; 
in  the  lipaemia  of  diabetes  mellitus ;  in  obesity,  leucaemia,  chronic 
alcoholism,  and  some  diseases  of  the  heart  and  the  pancreas.  The 
fat  may  be  derived  from  fatty  degeneration  of  the  renal  epithelium 
in  chronic  nephritis,  of  pus  cells  in  pyonephrosis,  or  of  neoplasms 
somewhere  along  the  urinary  tract.  If  the  urine  is  so  crowded  with 
minute  particles  of  fat  as  to  present  a  milky  appearance  to  the  naked 
eye,  it  constitutes  chyluria  or  galacturia.  It  may  clot  more  or  less 
extensively,  and  contain  leucocytes,  red  corpuscles  in  sufficient  num- 
bers to  colour  the  coagulum,  and  albumin.  Chyluria  may  be,  and 
usually  is,  of  parasitic  origin,  due  to  the  presence  of  the  Filaria  sail' 


640  THE  EVIDENCES  OF   DISEASE 

guinis  Jiominis ;  but  in  rare  instances  the  parasites  are  not  found 
and  the  etiology  is  obscure. 

(2)  Pus  in  the  Urine. — Pyuria  is  found  as  a  very  important 
symptom  in  a  number  of  affections  of  the  urinary  tract,  from  the 
kidney  to  the  end  of  the  urethra  inclusive.  It  occurs  a,lso  in  some 
instances  as  an  evidence  of  disease  in  neighbouring  organs.  The 
amount  of  pus  varies  from  a  moderate  increase  in  the  number  of 
leucocytes  normally  found  in  the  urine  and  to  be  perceived  only  by 
microscopical  examination,  to  a  quantity  which,  when  allowed  to 
settle,  will  form  a  deposit  an  inch  or  more  in  depth.  In  neutral  and 
acid  urines  the  form  and  character  of  the  pus  cells  may  be  well  pre- 
served, but  in  strongly  alkaline  urine  they  are  swollen  and  perhaps 
completely  disintegrated.  If  an  old  abscess  has  ruptured  into  the 
urinary  passage  nothing  but  granular  or  fatty  detritus  may  be  found. 

When  pus  is  discovered  in  the  urine  the  question  immediately 
arises  as  to  its  source.  Not  infrequently  the  determination  of  the 
condition  giving  rise  to  the  pyuria  is  extremely  difficult,  but  in  the 
majority  of  cases  attention  to  the  following  points,  together  with  a 
consideration  of  the  history  and  associated  symptoms,  will  enable  a 
satisfactory  answer.  It  may  be  stated  in  general  that  the  largest 
amounts  of  pus  come  from  an  inflamed  bladder,  or  from  the  rupture 
of  an  abscess  into  the  urinary  tract,  although  very  considerable 
quantities  may  be  discharged  from  the  kidney.  tTrine  containing 
pus  from  the  kidney,  or  from  an  outside  source,  is  usually  acid ; 
from  the  bladder,  more  or  less  strongly  alkaline.  It  is  of  course 
alkaline  if  pyelitis  and  cystitis  coexist.  If  the  pus  appears  and  dis- 
appears rather  suddenly,  or  varies  notably  in  quantity  at  different 
times,  either  its  renal  or  its  outside  origin  may  be  suspected. 

(«)  Urethritis. — If  the  pyuria  is  due  to  urethritis  (simple  or 
gonorrhoeal),  a  drop  of  pus  may  be  squeezed  from  the  urethra,  and 
if  the  two-glass  test  is  employed,  the  first  portion  of  urine  voided 
contains  pus,  while  the  second  is  clear.  If  the  second  portion  also 
contains  pus  in  even  larger  quantity  and  is  alkaline,  the  presence  of 
a  coexisting  cystitis  may  be  inferred.  A  gonorrhoeal  ulcer,  or  a  sub- 
urethral abscess  (especially  in  women),  may  also  be  responsible  for 
pyuria.     These  conditions  are  to  be  discovered  by  the  urethroscope. 

{h)  Cystitis. — If  the  urine  is  alkaline  (frequently  offensive)  and 
the  pus,  which  is  often  gelatinous  and  ropy,  issues  with  the  last  por- 
tion of  the  urine,  the  pyuria  is  due  to  cystitis.  The  cystoscope  may 
be  employed  to  confirm  the  diagnosis,  and  the  sound  to  discover  a 
possible  calculus. 

(c)  Ureteritis. — The  nature  of  a  pyuria  due  to  a  tuberculous  or 
gonorrhoeal   stricture   at    the   lower,  middle,  or  upper  part  of  the 


EVIDENCE  FROM  MICROSCOPIC  URINALYSIS  641 

ureter,  above  which  the  pus  may  collect,  is  to  be  determined  only 
by  ureteral  catheterization. 

{d)  Pyelitis  or  Pyelonephritis. — The  continuous  but  remittent 
presence  of  pus  in  an  acid  urine  suggests  tuberculous,  calculous,  or 
obstructive  pyelitis.  If  the  pus  flows  intermittently  it  is  more  likely 
to  be  caused  by  suppurative  or  surgical  kidney  with  abscesses  of  con- 
siderable size.  A  coexisting  cystitis  causes  the  urine  to  assume  the 
cystitic  type,  (b)  preceding,  but  also  suggests  the  possibility  of  an 
ascending  renal  infection.  Ureteral  catheterization  may  determine 
beyond  doubt  the  presence  or  absence  of  pyelitis. 

(e)  Outside  Sources  of  Pyuria. — Certain  suppurative  foci  may 
rupture  into  the  urinary  tract,  almost  invariably  into  the  bladder, 
and  utilize  it  for  drainage.  Pyuria  of  this  kind  is  most  frequently 
due  to  salpingitis,  simple  or  tuberculous,  but  may  also  arise  from  an 
abscess  of  the  ovary  or  extra-uterine  pregnancy,  suppurating  ovarian 
or  dermoid  cyst,  and  psoas  or  acetabular  abscess  connected  with  dis- 
ease of  the  vertebra  or  hip  joint.  A  vesico-intestinal  fistula  or  malig- 
nant disease  involving  the  bladder  by  contiguity  may  also  be  classed 
under  this  head. 

A  bacteriological  examination  of  the  pus  may  afford  valuable  evi- 
dence by  revealing  the  gonococcus,  the  tubercle  bacillus,  colon  bacil- 
lus, or  the  bacillus  of  typhoid  fever,  as  well  as  the  ordinary  pyogenic 
organisms. 

(3)  Red  Blood  Corpuscles. — See  Haematuria,  page  635. 

(4)  Epithelial  Cells. — Under  normal  circumstances  only  a  small 
number  of  epithelial  cells  are  found  in  the  urine,  representing  the 
slight  physiological  desquamation  constantly  occurring  in  the  whole 
length  of  the  urinary  tract.  Large  quantities  of  epithelium  when 
found  in  urinary  sediments  are  indicative  of  some  pathological  con- 
dition (disturbances  of  circulation  or  inflammatory  changes)  affecting 
the  kidney  or  the  urinary  passages.  Unhappily,  the  place  of  origin 
of  the  cells,  and  in  consequence  the  seat  of  the  disease,  can  not  be 
inferred  from  the  character  of  the  cells,  except  in  rare  instances, 
although  in  conjunction  with  the  history  and  the  associated  signs 
and  symptoms  the  cell  findings  may  afford  valuable  evidence  as  to 
the  nature  and  location  of  the  morbid  process.  The  uncertainty  as 
to  the  place  of  origin  of  the  epithelial  elements  arises  largely  from 
the  fact  that  similar  varieties  of  epithelium  are  found  in  widely 
separated  parts  of  the  urinary  tract.  Thus  a  certain  variety  of 
epithelium  when  derived  from  the  superficial  surface  of  the  mucous 
membrane  lining  a  definite  part  of  the  urinary  tract  may  be  quite 
characteristic  of  that  particular  area,  while  the  cells  of  the  deeper 
layers  of  the  membrane  at  the  same  point  may  exactly  resemble  the 


642  THE  EVIDENCES  OF   DISEASE 

superficial  cells  of  other  portions  of  the  tract.  If,  therefore,  as  hap- 
pens in  all  but  slight  pathological  processes,  there  is  a  more  or  less 
extensive  desquamation,  one  is  apt  to  find  a  deposit  of  the  mixed 
varieties.  Moreover,  by  their  sojourn  in  the  urine  if  it  be  alkaline, 
the  exfoliated  cellular  elements  tend  to  become  swollen,  large,  and 
round,  thus  interfering  with  the  characters  by  which  they  might 
otherwise  have  been  recognised. 

There  are  three  varieties  of  epithelium  the  recognition  of  which 
is  serviceable,  i.  e.,  round,  caudate,  and  flat. 

(a)  Round  Cells. — These  cells  are  usually  a  little  larger  than 
leucocytes,  but  may  be  of  the  same  size.  They  are  distinguished 
by  a  large  and  distinct  single  nucleus  which  is  visible  without  the 
aid  of  acetic  acid.  They  originate  mainly  from  the  uriniferous 
tubules,  the  deep  layers  of  the  mucous  membrane  of  the  pelvis  of 
the  kidney,  the  bladder,  and  the  male  urethra.  If  albumin  is  pres- 
ent, or  if  casts  are  found  to  which  some  of  the  round  cells  are  cling- 
ing, the  renal  origin  of  the  latter  may  be  inferred.  An  unusually 
large  number  of  well-preserved  and  typical  round  cells  occurring 
under  such  circumstances  is  indicative  of  an  acute  diffuse  nephritis ; 
while  if  the  cells  are  fatty,  markedly  granular,  or  partly  disin- 
tegrated, the  existence  of  a  chronic  diffuse  process  is  more  probable. 
If,  with  a  large  number  of  round  cells,  pus  is  present,  without  casts 
or  more  than  a  trace  of  albumin,  a  pyelitis  may  be  strongly  suspected. 

(b)  Caudate  Cells. — Conical,  columnar,  spindle-shaped,  cylindrical, 
or  "  tailed  "  epithelial  cells  originate  from  the  superficial  layer  of  the 
mucous  membrane  of  the  pelvis  of  the  kidney  and  the  deep  layers  of 
the  vesical  mucous  membrane.  The  cells  from  the  latter  location 
are  said  to  have  longer  "  tails  "  or  processes  by  which  it  may  be  pos- 
sible to  identify  them.  Although  by  no  means  characteristic,  tailed 
cells  are  usually  abundant  in  cases  of  pyelitis. 

(c)  Flat  Cells. — Large  squamous  or  pavement  epithelial  cells  are 
usually  derived  from  the  bladder  or  the  vagina.  The  vaginal  cells 
are  usually  larger  than  those  from  the  bladder,  and  are  very  com- 
monly grouped.  An  unusual  abundance  of  flat  vesical  epithelial 
cells  is  indicative  of  cystitis,  and  if,  in  addition,  many  columnar 
cells  are  present,  the  cystitis  is  probably  of  a  severe  grade,  involv- 
ing the  deeper  layers  of  the  vesical  mucosa.  If  in  a  woman  there  is 
doubt  as  to  whether  a  vaginitis  and  not  a  cystitis  is  the  source  of  the 
squamous  epithelium,  the  vulva  should  be  cleansed  and  a  catheter 
specimen  of  urine  obtained. 

(5)  Tube  Casts  in  the  Urine. — Urinary  tube  casts  are  perhaps 
the  most  important  of  all  findings  during  an  examination  of  the 
urine.     In  at  least  the  large  majority  of  cases  when  casts  are  dis- 


EVIDENCE  FROM  MICROSCOPIC  URINALYSIS  643 

covered  albumin  is  present,  although  it  may  be  in  such  small  amount 
as  only  to  be  discovered  by  the  more  delicate  tests.  There  are  three 
main  divisions  of  tube  casts :  First,  those  composed  of  cellular  ele- 
ments or  micro-organisms,  viz.,  red  corpuscles,  leucocytes,  epithelial 
cells,  or  bacteria ;  second,  casts  of  degenerated  cellular  elements  and 
unorganized  protoplasm — granular  casts ;  third,  casts  composed  of  a 
homogeneous,  hyaline  material — hyaline  and  waxy  casts. 

Judging  from  personal  experience,  it  seems  probable  that  casts  are 
found  more  frequently  in  sediments  obtained  by  centrifugation  than 
in  those  which  result  from  standing.  Certainly  of  late  years,  the  cen- 
trifugal apparatus  having  been  systematically  employed,  casts,  espe- 
cially of  the  hyaline  variety,  have  been  reported  as  occasionally  pres- 
ent in  a  much  larger  proportion  of  urines  in  my  own  practice  than 
was  formerly  the  case.  This  fact  emphasizes  the  truism  that  the 
presence  of  two  or  three  hyaline  casts,  like  that  of  a  trace  of 
albumin,  unless  found  in  repeated  examinations,  does  not,  per  sCy 
necessarily  imply  permanent  renal  disease. 

(a)  Epithelial  Tube  Casts. — These  occur  as  hollow  or  solid  cylin- 
ders composed  entirely  of  epithelial  cells ;  or  the  cells  are  adherent 
to  the  surface  of  a  cylindrical  hyaline  matrix.  The  cells  may  be 
granular  or  fatty.  When  found,  such  casts  always  signify  a  desqua- 
mative nephritis,  the  epithelial  lining  of  the  renal  tubules  having 
been  partly  or  entirely  exfoliated.  Granular  or  fatty  degeneration 
of  the  cells  argues  in  favour  of  a  chronic  process. 

(b)  Blood  Casts. — Casts  composed  of  red  corpuscles  bound  together 
by  a  fibrin  network  are  not  often  seen,  as  they  are  apt  to  be  obscured 
by  the  considerable  number  of  free  corpuscles  by  which  they  are  usu- 
ally accompanied.  Such  casts  are  encountered  in  acute  renal  hyper- 
aemia,  acute  nephritis,  hemorrhagic  infarction,  and  renal  haematuria. 
When  found  in  a  case  of  hematuria  their  presence  furnishes  indubi- 
table proof  that  the  blood  originates  from  the  kidney. 

(c)  Pus  Casts. — Very  seldom  casts  are  seen  which  are  formed  of 
leucocytes  alone.  When  found  they  are  indicative  of  a  multiple  sup- 
purative nephritis.  Small  numbers  of  leucocytes  adhering  to  other 
varieties  of  casts,  particularly  the  hyaline  form,  are  not  infrequently 
seen  in  the  non-suppurative  nephritides.  Plugs  or  balls  of  pus  are 
significant  of  pyelitis. 

(d)  Bacterial  Casts. — Casts  proved  to  consist  of  bacterial  masses 
(micrococci)  moulded  into  cylinders  in  the  urinary  tubules  are  some- 
times discovered.  Their  presence  is  significant  of  pyelonephritis  in 
which  the  infection  has  travelled  upward  through  the  ureters  to  the 
renal  pelvis,  or  suppurative  nephritis  due  to  the  lodgment  of  an 
infective  embolus  from  some  distant  septic  focus. 


Q4A:  THE  EVIDENCES  OP  DISEASE 

(e)  Granular  Casts. — Finely  or  coarsely  granular  casts,  often  frag- 
mentary, resulting  from  degenerative  changes  affecting  the  epi- 
thelium, red  corpuscles,  leucocytes,  or  hyaline  material  of  which 
they  were  originally  composed,  are  frequently  found.  If  such  casts 
are  present  it  is  safe  to  infer  the  existence  of  a  chronic  or  degenera- 
tive process  in  the  kidneys. 

(/)  Fatty  Casts. — Casts  whose  surfaces  are  completely  covered 
with  fat  droplets  or  globules  are  usually  significant  of  subacute  or 
chronic  nephritis  with  fatty  degeneration,  especially  the  large  white 
kidney. 

(g)  Hyaline  Casts. — These  are  transparent,  homogeneous  casts, 
sometimes  showing  fine  pale  granules  or  striations,  and  not  infre- 
quently presenting  a  few  adherent  epithelial  cells,  red  cells,  or 
leucocytes.  They  are  the  most  common  of  all  casts,  and  are  found 
not  only  in  all  inflammations,  acute  or  chronic,  of  the  renal  tubules, 
but  when  purely  hyaline  and  temporarily  present  may  result  from 
circulatory  disturbances  without  organic  changes. 

(h)  Waxy  Casts. — These  casts,  regarded  by  some  writers  as  merely 
a  variety  of  hyaline  cast,  are  not  at  all  indicative  of  amyloid  (waxy) 
degeneration  of  the  kidneys.  They  are  of  infrequent  occurrence, 
and  when  present  may  signify  any  one  of  the  subacute  or  chronic 
diseases  of  the  renal  substance. 

(i)  Cyllndroids. — These  structures  are  probably  of  renal  origin 
and  closely  affiliated  with  hyaline  casts.  Like  the  latter,  they  are 
indicative  of  renal  irritation  and  circulatory  disturbances,  as  in 
oxaluria  and  excessive  elimination  of  uric  acid,  but  may  be  present 
without  albumin  and  unaccompanied  by  indubitable  casts.  While 
their  exact  significance  is  a  matter  of  dispute,  some  writers  regard- 
ing them  with  suspicion,  it  is  very  likely  that  their  pathological 
importance  as  indicating  organic  changes  is  minimal.  They  are 
found  especially  in  the  urine  of  children. 

(6)  Prostatic  Threads. — Threads  of  mucus,  sufficiently  large 
to  be  easily  seen  without  the  aid  of  the  microscope,  are  significant  of 
prostatic  irritation. 

(7)  Spermatozoa. -^These  are  found  in  the  first  urine  passed 
by  men  after  emission  (coitus,  pollutions,  following  an  epileptic  con- 
vulsion), and  in  women  when  the  external  genitals  have  been  soiled 
during  coitus.  They*  occur  in  some  cases  of  injury  or  disease  of  the 
spinal  cord.  Occasionally  a  small  amount  of  semen  is  expressed  from 
the  vesiculae  seminales  by  hard  faecal  masses,  during  the  severe  expul- 
sive efforts  accompanying  obstinate  constipation.  The  persistent 
presence  of  spermatozoa  in  the  urine  is  the  cardinal  symptom  of  true 
spermatorrhoea. 


THE  URINALYSIS  IN  SPECIAL  DISEASES  645 

(8)  Elastic  Fibres  and  Tumour  Fragments. — Elastic  fibres 
"when  present  indicate  a  severe  ulcerative  process  in  the  bladder. 
Very  rarely  particles  of  papillomatous  or  villous  growths  of  the  blad- 
der are  detached,  and  appear  in  the  urine  as  vascular  connective 
tissue  formations  covered  with  epithelial  cells.  In  other  tumours 
nothing  but  disintegrated  and  unrecognisable  material  is  usually 
found. 

(9)  Parasites. — The  following  organisms  have  been  encountered 
in  the  urine,  either  by  centrifugation  and  the  preparation  of  dried 
And  stained  cover-glass  films,  or  by  cultures. 

(«)  Pathogenic  Bacteria. — The  typhoid  bacillus  is  present  in  the 
urine  at  some  period  in  the  course  of  almost  all  cases  of  typhoid 
iever,  and  its  finding  constitutes  one  of  the  diagnostic  tests  of  the 
disease.  The  discovery  of  the  tubercle  bacillus  in  the  urine  is  good 
evidence  of  tuberculous  disease  of  the  urinary  organs.  The  finding 
of  the  gonococcus  may  explain  the  true  nature  of  a  supposed  rheu- 
matism. While  the  presence  of  bacteria  in  the  urine  does  not 
necessarily  imply  renal  inflammation,  if  considerable  numbers  of  the 
diplococcus  of  pneumonia,  the  typhoid  bacillus,  the  Bacillus  colt 
communis,  or  the  pyogenic  staphylococci  and  streptococci  are  dis- 
covered in  the  urine,  and  the  clinical  symptoms  of  a  nephritis  or 
pyelonephritis  coexist,  it  may  safely  be  inferred  that  the  inflamma- 
tion is  due  to  infection  by  the  particular  organism  found. 

(b)  Other  Parasitic  Organisms. — Of  other  parasitic  forms  of  life, 
yeast  cells  may  occur  abundantly  in  urine  containing  sugar ;  rarely 
the  ova  of  distoma  haematobium  and  the  Filaria  sanguinis  hominis 
in  haematuria  and  chyluria ;  trichomonas  in  haematuria ;  also,  rarely, 
echinococciis  booklets  and  fragments  of  membrane  if  a  cyst  has 
ruptured  into  the  urinary  passages ;  and  very  infrequently  ascarides, 
in  cases  of  vesico-rectal  fistula. 

Before  deciding  that  the  urine  contains  bacteria  or  other  micro- 
organisms, a  specimen  should  be  examined  directly  after  voiding, 
having  taken  the  necessary  precautions,  especially  for  cultural  tests, 
of  carefully  disinfecting  the  external  genitals,  and  sterilizing  con- 
tainers, and  catheters,  if  the  latter  are  employed. 

IV.    COLLECTIVE    RESULTS    OF    URINALYSIS    IN 
SPECIAL    DISEASES    AND    CONDITIONS 

(1)  Movable  Kidney. — ^In  the  majority  of  movable  kidneys  the  urine  presents 
no  abnormality.  Occasionally,  when  the  ureter  becomes  badly  strangulated  or 
kinked  (Dietl's  crises)  and  its  lumen  temporarily  constricted,  the  urine  is  scanty, 
loaded  with  uric  acid  or  oxalates,  and  contains  blood,  albumin,  and  epithelial 
•cells.  This  condition  is  usually  followed  by  a  copious  discharge  of  pale  urine. 
43 


646  THE  EVIDENCES  OF   DISEASE 

(2)  Acute  or  Active  Menal  Hypercemia. — The  urine  is  acid,  somewhat  in- 
creased in  quantity,  and  contains  more  or  less  blood,  small  amounts  of  albumin,, 
and  a  few,  usually  hyaline,  casts. 

(3)  Passive  or  Mechanical  Renal  Congestion. — The  urine  is  scanty,  acid,  of 
high  specific  gravity,  usually  cloudy  with  urates,  and  contains  at  least  traces  of 
albumin,  with  a  few  small  hyaline  casts  and  occasional  red  corpuscles.  It  is 
the  typical  urine  of  chronic  valvular  disease  of  the  heart. 

(4)  Acute  Diffuse  Nephritis. — The  urine  is  greatly  diminished  in  amount  (4 
or  5  oz.  in  24  hours),  or  is  even  totally  suppressed  (anuria).  It  is  smoky, 
blackish,  or  of  a  chocolate  color.  The  specific  gravity  is  high.  Albumin  is; 
found  in  large  amount,  and  the  heavy  deposit  contains  abundant  red  corpuscles, 
blood,  hyaline,  and  epithelial  tube  casts.     The  total  urea  is  lessened. 

(5)  Chronic  Diffuse  Nephi'itis. — The  quantity  of  urine  is  diminished,  it  is 
cloudy  from  urates,  the  specific  gravity  may  be  high  in  the  early,  but  is  low  in 
the  later,  stages.  Albumin  is  abundant,  sometimes  more  so  than  in  any  other 
disease.  The  heavy  sediment  contains  large  numbers  of  nearly  all  the  varieties 
of  tube  casts,  hyaline,  epithelial,  granular,  and  fatty.  The  latter  are  especially 
characteristic.  Occasional  red  corpuscles,  many  leucocytes,  and  numbers  of 
degenerated  epithelial  cells  are  also  found.     The  amount  of  urea  is  decreased. 

(6)  Chr<mic  Interstitial  Nephritis. — The  urine  is  increased  in  quantity,  light 
yellow,  clear,  with  a  persistently  low  specific  gravity.  Albumin  is  scanty,  oc- 
curring in  traces,  and  is  sometimes  absent.  A  few  narrow  hyaline  casts  are 
almost  constantly  found  in  the  very  small  deposit.  Cellular  elements  are  as  a 
rule  no  more  abundant  than  in  normal  urine.  Polyuria,  persistent  low  specific 
gravity,  and  the  presence  of  a  few  hyaline  casts  constitute  the  urinary  signs  of" 
this  disease.     Albumin  may  or  may  not  be  present  in  small  quantity. 

(7)  Amyloid  Disease  of  the  Kidney. — There  is  polyuria,  the  urine  is  clear, 
pale,  and  of  low  specific  gravity,  with  a  scanty  sediment.  There  is  almost 
always  a  characteristically  abundant  amount  of  albumin,  perhaps  with  an  un- 
usually large  proportion  of  globulin.  Moderate  numbers  of  large  hyaline,  and 
occasional  waxy,  casts  are  found.  If  casts  are  numerous  a  certain  proportion* 
are  fatty  and  granular. 

(8)  Pyelitis. — (a)  In  the  simpler  forms  of  pyelitis,  such  as  occur  in  the 
specific  fevers,  the  urine  is  cloudy  and  acid,  containing  pus  cells,  young  epithe- 
lial cells  (mucous  corpuscles),  and  sometimes  red  blood  corpuscles.  Albumin 
is  present  in  traces. 

(J)  In  varieties  involving  both  pelvis  and  kidney,  the  urine  is  generally 
acid,  at  least  in  the  earlier  stages  and  when  not  complicated  by  cystitis.  The 
quantity  of  pus  is  considerable,  and  may  be  formed  into  plugs  or  rolled  into 
balls  by  its  passage  through  tlie  ureter.  The  pyuria  may  be  intermittent  be- 
cause of  a  varying  degree  of  obstruction  to  its  exit  from  the  renal  pelvis  (calcu- 
lus, kinks,  pressure).  If  the  obstruction  is  long  continued,  the  renal  pelvis 
becomes  distended  with  pus  (pyonephrosis).  The  epithelium  may  or  may  not 
be  abundant,  and  a  few  casts  and  red  corpuscles  may  be  present.  Albumin  is 
found,  generally  in  proportion  to  the  amount  of  blood  and  pus. 

(c)  In  acute  suppurative  nephritis  the  urine  is  cloudy,  containing  pus,  blood, 
epithelium,  bacteria,  and  casts.  The  latter  are  occasionally  composed  of  pus  or 
bacteria. 


THE  URINALYSIS  IN  SPECIAL  DISEASES  647 

(9)  Hydronephrosis. — When  the  ureter  is  partially  obstructed  and  the  urine 
is  secreted  under  pressure,  it  is  of  a  low  specific  gravity,  and  traces  of  albumin 
are  occasionally  present,  together  with  a  few  red  corpuscles  and  pus  cells. 
Tube  casts  are  not  common,  but  epithelium  is  abundant. 

(10)  Renal  Calculus. — The  urine  is  strongly  acid,  and  contains  blood,  usu- 
ally enough  to  give  a  smoky  tint.  Small  concretions  may  be  found.  Later  a 
calculous  pyelitis  may  be  present,  and  the  characters  of  the  urine  become  those 
previously  described  in  (i),  paragraph  (8)  preceding. 

(11)  Renal  Cancer. — Hsematuria  is  the  most  important,  and  sometimes  the 
first,  evidence  of  the  disease.  An  occasional  but  characteristic  finding  is  that 
of  blood  casts  of  the  renal  pelvis  and  the  ureter.  Tumour  particles  are  practi- 
cally never  found. 

(12)  Renal  Tuberculosis. — The  urine  presents  the  features  of  ordinary  pye- 
litis, pus,  blood,  albumin,  epithelium,  and,  occasionally,  caseous  masses.  Mi- 
croscopic examination  will  show  tubercle  bacilli,  or,  if  not  found  by  the  micro- 
scope, they  may  be  demonstrated  by  culture  and  inoculation. 

(13)  Cystic  Kidney. — Tlie  urine  resembles  that  of  interstitial  nephritis,  as 
previously  described  in  paragraph  (6),  except  that  there  may  be  a  larger  amount 
of  albumin,  a  decided  hsematuria,  and  the  tube  casts  found  are  usually  large 
and  granular. 

(14)  Renal  Embolism. — The  urine  becomes  suddenly  and  decidedly  albumi- 
nous, with  moderate  haematuria,  and  a  little  pus.  It  contains  varying  numbers 
of  hyaline  and  epithelial  tube  casts.  During  the  3  or  4  weeks  (or  less)  subse- 
quent to  the  attack  the  urine  steadily  regains  its  normal  characters. 

(15)  Diabetes  Insipidus. — The  quantity  of  urine  is  enormously  increased  (20 
to  40  pints),  it  is  pale,  and  the  specific  gravity  is  low  (1.002  to  1.007).  The 
total  urea  output  is  increased.  It  does  not  contain  albumin  (except  in  occa- 
sional traces),  sugar,  or  casts.     Inosite  (muscle  sugar)  is  infrequently  present. 

(16)  Diabetes  Mellitus. — The  quantity  of  urine  is  greatly  in  excess  of  the 
normal  (6  to  40  pints),  the  specific  gravity  is  usually  high  (1.030  to  1.045),  but 
exceptionally  is  low.  The  urine  is  pale,  acid,  has  a  sweetish  odour,  and  contains 
from  1  to  10  per  cent  of  glucose.  The  urea  is  increased.  Acetone,  diacetic 
acid,  and  /3-oxybutyric  acid  may  be  present,  and  traces  of  albumin  are  not  in- 
frequent. 

(17)  Uramia. — Although  this  condition  may  be  due  to  various  diseases  of 
the  kidney,  two  urinary  findings  are  practically  constant,  without  reference  to 
the  particular  variety  of  the  causative  lesion,  viz.,  a  considerable  reduction  in 
the  amount  of  urea  (200  to  100  to  50  grains  in  34  hours),  and  the  presence  of  tube 
casts. 

(18)  Cystitis. — In  acute  cystitis  the  urine  is  acid  and  contains  blood,  pus, 
albumin,  and  epithelium.  In  chronic  cystitis  the  urine  is  turbid,  alkaline,  and 
ammoniacal.  It  contains  a  considerable  amount  of  viscid  pus,  albumin,  much 
epithelium,  crystals  of  triple  phosphates,  and  numerous  bacteria  (coli  commu- 
nis, staphylococcus,  streptococcus).     Occasionally  blood  is  present. 

(19)  Vesicfd  Calculus. — Prior  to  the  development  of  cystitis  the  urine  per- 
sistently contains  uratic  or  phosphatic  deposits,  with  a  few  pus  cells  and  red 
corpuscles.  After  the  bladder  is  inflamed,  the  characters  of  the  urine  are  as 
stated  in  paragraph  (18),  except  that  blood  may  be  present  in  larger  amounts. 


548  THE  EVIDENCES  OF  DISEASE 

(20)  Vesical  Cancer.<— Marked  and  increasing  hsematuria,  the  presence  of 
blood  clots,  abundant  epithelium,  and,  in  rare  instances,  fragments  of  the 
growth  in  an  acid  urine,  characterize  malignant  disease  of  the  bladder.  "When 
cystitis  is  initiated  the  special  characters  of  vesical  inflammation  (18)  supervene. 

(21)  Vesical  Tuberculosis. — Blood  in  small  amount,  and  increasing  quanti- 
ties of  pus  in  an  acid  urine,  followed  by  the  evidences  of  a  chronic  cystitis  (18), 
constitute  the  urinary  findings  in  tuberculosis  of  the  bladder. 


SECTION  XLIII 

DIAGXOSTIC   PUXCTUEE  AND   THE   EVIDEXCE 
DERIVED   THEREFROM 

In  order  to  make  or  verify  a  diagnosis  it  is  sometimes  desirable 
to  ascertain  the  character  of  the  fluids  which  may  be  present  in  the 
cavities  of  the  body  or  in  cystic  or  abscess  cavities. 

Technic  of  the  Puncture. — A  diagnostic  or  exploratory  puncture 
may  be  made,  in  case  of  necessity,  by  an  ordinary  hypodermic  syringe, 
but  is  better  done  by  using  the  ordinary  aspirator  or  an  exploring 
syringe.  The  latter  is  simply  a  larger  hypodermic,  with  a  longer  and 
stouter  needle.  The  puncture  should  be  made  with  strict  antiseptic 
precautions.  The  needle  should  be  boiled  (conveniently  in  a  test 
tube)  for  5  to  10  minutes,  or  put  in  a  steam  sterilizer.  The  skin  at 
the  point  to  be  punctured  must  be  scrubbed  first  with  soap  and  wa- 
ter, then  with  bichloride  solution,  finally  \7ith  alcohol.  The  hands 
of  the  operator  should  be  similarly  treated.  To  minimize  the  pain 
of  the  needle  thrust,  a  few  minims  of  a  2-  to  4-per-cent  solution  of 
cocaine  may  be  injected  subcutaneously ;  or  local  anaesthesia  secured 
by  pressing  for  a  few  moments  a  bit  of  ice  sprinkled  with  salt  against 
the  selected  point,  or  using  an  ethyl  chloride  spray  for  the  same  pur- 
pose. The  needle  should  then  be  thrust  rapidly  but  steadily  to  the 
desired  depth.  If  a  vacuum  bottle  is  in  use  the  stopcock  should 
then  be  turned,  or  the  piston  of  the  syringe  slowly  pulled  out.  If 
the  attempt  is  unsuccessful,  the  needle  should  be  slowly  entered  a 
little  deeper,  or  gradually  withdrawn,  while  suction  is  continued. 
The  puncture  may  be  covered  with  sterilized  gauze,  or,  better,  sealed 
with  collodion  in  which  a  little  bismuth  iodide  has  been  mixed. 

The  following  points  of  puncture  are  those  commonly  employed : 

(1)  Pericardial  Cavity. — The  puncture  may  be  made  either  in 
the  fourth  interspace,  i^  to  1  inch  from  the  left  sternal  margin ;  or  in 
the  fifth  interspace,  1^^  inch  from  the  left  sternal  margin ;  or  if  the 
effusion  is  large,  by  entering  the  needle  in  the  left  costoxiphoid 


EVIDENCE  PROM  DIAGNOSTIC  PUNCTURE  649 

angle,  close  to  the  costal  margin,  and  passing  it  upward  and  back- 
ward, 

(2)  Pleural  Cavity. — The  puncture  may  be  made  either  in  the 
seventh  interspace  in  the  midaxillary  line,  or,  perhaps  better,  in  the 
eighth  interspace,  just  outside  of  the  lower  angle  of  the  scapula. 

(3)  Peritoneal  Cavity. — Ordinarily  the  puncture  is  made  in  the 
linea  alba,  midway  between  umbilicus  and  symphysis,  first  making 
sure  that  the  bladder  is  empty. 

(4)  Lumbar  Puncture  (Quincke). — As  this  is  most  frequently  re- 
quired to  be  done  in  children,  general  anaesthesia  is  often  necessary. 
The  patient  should  be  placed  in  the  right  or  left  lateral  position, 
bent  somewhat  forward,  back  toward  the  operator.  Identify  the 
12th  dorsal  spine  by  means  of  the  last  rib,  and  count  downward  to 
the  3d  (or  -ith)  lumbar  spinous  process.  An  exploring  needle 
is  then  entered,  about  ^  inch  to  right  or  left  of  the  median  line,  on 
a  level  with  the  tip  of  the  spinous  process,  in  a  direction  somewhat 
upward  and  inward.  It  should  be  introduced  slowly  to  a  depth  of  2 
to  4  centimetres  (f  to  1^  inch)  in  children,  4  to  8  centimetres  (1^ 
to  3  inches)  in  adults,  before  it  pierces  the  membranes  and  enters 
the  vertebral  canal.  Unless  the  pressure  is  great  the  cerebro-spinal 
fluid  escapes  drop  by  drop,  and  not  continuously.  Aspiration  is  not 
required.  The  fluid  should  be  collected  in  a  test  tube.  If  a  bac- 
teriological examination  is  to  be  made,  the  tube  should  have  been 
sterilized,  and  is  to  be  plugged  with  cotton  when  filled.  The  pro- 
cedure is  usually  free  from  danger.  It  is  wise  to  avoid  lateral  move- 
ment of  the  needle  while  obtaining  the  fluid,  in  order  to  prevent  un- 
necessary laceration  and  consequent  hemorrhage. 

(5)  Puncture  of  the  Liver. — Exploratory  aspiration  of  the  liver 
may  be  done  by  entering  the  needle  either  in  the  seventh  interspace 
in  the  midaxillary  line,  or  in  the  lowest  interspace  in  the  anterior 
axillary  line,  or  posteriorly  at  the  central  point  of  the  area  of  hepatic 
dulness.  General  anaesthesia  is  required.  This  procedure  may  be 
essential  for  diagnosis  in  abscess  or  hydatid  cyst  of  the  liver,  and  is 
unattended  by  danger.  Puncture  of  the  gall  bladder  is  rarely  done, 
as  there  is  danger  of  leakage  from  the  opening  into  the  peritoneal 
cavity. 

(6)  Cysts  and  Abscesses. — These  are  to  be  punctured  at  the  most 
prominent  point  (e.  g.,  hydronephrosis),  or  in  the  center  of  the  dul- 
ness caused  by  the  fluid  (e.  g.,  localized  empyema),  having  due 
regard  to  the  presence  of  important  structures  which  may  run  a  risk 
of  injury. 

Examination  of  the  Fluid  Obtained. — The  fluid  having  been  se- 
cured, it  is  necessary  to  note  its  colour,  transparency,  degree  of 


650  THE   EVIDENCES  OF  DISEASE 

'  fluidity,  and  odour.  After  taking  its  specific  gravity  with  an  accu- 
rate urinometer,  a  portion  may  be  set  aside  in  a  conical  glass  and 
allowed  to  settle,  observing  subsequently  the  appearance  of  a  deposit 
or  the  formation  of  a  coagulum.  Another  portion  should  be  filtered, 
and  the  filtrate  tested  with  regard  to  its  reaction  with  litmus  paper 
and  the  presence  of  albumin,  sugar,  mucin,  and  sometimes  of  urea. 

The  presence  of  albumin  is  ascertained  by  the  same  tests  as  those 
used  for  its  detection  in  urine.  Esbach's  albuminometer  may  be  em- 
ployed for  its  approximate  quantitative  estimation.  The  presence  of 
mucin  is  affirmed  by  the  appearance  of  a  precipitate  upon  adding 
acetic  acid  in  excess  to  a  portion  of  the  fiuid.  The  presence  and 
amount  of  urea  (rarely  found  except  in  hydronephrosis)  may  be  de- 
termined by  boiling  and  filtering  the  fiuid,  and,  after  evaporating 
the  filtrate  to  a  small  bulk,  testing  it  as  for  urea  in  urine. 

A  drop  of  the  sediment  obtained  by  standing  (or,  better,  by  cen- 
trifugation)  should  be  submitted  to  microscopical  examination,  with 
reference  to  the  presence  of  red  corpuscles,  leucocytes,  epithelial  or 
endothelial  cells,  booklets,  scolices  or  fragments  of  membrane  (echi- 
nococcus),  actinomyces,  and  the  Ammha  coli.  Pathogenic  bacteria 
may  be  sought  for  in  cover-glass  films  appropriately  stained,  or  by 
bacteriological  methods. 

The  Characters  of  the  Fluid  According  to  its  Source. — 
(1)  Dropsical  Fluids. — Fluid  effusions  obtained  in  pathological  quan- 
tities from  the  closed  (serous)  cavities  of  the  body  may  be  due  on  the 
one  hand  to  passive  congestion,  as  in  cardiac  valvular  disease,  or  to 
defective  drainage  by  way  of  the  kidneys,  as  in  nephritis.  On  the 
other  hand,  the  accumulation  may  be  the  result  of  inflammation. 
The  former  are  dropsical  fluids  or  transudates,  the  latter,  inflamma- 
tory fluids  or  exudates.  It  is  not  always  easy  to  distinguish  one  from 
the  other.  Both  may  be  clear,  serous  fluids  of  a  light  yellow  or  yel- 
lowish-green colour,  and  both  contain  albumin.  If  the  specific  gravity 
of  the  fluid  is  under  1.015,  and  the  percentage  of  albumin  is  less  than 
2.5,  it  may  be  definitely  inferred  that  it  is  a  transudate.  Trans- 
udates are  sometimes  reddish  (sanguineous),  very  rarely  milky  (chy- 
lous). If  a  transudate  contains  blood,  clotting  on  standing  may  occur, 
usually  to  a  moderate,  sometimes  to  a  considerable,  extent. 

(2)  Injiammato7"y  Fluids. — If,  on  the  contrary,  the  specific  gravity 
is  above  1.018,  and  there  is  more  than  4  per  cent  of  albumin,  usually 
(but  not  necessarily)  with  the  formation  of  a  considerable  coagu- 
lum, the  fluid  is  an  exudate.  As  a  general  rule  fluids,  whether  of 
inflammatory  or  non-inflammatory  origin,  derived  from  the  pleural 
cavity,  are  richer  in  albumin  than  those  obtained  from  the  perito- 
neal sac. 


EVIDENCE  FROM  DIAGNOSTIC   PUNCTURE  651 

(3)  Serous,  Serofibrinous,  and  Hemorrhagic  Fluids. — It  is  mainly 
■with  these  forms  of  effusion  that  difficulties  may  arise  in  determin- 
ing whether  a  given  specimen  is  a  transudate  or  an  exudate.  The 
points  of  distinction  have  just  been  described.  Under  the  micro- 
scope serous  and  sero-fibrinous  exudates  will  show  small  numbers  of 
fattily  degenerating  endothelial  cells,  polymorphonuclear  leucocytes, 
and  red  corpuscles,  the  latter  usually  from  the  puncture.  Bloody 
pleural  exudates  are,  in  the  majority  of  cases,  due  either  to  tubercu- 
lous or  carcinomatous  disease  of  the  lungs  or  pleura.  The  micro- 
scope shows,  in  addition  to  leucocytes  and  endothelial  cells,  large 
numbers  of  red  corpuscles  and,  occasionally,  crystals  of  cholesterin. 
A  search  for  bacilli  may  be  made  in  suspected  tuberculous  pleurisy, 
but  they  are  rarely  found.  In  supposed  malignant  disease  of  the 
pleura  a  diagnosis  often  may  be  made  possible  by  the  finding  of  an 
unusually  large  number  of  epithelial  cells  exhibiting  mitotic  figures, 
many  of  them  atypical  (Dock).  To  recognise  these  figures,  prepare 
A  cover-glass  film  of  the  sediment,  dry  in  the  air,  fix  for  one  hour  in 
■equal  parts  of  absolute  alcohol  and  ether,  and  stain  with  dilute 
haematoxylin.  The  discovery  of  very  large  epithelial  cells,  especially 
if  grouped,  or  of  solid  particles  presenting  an  alveolar  structure,  con- 
stitutes good  evidence  of  malignancy.  The  presence  of  globules  of 
fat  (rendering  the  fluid  milky),  or  grouped  crystals  of  the  fatty  acids, 
speaks  in  favour  of  carcinoma. 

(4)  Sero-purulent,  Purulent,  or  Putrid  Fluids. — Fluids  possess- 
ing the  characters  indicated  by  these  names  are  unquestionably  exu- 
dates or  inflammatory  effusions.  Sero-pus  and  pus  are  usually  readily 
recognised.  The  microscope  shows  a  vast  number  of  leucocytes, 
mainly  of  the  polymorphonuclear  variety,  which,  if  the  pus  is  old, 
present  fatty  granules  and  vacuolations,  or  are  shrunken  and  cre- 
nated.  A  certain  number  of  red  corpuscles  are  also  found.  A  brown 
or  brownish-green  fluid,  having  an  extremely  offensive  and  charac- 
teristic odour,  is  a  putrid  exudate  containing  degenerated  pus  cells 
and  crystals  of  fatty  acids,  cholesterin,  and  haematoidiu.  The  find- 
ing of  a  putrid  fluid  in  the  pleural  sac  may  indicate  the  perforation 
of  a  subphrenic  abscess  or  a  gangrenous  spot  of  lung  into  the  cavity; 
in  the  peritoneal  cavity,  a  similar  perforation  of  a  gastric  or  intesti- 
nal ulcer ;  although  in  either  case  it  may  occur  as  the  result  of  a 
malignant  growth  or,  more  rarely,  without  an  assignable  cause. 

Pus  may  be  examined  for  the  possible  presence  of  actinomyces, 
the  Amoeba  coli,  and  various  pathogenic  bacteria,  especially  the  Dip- 
lococcus  pneumonice  and  the  streptococcus. 

(5)  Chylous  Fluids. — A  turbid  milky  fluid  may  be  found,  most 
frequently  in  the  peritoneal  cavity,  less  commonly  in  the  pleural 


652  THE  EVIDENCES  OF  DISEASE 

cavity,  and,  as  a  rare  occurrence,  in  the  pericardial  sac.  The  milki- 
ness  is  almost  always  due  to  the  presence  of  fat,  sometimes  in  dis- 
tinct droplets  (chyloid  exudate),  in  other  cases  in  a  state  of  fine 
molecular  division  (chylous  exudate).  A  few  instances  have  been 
reported  (Lion)  in  which  the  turbidity  was  caused  by  the  presence 
of  numerous  albuminous  granules.  Chylous  and  chyloid  fluids  are 
found  in  connection  with  filariasis,  cancer  of  the  mesenteric  glands, 
peritoneum,  or  pleura,  and  in  conditions  which  lead  to  the  presence 
of  large  numbers  of  fattily  degenerating  endothelial  cells.  When 
found  in  the  peritoneum  (chylous  ascites)  the  fluid  may  have  come 
from  a  perforation  of  the  thoracic  duct.  It  has  been  suggested 
(Osler)  that  mild  grades  of  chylous  ascites  occurring  in  patients 
upon  a  strict  milk  diet  may  be  due  to  the  excess  of  fat  which  is  in 
the  blood  (lipaemia)  under  such  circumstances. 

(6)  Cerehro-spinal  Fluid. — Normally  this  is  a  clear,  colourless,  or 
slightly  yellow,  watery  fluid,  with  a  specific  gravity  varying  from 
1.005  to  1.007.  It  contains  albumin  (0.1  per  cent),  and  a  substance 
which  reduces  Fehling's  solution.  A  coagulum  seldom  forms. 
Microscopic  examination  shows  only  a  few  leucocytes  and  endothe- 
lial cells. 

If  the  fluid  is  cloudy,  forms  a  considerable  coagulum,  and  under  the 
microscoj^e  presents  large  numbers  of  leucocytes,  the  existence  of  a 
purulent  meningitis  is  assured.  The  fluid  may  have  a  specific  gravity 
as  high  as  1.012,  and  may  be  sero-purulent  or  even  consist  of  pure  pus. 

The  fluid  obtained  in  cases  of  brain  tumour,  as  well  as  in  serous 
and  tuberculous  meningitis,  is  normal  in  appearance  and  composi- 
tion, but  owing  to  increased  intracranial  pressure  it  flows  in  much 
larger  quantities,  varying  from  a  few  to  100  cubic  centimetres.  If 
only  a  few  drops  can  be  obtained  it  is  usually  safe  to  exclude  the 
diseases  just  mentioned. 

Microscopical  examination  of  the  centrifugalized  fluid  (by  stained 
cover-glass  films)  and  bacteriological  examination  by  cultures  may 
afford  most  valuable,  and  sometimes  indispensable,  evidence  of  the 
nature  of  a  meningitis.  Thus  may  be  found  the  Diplococcus  intra- 
cellularis  meningitidis  (meningococcus),  the  organism  causing  epi- 
demic cerebro-spinal  meningitis,  the  bacillus  of  tuberculosis,  the  dip- 
lococcus of  pneumonia,  and  the  streptococcus  of  septic  meningitis. 

(7)  Pancreatic  Cyst. — The  fluid  obtained  from  a  cyst  of  the  pan- 
creas is  watery,  clear,  colourless,  or  slightly  yellow,  of  a  low  specific 
gravity,  and  may  or  may  not  form  a  slight  coagulum.  If  its  origin 
from  the  pancreas  is  suspected  it  may  be  tested  with  regard  to  its 
power  of  digesting  egg  albumen.  A  few  small  particles  of  the  latter 
are  placed  in  the  fluid,  which  is  usually  alkaline,  but  if  not,  is  ren- 


EVIDENCE  PROM  DIAGNOSTIC  PUNCTURE  653 

dered  so  by  adding  10  per  cent  sodium-hydrate  solution.  After  two 
or  three  liours  a  drop  of  very  dilute  solution  of  sulphate  of  copper  is 
added,  and  if  a  reddish  violet  colour  appears  (biuret  reaction)  the 
presence  of  albumose,  and  therefore  of  trypsin,  is  assured.  A  nega- 
tive result,  however,  does  not  mean  that  the  fluid  is  not  from  the 
pancreas,  as  the  trypsin  disappears  unless  the  fluid  is  recent. 

(8)  Hydatid  Cyst. — The  fluid  is  watery,  colourless,  clear,  or 
slightly  cloudy,  with  a  specific  gravity  of  1.006  to  1.010.  If  this  rare 
condition  is  suspected,  a  careful  microscopic  examination  should  be 
made  for  shreds  of  the  cyst  wall,  booklets,  and  scolices. 

(9)  Distended  Gall  Bladder. — As  previously  stated,  puncture  of 
the  gall  bladder  is  rarely  done  for  diagnostic  purposes.  If  occasion 
arises  for  the  identification  of  its  contents  the  fluid  will  be  found  to 
be  viscid,  colourless,  or  stained  with  bile,  and  of  a  low  specific  gravity. 
Mucin  can  generally  be  found  by  the  usual  tests. 

(10)  Hydronephrosis. — The  fluid  is  watery,  colourless,  or  slightly 
yellow,  with  a  specific  gravity  of  1.008  to  1.020.  A  chemical  examina- 
tion may  reveal  urea  and  uric  acid  in  considerable  quantities,  which, 
together  with  the  finding  of  renal  epithelium  by  the  microscope,  con- 
stitute characteristic  features. 

(11)  Ovarian  Cysts. — The  fluid  from  an  ovarian  cyst  varies  con- 
siderably in  colour,  consistence,  and  composition.  It  may  be  of  a 
greenish,  yellowish,  or  brownish  tint ;  watery,  viscous,  or  colloid  in 
consistence ;  and,  according  to  the  amount  of  albumin  contained,  the 
specific  gravity  runs  from  1.002  to  1.050. 

If  it  is  suspected  that  the  fluid  under  examination  is  from  an 
ovarian  cyst,  one  should  test  for  metalbumin  (paralbumin).  Mix  a 
portion  of  the  fluid  with  3  times  its  volume  of  alcohol,  let  it  stand 
for  24  hours,  filter,  shake  the  precipitate  with  water,  filter  again,  and 
apply  the  following  tests  to  the  watery  filtrate :  Boil  a  portion,  and 
if  the  fluid  becomes  more  or  less  opaque  without  the  formation  of  a 
precipitate,  metalbumin  is  present.  Acidify  another  portion  with 
acetic  acid,  and  add  a  few  drops  of  a  10  per  cent  solution  of  potas- 
sium ferrocyanide.  In  the  presence  of  metalbumin  the  fluid  thick- 
ens and  becomes  of  a  yellowish  colour. 


^54  THE  EVIDENCES  OF  DISEASE 

SECTION  XLIV 

THE  USES   OF  THE  EOXTGEN  LIGHT  IN   MEDICAL 

DIAGNOSIS 

The  very  considerable  expense  ($500)  of  the  necessary  apparatus, 
the  technical  skill  required  in  its  management,  and  the  personal 
training  and  large  experience  which  is  requisite  before  trustworthy 
work  can  be  done,  places  X-ray  medical  diagnosis,  for  the  present, 
in  the  hands  of  the  expert. 

Medical  fluoroscopy  and  skiagraphy  have  proved  their  usefulness 
in  detecting  gouty  deposits,  tumours  of  the  stomach,  and  renal  or 
vesical  calculi ;  the  presence  of  thoracic  aneurism,  pericardial  effu- 
sion, emphysema,  pleural  effusion,  pneumothorax,  pulmonary  tuber- 
culosis, and  pneumonia ;  and  in  determining  the  position  of  the  dia- 
phragm and  the  size  of  the  heart. 


PAET  II 

DIAGNOSIS,  DIRECT  AND  DIFFERENTIAL 

Having  enumerated,  in  Part  I  of  this  volume,  the  symptoms, 
signs,  and  other  evidences  of  disease,  mainly  with  reference  to  their 
diagnostic  indications — i.  e.,  to  what  morbid  processes  each  sign  or 
symptom  may  point — it  remains  to  consider  such  evidence  from  an 
entirely  different  aspect.  Instead  of  inquiring,  "  What  disease  may 
the  symptoms  indicate?"  one  queries,  "Do  the  symptoms  found 
form  a  combination  which  is  characteristic  of  a  nosological  entity — 
i.  e.,  a  recognised  and  named  disease  ?  "  Furthermore,  another  ques- 
tion arises,  "  Are  there  any  other  diseases  with  which  the  one  in 
question  may  be  confounded,  and  in  what  manner  is  the  distinction 
to  be  made  ?  "  In  other  words,  the  physician  having  been  led  by  the 
result  of  his  examination  to  suspect  the  existence  of  a  certain  disease 
or  diseases,  it  is  evident  that  he  must  know  what  assemblage  of  symp- 
toms is  diagnostic  of  that  particular  ailment,  as  well  as  the  differences 
between  it  and  the  symptom  groups  of  other  diseases  which  may 
closely  resemble  it.  This  knowledge  can  be  obtained  only  from  a 
study  of  diseases  and  their  characteristics  as  distinguished  from  a 
study  of  more  or  less  isolated  symptoms  and  their  indications.  Con- 
sequently, Part  II  deals  in  detail  with  symptomatology  and  with 
diagnosis,  direct  and  differential.  Pathology,  etiology,  and  prognosis 
are  considered  in  a  cursory  manner,  not  from  choice,  but  from  con- 
siderations of  space  and  consistency. 


SECTION    I 
INFECTIOUS  DISEASES 

I.   TYPHOID    FEVER 

Ax  infection  by  the  Bacillus  ti/phosiis,  most  common  between  15 
and  25  years  of  age.  Prevails  especially  during  the  autumn.  Period 
of  incubation  varies  from  8  to  23  days.  During  this  period  there  may 
be  weakness,  lassitude,  and  general  ill-feeling. 

655 


656  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

Symptoms. — Prodromata  are  headache,  pains  in  back  and 
legs,  chill  (rare),  chilliness,  cough,  nosebleed,  anorexia,  nausea, 
or  slight  diarrhoea.  The  patient  finally  takes  to  his  bed,  from 
which  time  the  onset  of  the  disease  may  be  definitely  dated,  al- 
though of  necessity  this  point  of  departure  is  variable.  In  the 
majority  of  cases  the  disease  lasts  28  days,  in  the  severer  cases  42 
days,  or  even  longer. 

(1)  Onset. — Usually  gradual,  may  be  sudden,  especially  in  chil- 
dren.    May  begin  exceptionally  as 

Nephro-typlioid,  with  all  the  symptoms  of  an  acute  nephritis. 

Fnewno-typhoidj  with  a  severe  bronchitis,  a  lobar  pneumonia,  or 
an  acute  pleurisy. 

Gastro-enteric  typhoid^  with  vomiting  and  diarrhoea. 

Cerebrospinal  typhoid,  with  nausea,  delirium,  severe  headache,  or 
facial  neuralgia,  photophobia,  cervical  retraction,  twitching  of  mus- 
cles, convulsions,  drowsiness  or  stupor. 

Typhoid  septiccemia,  with  delirium,  high  fever,  and  symptoms  in- 
dicating a  severe  infection,  without  localizing  lesions. 

(2)  Fever. — Tyjncdl. — In  the,  typical  case  the  temperature  rises 
gradually  during  the  1st  week,  reaching  104°  to  105°,  with  morning 
remissions  of  1  to  1^  degrees.  During  the  2d  week  it  remains 
high,  with  slight  remissions;  so  also  during  the  3d  week,  except 
that  the  remittent  character  is  more  marked.  During  the  4th 
week,  or  at  the  end  of  the  3d  week,  the  morning  record  approaches 
or  becomes  normal,  while  the  evening  temperatures,  which  are  from. 
1  to  4  degrees  higher  than  those  of  the  morning,  persist,  but  with 
gradually  decreasing  height,  until  by  the  end  of  the  4th  week  the 
record  is  Oae**  (Chart  X). 

Irregularities  in  the  Temperature.  —  Very  commonly  variations 
from  the  type  just  described  are  found.  A  low  evening  and  high 
morning  temperature  (inverse  type)  is  of  no  importance.  The  fever 
may  terminate  at  the  end  of  the  second  week,  the  temperature  reach- 
ing normal  in  from  12  to  48  hours.  In  children,  or  in  cases  beginning 
with  a  chill,  the  fever  may  rise  abruptly.  A  sudden  fall  of  3  to  10 
degrees  suggests  intestinal  hemorrhage  or  perforation.  During  con- 
valescence, usually  as  a  result  of  emotional  excitement,  dietetic  im- 
prudences, or  constipation,  the  temperature  may  rise  quickly  to  102° 
or  103°  (recrudescence),  returning  to  normal  in  2  or  3  days.  Aside 
from  the  fever,  the  condition  of  the  patient  is  satisfactory.  A  per- 
sistent slight  fever  (99.5°  to  100.5°)  may  be  due  to  anaemia,  to  insuffi- 
cient food  (Da  Costa),  to  latent  pleurisy,  to  beginning  disease  of  the 
bones,  or,  in  the  absence  of  other  symptoms,  have  no  assignable  cause. 
A  relapse  is  a  replica  of  the  original  attack,  with  characteristic  symp- 


Temperature    (Fahrenheit ) . 
97"             98'        ^99"           100°          101°          102°          103"          104"           105'          106' 

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Chabt  X.-Showmg  the  typical  temperature  curve  of  typhoid  fever.  Also  the  average 
times  of  appearance  and  the  duration  of  prominent  signs  or  symptoms  (shown  by  black 
pointing  lines),  e.g.,  the  dicrotic  pulse  is  manifest  on  the  3d  day,  and  continues  to  the 
14th  day ;  rose  spots  appear  on  the  6th  day,  and  continue  to  appear  until  the  12th  day. 

657 


658  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

toms,  but  is  of  shorter  duration.    A  recrudescence  is  a  return  of  fever, 
without  characteristic  typhoid  symptoms. 

(3)  Circulatory  Symptoms. — The  pulse  is  rapid,  but  the  pulse  rate 
is  often  lower  than  would  be  expected  in  comparison  with  the  tem- 
perature (e.  g.,  pulse  rate  90,  temperature  104°).  It  is  often  dicrotic, 
even  in  the  early  stage  of  the  disease.  As  the  disease  progresses  it 
becomes  weak  and  rapid  or,  in  grave  cases,  running  and  thready. 
The  heart  sounds  become  weak,  the  first  resembling  the  second. 

Blood  examination  shows  an  absence  of  leucocytosis,  provided  no 
inflammatory  or  suppurative  complications  are  present.  The  relative 
number  of  lymphocytes  and  transitional  forms  is  increased  at  the 
expense  of  the  polymorphonuclear  neutrophiles,  which  may  sink  to 
50  or  60  per  cent.  Ansemia  (post-typhoid)  may  be  pronounced  dur- 
ing the  3d  and  subsequent  weeks. 

(4)  Respiratory  Symptoms. — Ordinarily  there  is  some  cough,  with 
an  increased  respiration  rate  and  sonorous  or  sibilant  rales,  indica- 
tive of  a  mild  bronchitis.  Nosebleed  is  a  rather  common  and  early 
symptom. 

(5)  Gastro-intestinal  Symptoms. — There  is  apt  to  be  tympanites, 
with  tenderness,  either  general,  or  localized  in  the  right  iliac  fossa. 
In  the  latter  area  gurgling,  a  symptom  of  little  or  no  significance,. 
may  be  found.  Diarrhoea  is  not  a  constant  symptom,  occurring, 
generally  during  the  2d  week,  in  about  ^  of  the  cases  ;  the  stools,  thin 
and  yellowish,  vary  from  3  to  10  in  24  hours.  Xausea  and  vomiting 
seldom  occur,  but  when  severe  and  persistent  may  constitute,  or 
indicate,  a  serious  complication.  The  spleen  is  usually  enlarged  and 
palpable. 

(6)  Nervous  Symptoms. — At  the  onset  there  may  be  persistent 
and  severe  headache  ;  in  the  2d  or  3d  week  delirium  (usually  quiet), 
stupor,  moderate  deafness,  and  retention  of  urine ;  and  in  grave  cases 
involuntary  passage  of  urine  and  faeces,  coma-vigil,  subsultus  tendi- 
num,  and  carphologia — i.  e.,  the  fully  developed  typhoid  status  (page 
153).     Convulsions  occur  with  extreme  rarity. 

(7)  Urinary  Symptoms. — The  urine  is  scanty  and  contains  traces 
of  albumin. 

(8)  Cutaneous  Symptoms. — The  rose  rash  or  exanthem  of  tyjihoid 
fever,  although  not  invariably  present,  is  very  characteristic.  It  con- 
sists of  flattened,  somewhat  raised  and  palpable,  rose-red  papules 
varying  from  2  to  4  millimetres  in  diameter,  which,  unless  petechial, 
disappear  upon  pressure.  They  appear  between  the  6th  and  12th 
day  of  the  disease,  each  spot  lasting  2  or  3  days,  and  leaving  a  slight 
brownish  stain.  Coming  in  successive  groups,  perhaps  up  to  the 
middle  of  the  3d  week,  they  are  found  most  commonly  upon  the^ 


TYPHOID  FEVER  659* 

abdomen,  but  very  frequently  upon  the  chest  and  back.  This  rash 
may  be  absent  in  the  very  young  or  the  aged.  An  erythema,  a  bril- 
liant redness  of  the  skin  of  the  chest  and  abdomen,  sometimes  of 
the  extremities,  may  be  present  during  the  1st  week  of  the  disease^ 
Sudamina  (page  85)  are  common.  The  infrequency  of  herpes  labialis- 
in  this  disease,  as  compared  with  pneumonia  or  malaria,  has  consider- 
able diagnostic  value.  Peliomata — taches  bleudtres — irregular,  deep- 
seated,  pale-blue  spots,  4  to  10  millimetres  in  diameter,  and  situated 
upon  various  parts  of  the  body,  especially  upon  the  chest,  abdomen,, 
and  thighs,  are  occasionally  met  with  as  a  diagnostic  sign  of  the 
presence  of  body  lice.  Urticaria  may  be  present.  The  palms  of  the 
hands  may  be  unusually  yellow.  Cutaneous  vasomotor  manifesta- 
tions are  common  in,  but  not  peculiar  to,  this  fever.  Stroking  the 
skin  causes  the  development  of  a  red  line  {tache  cerebrate) ;  or  simple 
exposure  to  the  air  produces  a  pink-and-white  mottling  of  the  skin. 
Profuse  sweating  rarely  occurs,  but  to  a  moderate  degree  is  not 
uncommon.  A  rather  characteristic  odour  or  exhalation  from  the 
skin  is  often  mentioned  by  experienced  nurses,  and,  I  believe,  has  a 
certain  limited  diagnostic  value.  During  convalescence  the  skin, 
may  desquamate  and  the  hair  fall  out. 

(9)  Miscellaneous  Symptoms. — The  cheeks  are  flushed  and  the  face 
has  a  dull,  heavy  expression.  The  pupils  are  apt  to  be  dilated.  The 
tongue  at  first  is  red  at  its  tip  and  edges,  with  a  white  coating  else- 
where. A  deep  longitudinal  furi'ow  is  often  present.  In  severe 
cases  it  becomes  dry,  brown,  fissured,  and  tremulous.  Sordes  collect 
upon  the  teeth. 

Varieties. — (1)  Ordinary  or  Moderately  Severe  Form. — During 
the  first  toeek  the  temperature  slowly  rises  to  103°  to  104° ;  the  pulse- 
runs  to  100  or  110,  often  less,  and  is  soft  and  dicrotic ;  the  tongue 
shows  a  white  coating ;  there  may  be  a  moderate  diarrhoea ;  the 
patient  coughs,  complains  of  headache,  and  there  may  be  some  noc- 
turnal confusion  and  delirium.  Toward  the  close  of  this  week  the 
abdomen  is  tumid,  perhaps  tender,  the  spleen  is  enlarged,  and  the 
rose  rash  appears.  During  the  second  iceeh  the  patient  becomes  men- 
tally dull,  the  headache  disappears,  the  pulse  loses  its  dicrotism  and 
becomes  more  rapid,  the  temperature  remains  high,  and  the  other 
symptoms  are  aggravated.  During  the  third  week  the  fever  shows 
marked  morning  remissions,  the  pulse  varies  from  110  to  130,  and 
weakness  and  emaciation  are  very  noticeable.  During  the  fourth 
week  the  fever  slowly  subsides,  the  diarrhoea  ceases,  the  tympanites, 
disappears,  the  tongue  clears,  the  mental  condition  improves,  and 
a  fierce  hunger  begins  to  possess  the  patient.  Chart  X  represents. 
the  course  of  the  average  case,  with  the  times  of  appearance  and 


660  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

duration  of  the  principal  symptoms,  and  some  of  the  possible  com- 
plications. 

(2)  Grave  or  Severe  Forms. — Bad  cases  present  high  fever  (105° 
or  over),  a  dry,  brown  tongue,  twitching  of  the  tendons,  picking  at 
the  bedclothes,  excessive  meteorism,  constant  and  marked  delirium, 
rapid  and  feeble  pulse,  weak  heart,  pulmonary,  renal,  gastro-intes- 
tinal,  or  nervous  complications,  involuntary  voiding  of  urine  and 
faeces ;  and,  if  death  does  not  occur,  the  fever  persists  into  the  5th, 
6th,  or  7th  week,  or  even  longer. 

(3)  Mild  Fonn. — The  disease  does  not  last  over  two  weeks,  the 
temperature  does  not  exceed  103°,  the  rose  spots  are  present  in 
scanty  numbers,  the  spleen  is  enlarged — in  short,  while  the  symp- 
toms of  the  ordinarily  severe  form  are  present,  they  are  of  much  less 
intensity. 

(4)  Abortive  Form. — The  onset  is  sudden  and  definite,  with  shiv- 
ering and  a  temperature  of  103°.  Splenic  swelling,  meteorism,  and 
rose  spots  appear  promptly  (2d  to  5th  day).  The  fever  lasts  from  7 
to  12  days,  and  terminates  rather  abruptly,  often  with  free  sweat- 
ing. Relapses  may  occur,  and  are  sometimes  more  severe  than  the 
original  attack. 

(5)  Latent  or  Walking  Typhoid. — The  symptoms  are  so  slight 
(languor,  diarrhoea,  anorexia)  that  they  are  disregarded  until  the 
disease  is  well  advanced.  On  examination,  characteristic  symptoms, 
especially  rose  spots,  are  found  ;  or  delirium,  intestinal  hemorrhage, 
or  perforation  leads  to  an  imperative  demand  for  medical  aid. 

(6)  Afebrile  Typhoid. — While  the  existence  of  these  cases  is 
affirmed  by  good  authority,  they  must  be  of  excessively  rare  occur- 
rence or  often  pass  unrecognised.  Headache,  weakness,  coated 
tongue,  anorexia,  slow  pulse,  splenic  swelling,  the  rose  rash,  and 
perhaps  an  occasional  evening  rise  of  temperature  to  100.5°,  are  said 
to  characterize  such  cases. 

(7)  Typhoid  Fever  in  Children. — The  onset  is  less  gradual,  nose- 
bleed is  not  frequent,  delirium  and  insomnia,  as  well  as  bronchitis, 
are  more  common,  diarrhoea  is  not  infrequently  absent,  the  rose  rash 
may  be  absent,  and  the  duration  is  usually  shorter  (2  to  3  weeks). 

In  infants,  inflammation  of  the  bladder,  occurring  without  cys- 
titic  symptoms,  and  due  to  infection  by  the  coli  communis,  may  be 
mistaken  for  typhoid  fever.  There  is  continuous  high  fever  and 
rapid  pulse,  perhaps  with  symptoms  of  bronchitis  or  broncho-pneu- 
monia. Aside  from  the  rarity  of  typhoid  fever  in  infants,  deep 
pressure  over  the  pubis  is  painful,  bacteriological  examination  of  the 
urine  (if  it  can  be  obtained)  will  show  the  presence  of  the  Bacillus 
coli  communis^  and  the  Widal  reaction  is  negative. 


TYPHOID   FEVER  QQl 

(8)  Typhoid  Fever  in  the  Aged. — In  patients  over  40  years  of  age 
the  temperature  curve  is  lower  and  less  characteristic  ;  cardiac  weak- 
ness, pneumonia,  and  renal  inflammations  are  more  common,  and 
splenic  swelling  and  rose  rash  more  frequently  absent. 

Complications  and  Sequelae. — There  is  in  typhoid  fever  a 
large  variety  of  complicating  conditions  or  lesions,  as  follows : 

(1)  Exaggeration  of  an  Ordinary  Symptom  as  a  Complication. — 
Hyperpyrexia  may  be  considered  a  complication,  although  it  is  more 
an  indication  of  the  severity  of  the  infection  than  a  danger  in  itself* 
Excessive  tympanites  embarrasses  the  action  of  the  heart  and  lungs, 
and  favours  intestinal  perforation  by  overstretching.  Severe  diar^ 
rhoea  and  excessive  vomiting  seriously  decrease  the  strength  of  the 
patient  and  may  cause  fatal  exhaustion.  Epistaxis  may  be  profuse 
and  serious. 

(2)  Hesj)iratory  Complications. — Lobar  pneumonia  rarely  initiates 
the  disease,  but  occurs  more  commonly  during  the  2d  or  3d  week. 
Hypostatic  congestion,  announced  by  a  somewhat  increased  respira- 
tion rate,  dulness,  weakened  voice  sounds,  and  moderately  fine,  moist 
rales  during  inspiration  at  both  bases,  is  found  not  infrequently  in 
the  later  stages.  Bronchitis  (usually  present)  may  extend  to  the  air 
cells  (broncho-pneumonia)  with  associated  atelectasis.  Rarely  in- 
farcts, abscess,  or  gangrene  of  the  lung  or  haemoptysis  may  occur. 
Pleuritis  (during  convalescence  apt  to  be  an  empyema)  is  not  very 
common ;  still  less  so  is  pneumothorax,  due  to  the  rupture  of  a  small 
abscess  or  to  overstraining  of  the  lung.  Laryngitis  and  ulceration  of 
the  larynx  with  sequent  perichondritis  may  occur ;  and  laryngeal 
paralysis  (neuritis)  may  show  itself  during  convalescence. 

(3)  Circulatory  Complications. — Endocarditis  or  pericarditis  may 
occur.  Thrombosis  of  veins  is  not  uncommon,  particularly  of  the 
left  femoral  vein,  sometimes  of  both  veins,  announced  by  increased 
fever,  pain,  swelling,  and  a  hard  oedema  of  the  leg,  generally  begin- 
ning in  the  foot.  The  affected  vein  may  be  felt  as  a  hard  cord,  and 
the  superficial  veins  are  plainly  visible  as  bluish  lines.  One  or  both 
arms  may  also  be  involved.  Less  frequently  there  may  be  embolism 
or  thrombosis  of  the  femoral  artery.  The  limb  becomes  cold,  numb, 
anaesthetic,  and  partly  paralyzed.  Gangrene  of  the  foot  and  leg  may 
follow. 

(4)  Gastro-intestinal  and  Abdominal  Complications. — Typhoid 
ulcers^  may  form  in  the  pharynx  and  esophagus.  Membranous 
pharyngitis,  developing  in  the  3d  week,  with  dysphagia,  is  a  rare 
and  usually  fatal  complication.  Suppurative  parotitis,  generally  of 
one  side,  is  not  common,  but  when  present  is  a  grave  and  usually 
fatal  sequel. 

44 


662 


DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 


Intestinal  hemorrhage  occurs  in  from  3  to  5  per  cent  of  all  cases^ 
mainly  during  the  3d  or  4th  week,  and  terminates  fatally  in  from  SO' 
to  40  per  cent.  The  symptoms  are  a  sudden  fall  of  temperature 
(Chart  XI),  with  signs  of  collapse,  and  in  a  few  hours  the  voiding  of 
bloody  or  tarry  stools.  If  the  hemorrhage  is  large  and  rapid,  death 
may  occur  before  the  blood  issues  from  the  rectum. 

Intestinal  perforation,  most  common  at  the  end  of  the  2d  or  dur- 
ing the  3d  week,  occurs  in  from  5  to  6  per  cent  of  all  cases,  more 
frequently  in  men  than  in  women.  In  the  majority  of  instances  (75 
per  cent)  it  is  announced  by  sudden  acute  abdominal  pain,  with  a 
rapid  development  of  rigidity  and  tenderness.  Vomiting,  a  weak 
and  rapid  pulse,  and  a  marked  condition  of  collapse  accompany  the 
abdominal  symptoms.  If  the  pre-existing  tympanites  is  great  and 
the  general  symptoms  already  severe,  the  occurrence  of  perforation 
may  be  difficult  to  determine.  The  distention  increases,  and  tender- 
ness may  be  detected 
by  deep  and  firm  pres- 
sure ;  or,  in  the  absence 
of  any  local  inflamma- 
tory (especially  sup- 
purative) process,  the 
question  may  be  decid- 
ed in  the  affirmative  by 
finding  a  leucocytosis. 

Cholecystitis,  cho- 
langitis, and  jaundice 
(obstructive  or  toxae- 
mic)  are  not  uncom- 
mon ;  hepatic  abscess  is 
very  rare.  Gallstones 
form  after  typhoid  fever 
with  notable  frequency. 
The  softened,  pulpy 
spleen  may  in  rare  in- 
stances rupture.  Peritonitis  may  be  a  consequence  and  symptom 
of  perforation  or,  less  commonly,  arise,  by  extension  through  the 
intestinal  walls,  from  an  ulcer,  or  a  ruptured  suppurating  mesenteric 
gland. 

(5)  Nervous  Complications. — Neuritis,  which  may  be  multiple,  is 
not  infrequent.  It  may  be  localized,  involving  one  arm  or  leg.  The 
affected  nerves  are  excessively  painful  and  hyperaesthetic,  and  the 
muscles  supplied  by  them  lose  power.  The  extensors  of  the  arm  or 
leg  may  be  involved,  causing  wrist-drop  or  foot-drop.     Especially 


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Chaet  XI. — Fatal  hemorrhage  in  typhoid  fever. 


TYPHOID  FEVER 


663 


after  cold  bathing  "  tender  toes  "  (probably  a  neuritis)  may  develop, 
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movement.     It  is  non-febrile,  and  probably  a  neurosis. 


Sept.  8th, 
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TYPHOID  FEVER  RECOVERY. 

peratures  at  8  A.M.  and  8  P.  M. 
ntermedlate  temperatures. 

Chart  XII. 


Among  the  rare  nervous  complications  are  meningitis ;  hemi- 
plegia, Avith  or  without  aphasia,  generally  due  to  arterial  thrombosis, 
less  often  to  a  meningo-encephalitis ;  poliomyelitis,  which  may  be 
confused  with  multiple  neuritis ;  and  tetany.  Convulsions  seldom 
occur,  except  perhaps  at  the  onset  of  the  disease  in  children ;  in 
adults,  if  present,  they  are  due  to  arterial  or  venous  thrombosis,  or 
encephalitis.  Post-typhoid  insanity  is  a  possible  event  during  con- 
valescence. 

(6)  Complicating  Diseases  q/'-6o«e.— Inflammation  of  the  joints 
(arthritis,  single  or  multiple)  is  rare.  Periostitis,  caries,  or  necrosis 
of  bone,  usually  of  the  tibia,  less  often  of  the  ribs,  is  not  uncommon. 
These  processes  are  essentiall}^  chronic  and  recurring,  and  may  con- 
stitute a  possible  cause  of  protracted  convalescence. 


664  DIAGNOSIS,  DIRECT  AND   DIFFERENTIAL 

(7)  Genito-urinary  ComjMcations. — An  acute  nephritis  may  usher 
in  the  disease,  more  commonly  it  occurs  in  a  mild  form  during  con- 
valescence. Haemoglobinuria  is  a  rare,  pyelitis  an  occasional,  event. 
Ovaritis  and  orchitis  have  been  noted. 

(8)  Eye  and  Ear  Complications. — Conjunctivitis,  iritis,  and  cor- 
neal inflammation  may  occur ;  and  oculo-motor  paralysis  of  neuritic 
origin  has  been  observed.  Inflammation  of  the  middle  ear  (not  infre- 
quent) should  be  watched  for,  as  it  may  be  overlooked  on  account  of 
the  mental  hebetude  of  the  patient. 

(9)  Other  Complications. — Bedsores  are  usually  preventable,  but 
with  great  emaciation,  especially  if  the  nerve  centers  are  gravely 
affected,  acute  decubitus  may  occur  over  the  sacrum,  scapulae,  or 
heels.  In  some  instances  irregular  fever  and  recurring  chilliness  or 
rigours  announce  the  existence  of  septicaemia  or  pyaemia,  attended  by 
the  formation  of  boils,  multiple  subcutaneous  or  intramuscular  ab- 
scesses, or  even  a  perinephric  or  ischio-rectal  abscess. 

Direct  Diagnosis. — The  cardinal  diagnostic  symptoms  are  the 
peculiar  temperature  curve  (slow  ascent,  maintenance,  slow  descent), 
the  rose  rash,  and  the  enlarged  spleen.  To  these  may  be  added  a 
decided  diazo-reaction  in  the  urine  and — of  extreme  value — a  posi- 
tive result  of  the  Widal  serum  test ;  but  a  negative  result  in  either 
does  not  positively  exclude  typhoid  fever.  The  finding  of  typhoid 
bacilli  in  the  blood,  urine,  or  faeces  may  be  useful,  but  is  clinically 
unsatisfactory  and  unavailable.  Epistaxis,  early  dicrotism  of  the 
pulse,  and  absence  of  leucocytosis  also  possess  a  distinct  diagnostic 
value. 

It  should  be  clearly  understood  that  as  different  organs  may  bear 
the  brunt  of  the  infection,  so  may  the  manifestations  of  the  disease 
be  extremely  variable.  Thus,  while  in  many  cases  the  usual  abdom- 
inal symptoms  (meteorism,  diarrhoea)  are  present,  in  others  they  may 
be  entirely  lacking  during  the  whole  course  of  the  disease ;  or  certain 
symptoms  may  be  replaced,  or  masked,  by  symptoms  referable  to  the 
kidneys  (nephritis),  lungs  (pneumonia),  or  other  organs.  In  view  of 
the  inconstancy  of  any  one  or  two  symptoms,  the  diagnosis  of  typhoid 
fever  should  not  be  made  unless  based  upon  a  study  of  the  entire 
clinical  picture.  It  is  best  not  to  make  a  positive  affirmation  of  its 
existence  until  the  disease  has  progressed  far  enough  to  present  a 
sufficient  assemblage  of  symptoms  to  warrant  such  a  diagnosis.  On 
the  other  hand,  any  continued  fever  should  be  considered  as  a  possi- 
ble typhoid  until  the  assumption  can  be  disproved  by  its  course  and 
the  evolution  of  its  symptoms.  As  a  matter  of  fact,  the  great  ma- 
jority of  cases  of  typhoid  fever  are  correctly  diagnosed  as  such,  by 
competent  observers,  within  the  first  week  or  ten  days ;  in  a  certain 


TYPHOID   FEVER  665 

small  proportion  the  diagnosis  remains  uncertain  for  a  longer  period ; 
in  a  still  smaller  number  no  positive  diagnosis  is  made,  even  after  re- 
covery ;  and  in  a  few  instances  'the  autopsy  reveals  the  presence  of 
the  disease,  when  it  had  not  been  suspected  during  life. 

Differential  Diagnosis. — As  Herrick  cleverly  puts  it,  typhoid 
fever  is  not  only  an  imitator  of  diseases,  but  many  diseases  imitate 
typhoid  fever. 

Diseases  Simulated  by  Typhoid  Fever.— (1)  Certain  cases  are  met 
with  and  usually  diagnosed  as  simple  continued  fever  in  which  there 
are  no  symptoms  except  malaise,  slight  headache,  moderate  fever, 
and  a  barely  perceptible  swelling  of  the  spleen.  The  illness  con- 
tinues for  from  5  to  8  days  only,  and  yet  the  Widal  test  (the  sole 
available  diagnostic  evidence  in  such  cases)  affords  a  positive  reaction 
during  convalescence. 

(2)  In  rare  instances  the  typhoid  infection  may  be  localized  in 
the  meninges  and  simulate  sporadic  cerehro-spinal  meningitis,  pre- 
senting headache,  delirium,  photophobia,  cervical  retraction,  and 
muscular  rigidity.  Similarly,  an  acute  nephritis,  with  scanty,  smoky 
urine,  loaded  with  albumin,  and  containing  many  casts,  may  be  the 
earliest  evidence  of  a  typhoid  infection.  In  other  instances  the  poi- 
son first  attacks  the  lungs,  causing  a  lobar  jmeumonia,  with  its  typical 
signs  and  symptoms.  Or  the  infection  may  be  general  and  sudden, 
with  repeated  chills,  high  fever,  the  early  onset  of  delirium,  and 
other  symptoms  of  a  profound  septicemia.  In  every  such  case  it  is 
well  to  have  in  one's  mind  a  lurking  suspicion  that  it  may  turn  out 
to  be  of  typhoid  origin,  and  to  watch  for  diarrhoea,  meteorism,  splenic 
swelling,  and  especially  the  rose  spots ;  not  omitting  the  Widal  test 
in  suspicious  cases. 

(3)  Malaria. — Intermittent  fever  (tertian  organism)  can  not  be 
confounded  with  typhoid  fever.  Aside  from  the  finding  of  the  Plas- 
modium, the  paroxysms  are  promptly  stopped  by  quinine. 

Infection  by  the  aestivo-autumnal  variety,  however,  may  simulate 
typhoid  fever  very  closely  for  a  time.  But,  if  the  work  of  Osier  is  to 
be  trusted,  it  may  be  confidently  stated  that  in  the  Xorthern  and 
Middle  States  this  form  of  infection  is  very  rare,  and  a  continued 
fever  due  to  malaria  very  exceptional.  Furthermore,  the  studies  of 
Dock  and  Vaughn  prove  conclusively  that  many  cases  diagnosed  as 
malaria  are  in  reality  typhoid  fever.  In  view  of  the  vast  importance 
of  prophylactic  disinfection,  even  omitting  the  imperative  need  for 
rest  and  careful  diet  in  the  individual  case,  it  is  best  to  accept  the 
dictum  that  typhoid  fever,  and  not  malaria,  is  to  be  suspected  "  in 
every  case  of 'fever  of  6  or  7  days'  duration,  particularly  if  it  resists 
the  action  of  quinine." 


666  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

The  distinction  between  a  malarial  remittent  and  typhoid  fever 
depends  upon  the  following  points  : 

In  malarial  fever  the  remittent  character  of  the  fever  is  marked 
from  the  outset :  anaemia  with  a  subicteric  complexion  occurs  early  in 
the  disease,  herpes  labialis  is  more  frequent,  the  pulse  is  rarely  dicrot- 
ic, abdominal  symptoms  are  not  marked,  and  the  rose  spots  do  not 
appear.  On  the  other  hand,  there  may  be  splenic  enlargement,  and 
the  general  condition  may  so  closely  resemble  typhoid  fever  that  it  is 
impossible  to  make  a  differential  diagnosis  until  the  end  of  the  first 
week.  This  limit  is  set,  because  the  crucial  test — the  finding  of  the 
Plasmodium  in  the  blood — can  not  in  many  cases  be  successfully 
made  during  this  period  for  the  reason  that  the  hyaline  bodies  of  the 
aestivo-autumnal  parasite  are  seldom  to  be  found  in  the  blood,  and 
one  must  wait  until  the  pigmented  crescents  and  ov'oids  appear,  at 
least  7  days  as  a  rule,  after  the  onset  of  the  disease. 

Two  other  distinctive  points  are  a  failure  to  obtain  the  Widal  re- 
action during  the  course  of  the  disease,  and  the  therapeutic  test — 
the  subsidence  of  the  fever  in  4  or  5  days  as  a  result  of  the  adminis- 
tration of  quinine.  Kecurring  chills  have  little  diagnostic  value,  as 
they  may  occur  in  both  diseases  :  in  malaria  as  a  frequent  but  not 
necessary  symptom,  in  typhoid  fever  at  its  beginning,  or  at  the  on- 
set of  a  relapse  or  a  complication,  or  when  the  temperature  rises  after 
having  been  thrust  down  by  antipyretics. 

In  rare  instances  there  may  be  a  double  infection  with  the  Bacillus 
typJiosus  and  the  Plasmodium  malarice,  but  the  weight  of  evidence  is 
decidedly  against  the  existence  of  the  so-called  typho-malarial  fever 
as  a  separate  disease. 

Diseases  Simulating  Typhoid  Fever. — (1)  Amife  Miliary  Tuber- 
culosis.— In  this  the  fever  is  much  more  irregular,  the  pulse  and 
respiration  are  more  rapid,  there  is  usually  noticeable  cyanosis,  con- 
stipation is  the  rule,  and  the  rose  spots  do  not  appear.  On  the  other 
hand,  the  simulation  of  typhoid  fever  may  be  so  close  that  the  acut- 
est  diagnostician  is  at  fault.  A  positive  "Widal  test,  the  finding  of 
tubercles  in  the  choroid,  or  more  rarely  of  tubercle  bacilli  in  the 
blood  (or  in  the  sputum  if  signs  of  apparent  pulmonary  tuberculosis 
become  manifest),  constitute  the  only  reliable  differential  evidences. 
Time  alone  may  settle  the  diagnosis.  The  diazo-reaction  may  possi- 
bly be  of  service  (page  639). 

(2)  Pycemia. — The  marked  prostration,  irregular  fever,  delirium, 
diarrhoea,  and  splenic  enlargement  attending  some  pyaemias  may 
simulate  typhoid  fever,  but  a  negative  Widal  test,  or  a  marked  leuco- 
cytosis,  with  perhaps  the  finding  of  foci  of  suppuration,  will  elimi- 
nate typhoid  fever. 


TYPHOID  FEVER  667 

(3)  Tuberculous  Peritonitis. — This,  when  coining  on  slowly,  with 
a  continuous  low  fever,  tympanites,  and  abdominal  tenderness,  may 
imitate  typhoid  fever.  The  Widal  and  the  tuberculin  tests  may  aid 
in  separating  the  two,  but  continued  observation  may  be  required. 

(4)  Appendicitis. — This  disease  may  simulate,  or  be  simulated  by, 
typhoid  fever.  On  account  of  right  iliac  tenderness  and  tumefac- 
tion due  to  the  swollen  ileum  and  mesenteric  glands  of  typhoid  fever, 
a  surgeon  has  more  than  once  been  called  to  operate  for  a  supposed 
appendical  inflammation.  But  in  the  majority  of  cases  of  appendi- 
citis the  onset  is  so  abrupt  and  the  symptoms  and  physical  signs  so 
distinctive,  as  compared  with  typhoid  fever,  that  this  mistake  is  sel- 
dom made.  Conversely,  appendicitis  may  be  taken  for  typhoid  fever, 
but  the  history,  together  with  a  careful  physical  examination,  and,  in 
addition,  the  blood  examination  and  serum  test,  will  usually  settle 
the  differential  diagnosis  in  such  rare  cases. 

(5)  Ulcerative  Eyidocarditis. — The  more  chronic  forms  of  this 
disease  are  commonly  diagnosed  as  typhoid  fever.  The  presence  or 
absence  of  a  leucocytosis,  and  the  result  of  the  Widal  test  may  decide 
the  question.  Kecurring  chills,  irregular  fever,  substernal  pain,  the 
development  of  endocardial  murmurs,  and  the  absence  of  abdominal 
symptoms  and  the  rose  spots,  point  toward  ulcerative  endocarditis 
rather  than  typhoid  fever. 

(6)  Salpingitis  {right). — I  have  known  one  case  in  which  the 
occurrence  of  continued  fever  and  the  typhoid  status  with  right  iliac 
tenderness  in  this  disease  led  to  a  diagnosis  of  typhoid  fever,  but 
a  vaginal  examination,  not  previously  made,  settled  the  question 
at  once  by  disclosing  a  fixed  uterus  and  a  tender  mass  in  the  right 
pelvis. 

(7)  Catarrhal  Enteritis. — This,  especially  in  children,  may  be 
taken  for  tjrphoid  fever,  but  enteritis  lacks  the  epistaxis,  bronchi- 
tis, high  fever,  splenic  enlargement,  rose  spots,  and  positive  Widal 
reaction. 

(8)  Pneumonia. — When  lobar  pneumonia  is  the  initial  symptom 
of  typhoid  fever,  or  when  pneumonia  presents  the  typhoid  status 
(especially  if  the  patient  is  seen  for  the  first  time  after  this  condition 
has  developed),  a  differential  diagnosis  may  be  quite  impracticable 
until  the  rose  spots  appear,  or  a  positive  Widal  reaction  is  obtained. 
Ordinarily  no  confusion  need  arise. 

(9)  Epidemic  Influenza. — Earely  this  disease  may  cause  an  eleva- 
tion of  temperature,  lasting  for  3  or  4  weeks,  and  closely  resembling 
typhoid  fever.  The  non-appearance  of  the  rose  rash,  and  the  absence 
of  a  positive  Widal  reaction,  with  perhaps  the  discovery  of  the 
Pfeiffer  bacillus  in  the  nasal  or  bronchial  secretions,  will  serve  for 


668  DIAGNOSIS,    DIRECT   AXD   DIFFERENTIAL 

differentiation.    Furthermore,  the  prevalence  of  an  epidemic  of  influ- 
enza is  suggestive. 

(10)  Urcemia. — The  more  chronic  forms  of  urasmia  may  closely 
simulate  typhoid  fever  because  of  the  presence  of  stupor,  rapid  and 
feeble  pulse,  dry,  brown  tongue,  subsultus  tendinum,  and  continuous 
slight  fever,  lasting  for  weeks.  The  absence  of  the  rose  rash,  the 
negative  Widal  test,  the  presence  of  the  urinary  characters  of  uraemia 
(page  647),  and  the  condition  of  the  heart  and  arteries,  must  be  relied 
upon,  perhaps  with  an  ascertained  previous  history  of  chronic  renal 
disease. 

(11)  TricMniasis. — The  severe  cases  of  this  disease  have  been 
diagnosed  as  typhoid,  because  of  the  prolonged  fever,  delirium,  dry, 
brown  tongue,  abdominal  pain,  and  diarrhoea  which  may  be  present. 
CEdema  of  the  eyelids,  swelling  and  tension  of  the  muscles,  and 
dyspnoea  should  suggest  trichiniasis.  In  suspected  cases  the  blood 
should  be  examined  for  a  marked  eosinophilia,  and  the  stools  and  an 
excised  bit  of  muscle  for  the  trichina. 

(12)  Typhus  Fever. — In  modern  times  and  civilized  countries  an 
occasion  for  differentiating  between  typhus  and  typhoid  fever  rarely 
arises.  The  onset  of  the  former  is  sudden,  delirium  is  early  and 
often  active,  the  stupor  becomes  profound,  the  pupils  are  contracted, 
the  conjunctivae  are  brilliantly  injected,  and  about  the  4tli  day  of 
the  disease  the  macular  and  petechial  rash  appears.  The  fever  lasts 
12  to  14  days  and  terminates  by  crisis.  When  an  epidemic  of  typhus 
is  present  the  diagnosis  is  usually  easy,  but  it  may  be  almost  or  quite 
impossible  to  distinguish  a  sporadic  case  of  this  disease  from  typhoid 
fever. 

(13)  Relapsing  Fever. — The  early  cases  of  an  epidemic  of  this 
disease  may  be  diagnosed  as  irregular  typhoid,  but  in  relapsing  fever 
the  onset  is  sudden,  with  chill  and  intense  general  aching,  and  in  6 
or  7  days  the  temperature  falls  suddenly  to  or  below  the  normal.  In 
a  week  the  attack  is  repeated,  and  a  3d  or  4tli  similar  relapse  may 
occur.  If  this  disease  is  suspected  its  nature  can  be  positively  deter- 
mined by  a  blood  examination,  which  reveals  the  presence  of  the 
spirilla. 

11.    TYPHUS    FEVER 

Symptoms. — Begins  suddenly  with  chills  (perhaps  recurrent), 
fever,  pain  in  head,  back,  and  extremities,  soon  followed  by  extreme 
prostration.  Cough  and  bronchitis  are  common.  The  pulse  is  rapid, 
full,  and  often  dicrotic.  The  tongue  is  white,  dry,  and  tremulous,  in 
bad  cases  becoming  brown  or  black.  The  expression  is  dull  and 
heavy,  the  face  duskily  flushed,  the  eyes  congested,  and  the  pupils 


TYPHUS  FEVER 


669 


contracted.  In  the  severer  cases,  delirium,  which  may  become  active 
or  maniacal,  together  with  subsultus  tendinum,  coma-vigil,  and  car- 
phologia,  constitute  prominent  symptoms.  Vomiting  may  be  trouble- 
some, and  constipation  is  the  rule. 


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Chart  XIII. —Typhus  fever. 


The  fever  rises,  with  moderate  morning  remissions,  during  the  first 
3  or  4  days,  reaching  a  maximum  of  from  103°  to  107°.  This  max- 
imum is  maintained  for  about  10  days,  and  then  falls  by  crisis  to  or 
below  the  normal  within  12  to  24  hours  (Chart  XIII).  Between  the 
3d  and  the  5th  day  the  eruption  appears,  partly  as  a  dusky  subcuticu- 
lar mottling,  partly  as  papular  rose  spots,  which  rapidly  become  pe- 
techial. The  rash  appears  first  upon  the  abdomen,  whence  it  spreads 
over  the  body.  The  urine  is  diminished  in  amount,  high-coloured, 
and  usually  albuminous.  Retention  of  urine  is  common.  Like  other 
infectious  diseases,  exceptional  cases  occur  which  may  be  either  mild, 
or  malignant  and  fatal  within  2  or  3  days. 

Complications. — The  most  common  of  these  is  broncho-pneu- 
monia, which  may  eventuate  in  gangrene  of  the  lung.  Suppurative 
arthritis,  parotid  abscess,  subcutaneous  abscesses,  gangrene  of  the 
smaller  extremities,  neuritic  paralysis,  hypostatic  congestion  of  the 
lungs,  and  hyperpyrexia  are  occasional  events.  Kephritis,  meningitis, 
and  haematemesis  are  rare  complicating  conditions. 


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DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 


Differential  Diagnosis.— (1)   Typhoid  fever  (page  G68). 

(2)  Cerebrospinal  Meningitis. — In  this,  one  finds  a  greater  irregu- 
larity of  the  fever,  greater  pain  in  the  back,  a  more  frequent  occur- 
rence of  convulsions,  facial  or  ocular  paralyses,  photophobia,  in- 
tolerance of  sounds,  and  cervical  retraction.  The  eruption  is  less 
constant,  and  does  not  appear  at  any  definite  period  in  the  disease. 
Finally,  lumbar  puncture  and  the  finding  of  the  meningococcus  may 
settle  the  question. 

(3)  Smallpox. — Malignant  smallpox  may  resemble  severe  typhus, 
but  the  hemorrhages  (subcutaneous,  haematuria,  haematemesis,  intes- 
tinal, conjunctival)  will  speak  for  the  former  disease. 

Prognosis. — The  mortality  varies  from  12  to  20  per  cent ;  in 
children  slight,  and  after  middle  age  high  (perhaps  50  per  cent). 
Death  results  from  toxasmia  or  a  complicating  pneumonia. 

III.    RELAPSING    FEVER 

Symptoms. — The  period  of  incubation  of  this  disease,  caused 
by  the  spirochwte  or  spirillum  of  Obermeier,  varies  from  5  to  7  days. 
The  invasion  is  sudden,  with  chill,  rapid  onset  of  fever  (104°  to  106°), 


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- 

Chart  XIV. — Relapsing  fever. 


intense  headache,  backache,  and  aching  in  the  extremities.     The 
pulse  runs  from  110  to  130.     Sweats,  jaundice,  and  delirium  (if  fever 


RELAPSING  FEVER— DENGUE  671 

is  high)  are  common,  and  the  spleen  swells  at  an  early  period.  In 
the  young  there  may  be  nausea,  vomiting,  and  convulsions. 

Tlie  fever  remains  high,  usually  for  7  days  (rarely  3  to  10),  and 
falls  by  crisis  (Chart  XIV),  with  profuse  sweating,  sometimes  diar- 
rhoea, and  (in  elderly  persons)  with  symptoms  of  collapse.  In  another 
week  (14th  day  of  disease)  the  attack  may  be  repeated.  The  relapse 
is  usually  shorter  than  the  original  attack.  A  second  relapse  may 
occur  about  the  21st  day,  and  a  3d,  4th,  or  5th  relapse  may  protract 
the  disease.  During  the  apyretic  periods  the  patient  may  feel  quite 
well  and  be  about.  The  finding  of  the  spirilla  in  the  blood  decides 
the  diagnosis. 

Complications. — Uncommon,  but  pneumonia  is  not  infrequent, 
and  nephritis,  haematuria,  jaundice,  haematemesis,  rupture  of  the 
sj)leen,  ophthalmia,  abortion,  and  post-febrile  paralysis  have  been 
noted. 

Differential  Diagnosis. — (1)  Typlioid  Fever. — In  the  early 
cases  of  an  epidemic  the  diagnosis  of  an  irregular  typhoid  may  be 
made,  but  the  course  of  the  temperature  declares  quite  certainly  the 
nature  of  the  disease,  and  the  blood  examination  with  the  finding  of 
sj^irilla  makes  a  positive  diagnosis  of  relapsing  fever. 

(2)  Yellow  Fever. — Absence  of  spirilla  and  splenic  swelling,  with 
presence  of  black  vomit  and  other  symptoms  of  yellow  fever  {q.  v.), 
Avill  separate  it  from  relapsing  fever. 

(3)  Malarial  Remittent  Fever. — In  this  the  fever  is  intermittent 
rather  than  remittent,  the  paroxysms  of  chill  and  fever  are  more  fre- 
quent, and  the  blood  examination  reveals  the  presence  of  the  Plasmo- 
dium and  the  absence  of  spirilla. 

Prognosis. — Kecovery  is  the  rule,  except  in  old  or  feeble  per- 
sons.    Tlie  mortality  is  about  4  per  cent. 

IV.    DENGUE 

Symptoms. — After  a  period  of  incubation  varying  from  3  to  5 
days,  the  attack  begins  suddenly  with  headache,  chilliness,  and  atro- 
cious aching  pains  in  the  muscles  and  joints.  From  the  latter  symp- 
tom arises  the  name  "  break-bone "  fever.  The  joints  are  swollen, 
red,  and  tender.  The  pulse  and  respiration  are  quickened ;  the  face 
is  suffused  and  swollen,  eyes,  skin,  and  mucous  membranes  congested. 
The  lymph  glands  are  frequently  enlarged.  Prostration  may  be 
decided,  and  slight  delirium  is  sometimes  noted.  In  severe  cases 
hemorrhages  from  the  mucous  membranes  (epistaxis,  haemoptysis, 
haematemesis,  etc.)  may  occur.  Extreme  hyperaesthesia  of  the  skin 
has  been  observed.  In  the  majority  of  cases  an  exanthem  occurs, 
sometimes  macular  and  resembling  measles,  or  diffuse  like  that  of 


672  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

scarlet  fever,  or  papular  or  urticarial.  It  has  no  definite  time  of  ap- 
pearance and  is  not  distinctive  in  its  characters. 

The  fever  steadily  rises  during  the  first  3  or  4  days,  reaching  a 
maximum  of  103°  to  107°,  at  which  time  it  rapidly  remits,  with  free 
sweating  and  an  almost  total  disappearance  of  the  painful  symptoms. 
The  period  of  apyrexia  lasts  from  2  to  4  days,  and  the  seizure  is  then 
repeated  in  a  milder  form.  The  average  duration  of  the  entire  attack 
is  from  7  to  10  days. 

Complications. — These  are  uncommon.  Convulsions  (in  chil- 
dren), insomnia,  active  delirium,  hyperpyrexia,  pericarditis,  and 
meningitis  (rare)  may  occur. 

Differential  Diagnosis. — (1)  Yelloiu  Fever. — As  dengue  and 
yellow  fever  are  frequently  prevalent  at  the  same  time,  the  two  diseases 
are  apt  to  be  confounded.  The  symptoms  which  in  the  majority  of 
cases  determine  the  disease  to  be  yellow  fever  are  the  facies,  red  and 
injected  eyes,  flushed  face  plus  an  icteric  hue,  slow  pulse  with  high 
fever,  albuminous  urine,  black  vomit,  and  early  jaundice  (2d  or  3d 
day).  Nevertheless,  good  authorities  may  disagree.  It  is  possible 
that  the  work  of  Sanarelli,  AVoodson,  and  others  may  develop  a 
reliable  serum  test  for  yellow  fever  analogous  to  that  of  "Widal  for 
typhoid  fever. 

(2)  Influenza. — In  this  there  is  usually  no  eruption  (except  herpes), 
the  fever  does  not  show  the  striking  remissions  of  dengue,  and  the 
joints  are  not  implicated.  Examination  of  the  nasal  and  bronchial 
secretions  will  discover  the  bacillus  of  Pfeiifer.  A  question  can  only 
arise  in  sporadic  cases,  as  the  existence  of  an  epidemic  of  either  will 
be  recognisable. 

(3)  Acute  Rheumatism. — A  sporadic  case  might  be  mistaken  for 
acute  rheumatic  fever  because  of  the  joint  symptoms,  but  in  the 
latter  there  is  generally  no  eruption,  and  the  course  of  the  fever  will 
prove  to  be  quite  unlike  that  of  dengue. 

Prognosis. — Seldom  fatal,  death  resulting  only  from  the  rare 
serious  complications. 

V.    CEREBRO-SPINAL    MENINGITIS 

This  disease,  most  common  in  children  and  young  adults,  and 
caused  by  the  Diplococcus  intracellularis,  presents  remarkably  wide 
clinical  variations. 

Symptoms. — (1)  Ordinary  or  Common  Form. — After  an  un- 
known period  of  incubation  the  disease  begins  abruptly  with  a  vio- 
lent headache,  severe  chill,  fever  (101°  to  102°),  vomiting,  and  pain 
in  the  back  and  limbs.  In  children  a  convulsion  may  occur.  Very 
soon  the  muscles  of  the  neck  and  back  become  painful  and  stiff,  with 


CEREBRO-SPINAL  MENINGITIS  673 

cervical  retraction  or  even  opisthotonus.  There  is  photophobia, 
hyperacusis,  delirium  (which  may  be  violent),  followed  in  bad  cases 
by  stupor  or  coma.  Strabismus  (frequent),  nystagmus,  ptosis,  irregu- 
larity of  the  pupils,  and  facial  spasm  may  be  noted.  Impairment 
of  sight  or  hearing  may  develop.  There  is  often  general  cutaneous 
hypersesthesia,  and  tenderness  along  the  spine,  with  tremor,  and  occa- 
sional tonic  or  clonic  spasms  of  the  extremities.  The  joints  may  be- 
come red  and  swollen. 

The  fever  is  irregular  and  not  characteristic.  In  severe  or  fatal 
cases  the  temperature  may  rise  to  105°  to  108°.  The  pulse  is  full 
and  rapid,  in  rare  instances  abnormally  slow.  The  respiration  is  not 
increased,  unless  pneumonia  coexists,  but  may  be  of  a  sighing  or 
even  a  Cheyne-Stokes  character.  The  bowels  are  generally  consti- 
pated, the  abdomen  is  not  tender,  and  vomiting  is  present,  as  a  rule, 
only  at  the  onset.  The  spleen  is  usually  swollen.  The  urine  may 
be  albuminous,  and  contain  sugar  and,  in  the  severer  cases,  blood. 
There  is  a  leucocytosis,  the  increase  affecting  the  polymorphonuclear 
cells.  The  eruption  is  variable  and  not  always  present.  Herpes  is 
frequently  seen  ;  in  many  cases  blotchy  purple  spots  and  petechise  are 
found  over  the  entire  surface  of  the  body  (hence  the  name  "  spotted 
fever").  Urticarial,  erythematous,  or  roseolous  rashes  have  been 
observed. 

In  many  cases  a  certain  diagnosis  may  be  made  by  lumbar  punc- 
ture and  examination  of  the  fluid  for  the  DipJococcus  intracellularis^ 
a  test  which  should  always  be  made  if  the  disease  is  suspected. 

The  duration  is  variable.  An  acute  case  may  last  but  a  few 
hours,  a  chronic  case  for  several  weeks,  or  even  months.  The  ma- 
jority of  deaths  occur  within  the  first  5  days.  In  favourable  cases,  at 
the  end  of  this  time  improvement  becomes  manifest. 

(2)  Malignant^  Fulminant,  or  Apoplectic  Form. — There  is  a  sud- 
den onset,  severe  chill,  perhaps  a  convulsion,  headache,  moderate 
fever,  extreme  prostration,  and  purpuric  spots.  Muscular  spasm, 
slow,  weak  pulse,  and  stupor  usually  appear,  and  death  takes  place 
from  collapse  in  from  5  to  24  hours. 

(3)  Abortive  Form. — The  attack  begins  with  great  intensity  as  in 
the  ordinary  form,  but  in  2  or  3  days  there  is  a  prompt  subsidence  of 
the  symptoms,  with  a  rapid  convalescence. 

(4)  Mild  Form. — During  an  epidemic  of  the  disease  there  are 
walking  cases  with  headache,  nausea,  vomiting  (occasional),  vertigo, 
languor,  and  slight  pain  and  stiffness  in  the  muscles  of  the  neck  and 
back.  Fever  is  slight  or  absent,  and  only  the  presence  of  the  epi- 
demic enables  a  diagnosis. 

(5)  Intermittent  Form. — The  fever  and  the  symptoms  remit  or 


674  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

intermit  every  day  or  every  2d  day,  or  present  an  irregular  remittent 
temperature  like  that  of  pyaemia. 

(6)  Chronic  Form. — There  is  a  series  of  recurrences  of  the  fever 
with  a  complex  symptomatology,  dependent  possibly  upon  chronic 
hydrocephalus  or  abscesses  of  the  brain  (Osler,  IIeubxer). 

Complications  and  Sequelae.  —  Pleurisy,  pneumonia  (fre- 
quent), bronchitis,  pericarditis,  arthritis  (frequent),  and  parotitis 
may  occur.  Chronic  headaches  (meningitis),  chronic  hydrocephalus, 
aphasia,  mental  impairment;  defective  vision  from  optic  atrophy, 
retinitis,  or  keratitis ;  defective  hearing  from  inflammation  of  the 
middle  or  internal  ear,  or  neuritis  of  the  auditory  nerve  ;  and  paral- 
ysis of  other  cranial  nerves,  may  result  from  an  attack  of  this  disease. 
Nephritis  with  haematuria  has  been  observed  as  a  complication. 

Differential  Diagnosis. — In  sporadic  or  doubtful  cases  a  diag- 
nostic lumbar  puncture  should  be  made  (page  649)  and  the  fluid 
examined  for  the  characteristic  organism. 

(1)  Typhoid  Fever. — In  the  majority  of  cases  of  this  disease  the 
slow  development  of  the  symptoms,  the  temperature  curve,  the  ab- 
dominal symptoms,  and  the  Widal  reaction  will  ultimately  separate 
it  from  cerebro-spinal  meningitis.  There  is,  as  a  rule,  no  cervical 
pain  and  retraction,  no  herpes,  and  no  leucocytosis.  In  exceptional 
cases  the  cerebral  form  of  typhoid  fever  begins  abruptly,  with  symp- 
toms indistinguishable  from  those  of  cerebro-spinal  meningitis. 

(2)  Typhus  Fever. — In  this  the  fever  is  more  regular  than  in 
cerebro-spinal  meningitis ;  facial  paralysis,  muscular  rigidity,  and 
the  severe  cervico-dorsal  pains  are  absent. 

(3)  Pneumonia. — When  this  is  complicated  by  meningitis,  the 
pneumonia  precedes  the  meningitis,  there  is  less  pain,  and  the  cervi- 
cal retraction  is  not  so  marked  as  in  cerebro-spinal  fever.  But  if  the 
case  is  not  seen  from  the  beginning,  one  can  not  be  certain  that  the 
meningitis  is  secondary  to  the  pneumonia,  and  it  may  be  difficult  or 
impossible  to  separate  it  from  a  case  of  cerebro-spinal  fever  compli- 
cated with  pneumonia. 

(4)  Acute  Rheumatic  Fever. — On  account  of  the  redness  and 
swelling  of  the  joints  which  may  occur  in  cerebro-spinal  meningitis 
it  may  be  mistaken  for  acute  rheumatic  fever,  but  in  the  latter  the 
joint  symptoms  occur  at  the  onset,  and  there  is  an  absence  of  cervi- 
cal retraction,  muscular  rigidity,  facial  paralysis,  and  cutaneous 
eruptions. 

(5)  Tuherculous  Meningitis. — Compared  with  cerebro-spinal  fever, 
the  onset  of  tuberculous  meningitis  is  not  so  sudden,  the  aching, 
hypersesthesia,  and  cervical  retraction  are  less,  and  there  are  usually 
no  cutaneous  eruptions ;  while  retraction  of  the  abdomen,  irregular 


INFLUENZA  675 

pulse,  and  Cheyne-Stokes  respiration  are  much  more  common.  Fur- 
thermore, a  pre-existing  tuberculous  focus  may  be  found,  and  tuber- 
cles discovered  in  the  choroid  by  ophthalmoscopic  examination. 

Prognosis. — The  mortality  varies  from  20  to  75  per  cent,  and  is 
greatest  in  children  under  5  years.  High  fever,  recurring  convul- 
sions, and  profound  coma  usually  presage  a  fatal  termination. 

VI.    INFLUENZA 

Symptoms. — After  an  incubation  of  from  1  to  4  days  the  disease 
(caused  by  Pfeiffer's  bacillus)  sets  in  abruptly  with  chilliness,  or  even 
a  severe  rigour.  The  fever  is  extremely  variable,  running  from  100° 
to  105°,  and  lasts  vnth  remissions  from  1  to  10  days.  There  is  in 
almost  all  cases  severe  headache  and  general  aching,  with  a  degree 
of  prostration  out  of  all  proportion  to  the  apparent  cause.  Delirium 
is  not  infrequent.  The  symptomatology  of  the  disease  is  variegated, 
and  one  symptom  group  may  quickly  merge  into  another.  The  fol- 
lowing forms  of  the  disease  are  recognised  : 

(1)  Respiratory  Form. — The  early  symptoms  are  those  of  a  severe 
coryza.  Usually  pharyngitis,  laryngo-tracheitis,  and  bronchitis  fol- 
low. The  general  aching  and  extreme  weakness  may  be  the  only  dis- 
tinguishing characteristics.  Very  frequently  a  slight  patchy  bron- 
cho-pneumonia, with  few  physical  signs,  coexists.  The  cough  is  apt 
to  be  paroxysmal,  violent,  and  extraordinarily  persistent. 

(2)  Xervous  Form. — In  many  cases  slight  fever,  with  atrocious 
headache,  pain  in  the  back  and  limbs,  and  marked  weakness  may  be 
the  only  symptoms. 

(3)  Gastro-intestinal  Form. — In  a  certain  proportion  of  cases^ 
nausea,  vomiting,  abdominal  pain,  and  profuse  watery  or  serous  diar- 
rhcea,  with  prostration  amounting  at  times  to  collapse,  may  consti- 
tute the  evidence  of  the  disease. 

(4)  Typhoid  or  Febrile  Form. — In  some  instances,  fortunately  in- 
frequent, there  may  be  a  continued  fever,  with  delirium,  dry,  brown 
tongue,  and  other  symptoms  of  the  typhoid  status.  In  certain  cases 
the  fever  remits  or  intermits,  with  recurring  chills,  and  simulates 
malaria. 

Com.plications,  Sequelae,  and  Occasional  Symptoms. — 
(1)  Respiratory  Organs. — Broncho-pneumonia  (common),  lobar  pneu- 
monia, pleurisy  terminating  in  empyema  (rare),  pulmonary  gangrene 
and  abscess  (rare),  pulmonary  oedema  (sequel  of  pneumonia),  and  en- 
largement of  the  bronchial  glands. 

(2)  Circulatory  Organs. — Tachycardia,  bradycardia,  or  persistent 
irregularity  of  the  pulse ;  angina  pectoris  (influenzal),  usually  with- 
out discoverable  organic  changes,  temporary  and  recoverable ;  cardiac 


676  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

weakness ;  endocarditis,  pericarditis,  phlebitis  and  thrombosis  of 
different  vessels.  Eecurring  syncope  is  not  infrequent  at  the  onset 
of  the  disease,  especially  in  women. 

(3)  Nervous  System. — True  meningitis,  or  the  symptoms  of  men- 
ingitis which  disappear  in  a  day  or  two ;  encephalitis,  with  resulting 
hemiplegia  or  monoplegia ;  and  abscess  of  the  brain,  are  uncommon 
complications.  Various  forms  of  neuritis  are  not  infrequent.  Ac- 
tive delirium,  depression  of  spirits,  melancholia,  dementia,  persistent 
insomnia,  neuralgias,  and  migraine  have  been  noted.  Neurasthenia, 
sometimes  severe  and  prolonged,  is  a  not  uncommon  sequel. 

(4)  The  spleen  may  become  enlarged,  and  catarrhal  jaundice  has 
occurred  with  some  frequency ;  (5)  haematuria,  acute  congestion,  and 
acute  nephritis  are  not  extremely  rare  ;  (6)  conjunctivitis  is  frequent, 
iritis  uncommon,  and  optic  neuritis  is  rare ;  (7)  acute  otitis  media  is 
common,  terminating  occasionally  in  mastoiditis,  and  vertigo,  as  a 
result  of  labyrinthine  disease,  has  been  observed ;  (8)  herpes  is  fre- 
quently seen ;  occasionally  diffuse  erythema  and  purpuric  spots  are 
witnessed. 

Differential  Diagnosis. —  In  doubtful,  anomalous,  or  sus- 
pected sporadic  cases  a  bacteriological  examination  of  the  bronchial 
or  nasal  secretions  should  be  made  in  order  to  find  Pfeiffer's  bacillus, 
which,  if  present,  will  declare  the  disease  to  be  influenza.  In  the 
midst  of  an  epidemic  there  is  usually  no  difficulty  in  making  a  diag- 
nosis, nor  in  a  sporadic  case  if  the  symptoms  come  under  the  head  of 
one  of  the  recognised  types.  The  cardinal  symptom  is  the  excessive 
and  disproportionate  weakness. 

(1)  Typhoid  Fever. — Influenza  begins  suddenly,  and  lacks  the 
regular  temperature  curve,  rose  spots,  and  positive  Widal  reaction  of 
typhoid  fever. 

(2)  Cerehro-spinal  Meningitis. — In  certain  cases  of  influenza  the 
sudden  onset,  headache,  backache,  delirium,  and  muscular  stiffness 
may  afford  a  clinical  picture  exactly  like  that  of  cerebro-spinal  men- 
ingitis, and  the  differential  diagnosis  must  depend  upon  the  bacteri- 
ological examination ;  in  the  one  case  for  the  Pfeiffer  bacillus,  in  the 
other  for  the  meningococcus. 

(3)  Broncho-pneumonia. — If  the  question  arises  as  to  whether  a 
given  case  of  broncho-pneumonia  is  of  influenzal  origin,  a  rather 
peculiar  and  anomalous  combination  of  physical  signs  may  answer 
the  question  in  the  affirmative,  viz.,  varying  degrees  of  dulness  over 
both  chests  posteriorly,  with  weak  respiratory  murmur,  impaired 
transmission  of  voice  sounds,  and  a  shower  of  fine  and  subcrepi- 
tant  rdles  at  the  end  of  a  deep  inspiration,  heard  in  scattered  areas 
or  patches,  especially  at  the  bases.     The  combination  is  probably 


WHOOPING  COUGH  677 

indicative  of  a  mixture  of  broncho-pneumonic  spots  and  collapsed 
lobules. 

Prognosis. — In  the  large  majority  of  cases  recovery  occurs. 
Tlie  mortality  varies  from  ^  to  2  per  cent,  and  is  generally  due  to 
a  complicating  severe  pneumonia,  especially  when  affecting  the  very 
young  or  the  aged. 

VII.    WHOOPING    COUGH 

Symptoms. — Period  of  incubation  varies  from  7  to  10  days. 
Two  stages  are  recognised.  (1)  Catarrhal  Stage. — Symptoms  those 
of  an  ordinary  cold :  coryza,  injected  conjunctivae,  and  a  bronchial 
(perhaps  slightly  spasmodic)  cough,  with  slight  fever.  In  a  week  or 
10  days,  instead  of  improving,  the  disease  enters  upon  the 

(3)  Paroxysmal  Stage. — This  stage  begins  with  the  first  "  whoop  " 
or  "  kink."  The  cough  becomes  paroxysmal,  and  the  child  is  usually 
conscious  of  the  approach  of  a  seizure  for  a  moment  or  two  prior  to 
its  occurrence  and  endeavours  to  restrain  it.  The  paroxysm,  fre- 
quently precipitated  by  emotional  causes,  begins  with  a  series  of 
short  coughs,  followed  by  a  deep  inspiration  during  which  the  char- 
acteristic whoop  is  heard.  A  2d,  3d,  or  4th  series  of  coughs,  each 
ending  with  a  whoop,  may  follow,  the  paroxysm  terminating  with 
the  ejection  of  thick  mucus,  and  frequently  with  vomiting.  Phys- 
ical examination  of  the  lungs  is  negative,  except  for  the  evidence  of 
a  slight  bronchitis.  The  number  of  paroxysms  varies  from  4  or  5  to 
40  or  50  in  24  hours.  During  the  seizure  the  face  is  swollen,  con- 
gested, and  cyanotic ;  the  veins  are  full  and  the  eyeballs  project. 
Urine  and  faeces  may  be  passed  involuntarily. 

After  the  disease  is  well  developed  the  facies  is  very  characteristic, 
with  its  swollen,  dusky  appearance,  reddened  eyes,  and  puffy,  pinkish 
lids.     Subconjunctival  extravasations  are  not  uncommon. 

The  paroxysmal  stage  lasts  usually  3  or  4  weeks,  after  which  the 
attacks  grow  milder  and  gradually  cease.  The  average  duration  of 
a  case  of  moderate  severity  is  6  weeks ;  in  aggravated  cases  it  may  be 
4  months. 

Com.plications  and  Sequelae. — Epistaxis,  haemoptysis  (infre- 
quent), intestinal  hemorrhage  (rare),  subconjunctival  extravasations, 
and  petechial  spots  on  the  forehead  and  face  may  occur  as  a  result 
of  the  extreme  venous  congestion.  The  pulmonary  complications 
are  important,  of  which  broncho-pneumonia  (sometimes  tuberculous) 
and  pulmonary  collapse  are  most  common  ;  lobar  pneumonia,  pneumo- 
thorax or  interstitial  emphysema  (from  strain),  pleurisy,  and  enlarge- 
ment of  bronchial  glands  (very  common).  Convulsions  are  not 
uncommon,  sometimes  succeeded  by  a  profound  coma ;  hemiplegia, 
45 


678  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

monoplegia,  and  subdural  hemorrhage  are  rare  events.  Irregularity 
of  the  pulse,  dilatation  of  the  right  ventricle,  and  perhaps  permanent 
valvular  lesions  may  result  from  the  great  paroxysmal  strain  upon 
the  heart.  Acute  nephritis  may  occur  (20  per  cent  of  200  cases, 
Anders).  As  sequelae,  chronic  bronchitis  and  pulmonary  tuberculosis 
may  be  found.  Gastro-intestinal  catarrh  is  not  an  infrequent  follow- 
ing, and  hernia  may  occur  as  a  result  of  strain. 

Diagnosis. — The  disease  can  not  be  recognised  until  the  parox- 
ysmal stage,  when  the  "  whoop  "  is  unmistakable.  The  paroxysmal 
cough  of  influenza  may  closely  simulate  pertussis,  but  the  onset  in 
the  former  disease  is  sudden,  and  the  spasmodic  character  of  the 
cough  is  usually  marked  from  the  outset.  Mild  cases  in  which  the 
whoop  does  not  develop  may  remain  doubtful.  The  swollen  face 
and  eyes  are  of  much  diagnostic  importance.  The  mortality  of  per- 
tussis, with  its  complications,  amounts  to  7  or  8  per  cent,  especially 
during  the  first  2  years  of  life, 

VIII.    EPIDEMIC    PAROTITIS    (MUMPS) 

Symptoms. — After  an  incubation  of  2  to  3  weeks  there  is  lassi- 
tude, with  fever  (rarely  above  101°),  and  pain  under  one  (usually  the 
left)  ear,  increased  by  taking  an  acid.  Headache  and  nausea  are 
sometimes  present.  Swelling  begins  on  the  affected  side,  which  in  2 
or  3  days  becomes  very  extensive.  The  bulk  of  the  swelling  lies 
under  the  lobe  of  the  ear,  which  is  pushed  outward,  and  extends 
forward  in  front  of  the  ear  and  backward  under  the  stern o-mastoid 
muscle  (anatomical  situation  of  the  parotid  gland).  The  opposite 
gland  usually  follows  suit  within  a  day  or  two.  The  pain  is  tensive 
rather  than  acute,  the  mouth  can  scarcely  be  opened,  and  there  is 
diflSculty  in  mastication,  swallowing,  and  speaking.  Tinnitus  and 
slight  dulness  of  hearing  are  very  common.  The  swelling  lasts  from 
6  to  10  days.  As  a  rule  the  disease  is  of  a  mild  type,  but  in  very 
exceptional  cases  there  may  be  high  fever  (103°  to  104°),  with  delir- 
ium, prostration,  and  other  symptoms  of  the  typhoid  status. 

Comiplications  and  Sequelae. — Orchitis,  usually  after  the 
parotitis  has  subsided,  sometimes  resulting  in  atrophy ;  and  at  the 
same  period,  ovaritis  (rare),  mastitis  or  tenderness  of  the  breasts, 
and  vulvovaginitis,  almost  invariably  after  puberty.  Other  complica- 
tions are  meningitis,  acute  mania,  insanity,  facial  paralysis,  convul- 
sions, hemiplegia,  peripheral  neuritis,  endocarditis,  arthritis,  jaun- 
dice, albuminous  urine,  acute  uraemia,  otitis  media  (not  uncommon), 
disease  of  the  auditory  nerve  with  permanent  deafness,  disease  of 
the  lachrymal  gland,  and  optic  atrophy.  The  majority  of  these  are 
either  very  rare   or   occur  very  infrequently.     Suppuration   of   the 


MUMPS— SMALLPOX 


679 


gland  in  epidemic  parotitis  seldom  occurs.     The  gland  may  become 
chronically  enlarged. 

Differential  Diagnosis. — Mumps  occurs  mainly  in  children. 
The  diagnosis  is  usually  readily  made  by  noting  that  the  bulk  of  the 
swelling  is  below  and  in  front  of  the  ear,  and  that  the  lobe  of  the  ear 
is  pushed  outward.  Inspection  of  the  throat  will  show  the  absence 
of  a  tonsilitis  or  other  inflammation  which  might  cause  swelling  of 
the  cervical  glands  and  thereby  simulate  a  parotitis.  A  parotitis 
may  result  from  various  septic  inflammations,  but  the  gland  usually 
suppurates,  an  occurrence  which  alone  will  almost  invariably  separate 
it  from  the  epidemic  form,  and  the  presence  of  the  causative  infec- 
tion, as  a  rule,  will  have  been  recognised.  The  prognosis  is  favour- 
able in  almost  all  cases. 

IX.    SMALLPOX   (VARIOLA) 

Four  varieties  of  smallpox  are  recognised :  the  discrete,  of  mod- 
erate severity ;  the  confluent,  of  great  severity ;  the  hemorrhagic  or 
malignant ;  and  varioloid,  or  smallpox  as  modified  by  vaccination. 

Symptoms.— (1)  Discrete  Form.—Aiter  an  incubation  of  from 
8  to  15  days  the  disease  usually  begins  with  a  chill  (perhaps  recur- 
rent) in  adults,  and  a  convulsion  in  children,  followed  by  intense 


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headache,  excessive  lumbar  pain,  nausea,  and  vomiting.  The  tem- 
perature rises  rapidly  during  the  1st  and  2d  days,  reaching  103"  to 
105°.     The  face  is  flushed,  eyes  bright,  and  delirium  present,  espe- 


680  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

cially  if  the  fever  runs  high.  The  pulse  is  rapid  (120  to  140),  full, 
seldom  dicrotic.  Generally  the  bowels  are  constipated,  the  urine 
scanty  and  albuminous.  The  initial  fever  continues  high  until  the 
3d  or  4th  day,  when  a  decided  remission  occurs,  lasting  until  the  7th 
or  8th  day,  when  it  again  rises  (fever  of  suppuration),  fluctuating 
more  or  less,  and  in  favourable  cases  gradually  falls  to  the  normal  by 
the  18th  day  of  the  disease  (Chart  XV). 

The  characteristic  eruption  appears  on  the  3d  or  4th  day  of  the 
disease  as  small  red  spots,  first  on  the  forehead  and  wrists,  appearing 
within  the  next  24  hours  upon  other  parts  of  the  face  and  limbs,  and 
to  some  extent  upon  the  trunk.  With  the  appearance  of  the  erup- 
tion the  fever  falls  and  there  is  an  improvement  in  the  general  symp- 
toms. The  rash  is  at  first  macular,  changing  rapidly  into  rounded 
papules  which  feel  like  shot  under  the  skin.  The  lesions  may  occur 
also  in  the  mouth,  pharynx,  and  larynx.  About  the  5th  or  6th  day 
of  the  disease  they  become  vesicular  and  umbilicated,  and  about  the 
8th  day  are  converted  into  non-umbilicated  pustules.  Each  pustule 
is  surrounded  by  a  red  areola,  and  the  intervening  skin  is  swollen. 
With  pustulation  the  fever  returns  and  the  general  symptoms  reap- 
pear. About  the  11th  or  12th  day  of  the  disease  the  pustules  begin 
to  desiccate  and  form  scabs  or  crusts,  which  cling  to  the  skin  for  a 
week  or  longer.  The  maturation  of  the  eruption  occurs  first  upon  the 
face  and  follows  the  order  of  its  appearance.  More  or  less  pitting  of 
the  skin  results.  In  the  discrete  form  the  lesions  are  not  very  abun- 
dant and  do  not  coalesce. 

(2)  Confluejit  Form. — The  papules  are  numerous,  thickly  set,  and 
soon  coalesce,  although  the  confluence  may  not  take  place  until  the 
stage  of  pustulation.  They  are  most  abundant  on  the  face  and  hands, 
less  so  on  the  limbs,  and  may  be  scattered  and  discrete  on  the  trunk. 
The  initial  symptoms  of  the  confluent  form  resemble  those  of  the 
discrete  variety,  but  are  usually  of  greater  severity.  Delirium,  stupor, 
subsultus ;  salivation,  diarrhoea ;  extreme  swelling  of  the  cervical 
glands ;  hoarseness,  cough,  and  offensive  discharges  from  the  nose 
and  throat  due  to  the  existence  of  the  eruption  in  the  nose,  mouth, 
pharynx,  and  larynx,  are  present  to  a  varying  extent. 

(3)  Malignant  or  Hemorrhagic  Form. — This  presents  2  varieties. 

Black  or  purpuric  smallpox,  beginning  with  intense  fever,  lum- 
bar pain,  and  prostration,  and  an  unusually  rapid  respiration  rate. 
On  the  2d  or  3d  day  small  ecchymoses  appear  on  various  portions  of 
the  skin,  growing  in  size  and  number,  so  that  in  the  severest  cases 
the  greater  portion  of  the  cutaneous  surface  may  be  purple  or  black- 
ish in  colour.  Extensive  conjunctival  ecchymoses  may  also  be  pres- 
ent.    Hemorrhages  from  the  mucous  membranes  are  common,  viz., 


SMALLPOX 


681 


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hgematuria,  haematemesis,  intestinal  hemorrhage,  haemoptysis,  or  me- 
trorrhagia. As  death  occurs  between  the  3d  and  6th  day,  the  vario- 
lous eruption  may  not 
have  time  to  appear, 
except  that  scattered 
papules  may  be  found. 

In  hemorrhagic  pus- 
tular smallpox  the  dis- 
ease progresses  like  an 
ordinary  severe  case  up 
to  the  vesicular  or  pus- 
tular stage,  at  which 
time  the  pocks  become 
hemorrhagic,  bleedings 
from  the  mucous  mem- 
branes occur,  and  death 
usually  takes  place  from 
the  7th  to  the  9th 
day. 

(4)  Varioloid.— The 
initial  symptoms  are 
mild,  a  few  papules  ap- 
pear on  the  face  and 
hands,  and  the  fever  of  suppuration  does  not  occur  (Chart  XVI). 

Complications  and  Sequelae. — Broncho-pneumonia  (com- 
mon), lobar  pneumonia  (rare),  pleurisy  (common) ;  laryngitis,  oede- 
ma of  glottis,  perichondritis  or  necrosis.  Endocarditis  and  pericar- 
ditis are  rare,  myocarditis  not  infrequent.  Diarrhoea  not  uncommon, 
especially  in  children ;  parotitis  is  rare ;  vomiting  usually  not  pro- 
tracted ;  swollen  spleen  and  liver,  albuminuria  common,  acute  nephri- 
tis infrequent ;  haematuria,  orchitis,  and  ovaritis  very  seldom  seen. 
Neuritis,  local  or  general ;  diffuse  myelitis  with  paraplegia  ;  hemiple- 
gia and  aphasia  due  to  encephalitis  (rare) ;  convulsions,  common  in 
children  ;  active  delirium  ;  coma ;  insanity  (post-febrile)  seldom  met ; 
epilepsy  rarely.  Arthritis,  perhaps  suppurative ;  acute  necrosis  of 
bone.  Boils  (frequent)  ;  local  gangrene  seldom ;  acne.  Otitis  me- 
dia ;  conjunctivitis,  iritis,  and  corneal  inflammation. 

Diflferential  Diagnosis. — The  so-called  "  initial  "  rashes  may 
cause  error.  There  are  2  forms,  one  resembling  the  rash  of  scarlet 
fever,  the  other  that  of  measles.  Generally  they  are  limited  to  the 
lower  abdomen,  the  inner  surface  of  the  thighs,  or  to  the  axillary 
regions  and  sides  of  the  chest,  and  appear  upon  the  2d  or  3d  day  of 
the  disease.     Until  shotty  papules  form  it  is  difficult  or  impossible 


Chart  XVI. — Varioloid. 


682  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

to  recognise  the  true  nature  of  these  rashes,  although  the  prodromal 
symptoms  may  be  suflBciently  characteristic  in  each  instance. 

Ordinarily  if  an  epidemic  is  present  the  diagnosis  of  smallpox  is 
readily  made ;  but  in  sporadic  cases,  or  during  the  period  prior  to 
the  appearance  of  the  papules  or  vesicles,  variola  may  require  differ- 
entiation from  the  following  diseases  : 

(1)  Gerehro-spinal  Fever. — The  hemorrhagic  form  of  smallpox 
may  be  mistaken  for  the  purpuric  spots  and  hemorrhages  of  cerebro- 
spinal fever,  and  irritative  meningeal  symptoms  may  also  be  present. 
If  death  occurs  early  a  correct  diagnosis  may  not  be  made,  but  other- 
wise the  papular  and  pustular  development  of  the  eruption  will  make 
the  discrimination. 

(2)  Typhus  Fever. — The  onset  of  this  disease  resembles  that  of 
smallpox,  but  may  be  discriminated  by  the  fact  that  in  typhus  fever 
the  macular  or  petechial  rash  appears  first  on  the  trunk  and  does  not 
become  papular  or  pustular ;  nor  is  there  a  remission  of  the  fever 
coincidently  with  the  appearance  of  the  eruption. 

(3)  Varicella. — It  is  at  times  exceedingly  difficult  to  discrimi- 
nate between  varicella  and  varioloid  or  very  mild  cases  of  discrete 
variola. 

In  varicella  the  eruption  usually  appears  first  upon  the  trunk, 
front  or  back,  beginning  more  rarely  on  the  forehead  and  face.  The 
vesicles  vary  in  size,  are  often  oval  in  shape,  are  rather  superfi- 
cial without  a  marked  red  areola,  and  not  infrequently  flattened  or 
umbilicated.  They  arrive  in  successive  crops,  so  that  by  the  4th  day 
lesions  in  the  various  stages  of  papules,  vesicles,  and  pustules  can  be 
seen  side  by  side,  which,  together  with  their  abundance  upon  the 
trunk,  constitute  most  important  differential  points.  Moreover,  the 
slightness  of  the  constitutional  symptoms  (fever,  backache,  prostra- 
tion) is  notable  in  varicella,  and  there  is  no  fever  of  suppuration. 
The  knowledge  of  previous  exposure  to  the  disease  may  be  helpful. 

In  varioloid  or  mild  variola  the  eruption  usually  appears  first 
upon  the  forehead  and  hands,  the  lesions  are  of  uniform  size,  not 
superficial,  are  more  pustular,  and  the  various  stages  do  not  exist 
side  by  side.  The  eruption  is  most  abundant  on  the  face,  hands,  and 
extremities.  The  constitutional  symptoms  are,  as  a  rule,  of  a  more 
decided  character.  There  may  be  a  history  of  exposure  to  a  known 
case  of  smallpox. 

Prognosis. — Varioloid  recovers  ;  in  discrete  smallpox  the  prog- 
nosis is  good ;  in  confluent  forms,  grave ;  in  the  malignant  and 
severe  hemorrhagic  forms  death  is  almost  inevitable. 


VACCINIA— VARICELLA 


68a 


X.    VACCINIA  (COWPOX) 

S3nnptoins. — Two  or  three  days  subsequent  to  vaccination  a 
papule  with  a  red  areola  is  seen  at  the  point  of  inoculation.  It 
increases  in  size,  and  by  the  6th  day  becomes  an  umbilicated  circular 
vesicle,  which  grows  larger  and  is  distended  with  lymph.  On  the 
10th  day  it  becomes  purulent,  and  on  the  12th  day  desiccation 
begins.  The  scab  separates  in  from  3  to  4  weeks  from  the  date  of 
inoculation,  leaving  a  pitted  scar.  There  is  usually  some  fever  and 
constitutional  disturbance,  beginning  on  the  3d  and  terminating  on 
the  9th  day.  The  axillary  or  inguinal  glands,  according  to  the  site 
of  the  operation,  become  swollen  and  tender. 

Irregularities  and  Complications. — A  non-characteristic, 
over-rapid  development  of  the  vesicle,  with  the  formation  of  a  crust 
by  the  7th  or  8th  day,  or  a  retarded  formation,  requires  revaccina- 
tion.  Injury  of  the  vesicle  causes  inflammation  or  the  formation  of 
an  ulcer.  Secondary  vesicles  may  form  in  the  neighbourhood  of  the 
pock ;  and  very  rarely  there  is  a  general  pustular  eruption  in  various 
parts  of  the  body,  successive  crops  appearing  for  several  weeks. 

The  possible  complications  are  as  follows  (Aclaxd)  : 

1.  During  the  first  3  days :  Erythema ;  urticaria ;  vesicular  and 
bullous  eruptions ;  in  vaccinated 
erysipelas.  2.  After  the  3d  day 
and  until  the  pock  reaches  ma- 
turity :  Urticaria ;  lichen  urti- 
catus, erythema  multiforme ;  ac- 
cidental erysipelas.  3.  About 
the  end  of  the  1st  week :  Gen- 
eralized vaccinia ;  impetigo ; 
vaccinal  ulceration ;  glandular 
abscess  ;  septic  infections ;  gan- 
grene. 4.  After  the  involution 
of  the  pocks  :  Invaccinated  dis- 
eases— for  example,  syphilis. 

XI.  VARICELLA  (CHICKEN 
POX) 

Symptoms. — After  a  peri- 
od of  incubation  (10  to  15  days) 
there  is  a  slight  fever,  sometimes  Chabt  xvii.— Varicella, 

chilliness,  vomiting,  and  aching 

in  back  and  legs,  followed  in  24  hours  by  the  appearance  of  a  papular 
eruption,  which  in  a  few  hours  becomes  vesicular.     The  lesions  are 


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684  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

discrete,  often  ovoid,  somewhat  superficial,  flattened,  not  infrequently 
umbilicated,  and  contain  clear  or  cloudy  fluid.  In  36  or  48  hours 
the  contents  become  purulent,  and  during  the  3d  and  4th  days 
shrivel  into  dark-brown  crusts,  which  become  detached,  usually  with- 
out leaving  scars.  The  vesicles  appear  in  successive  sets  during  the 
first  2  or  3  days  of  the  disease,  so  that  lesions  in  various  stages  of 
development  may  lie  side  by  side  (Chart  XVII). 

Complications. — Ordinarily  the  disease  is  mild.  If  the  vesi- 
cles are  disturbed  by  scratching,  ulcers  may  form,  and  in  some  cases 
the  vesicles  may  be  unusually  large  (bullae).  In,  rare  instances  vari- 
cella may  be  hemorrhagic,  with  bleeding  from  the  mucous  mem- 
branes and  the  presence  of  ecchymotic  spots  on  the  skin.  Other 
occasional  complications  are  acute  nephritis,  infantile  hemiplegia, 
and  gangrene  immediately  around  the  vesicles  in  tuberculous  or 
weakly  children.  The  diagnosis  is  from  smallpox  (page  682),  and 
the  prognosis  is  almost  invariably  favourable. 

XII.    SCARLET   FEVER  (SCARLATINA) 

Symptoms. — Period  of  incubation  varies  from  1  to  7  days 
(usually  2  to  4).  The  disease  begins,  as  a  rule,  abruptly,  rarely  with 
a  chill,  but  in  the  majority  of  cases  with  vomiting.  In  young 
children  convulsions  are  common.  The  fever  rises  rapidly  (perhaps 
104°  to  105°)  during  the  1st  day,  and  the  child  complains  of  sore 
throat. 

At  the  end  of  the  1st  or  the  beginning  of  the  2d  day  the  rash 
appears,  first  on  the  neck  and  chest,  whence  it  spreads  over  the 
whole  body,  usually  within  the  next  24  hours.  From  a  distance  the 
skin  is  uniformly  and  brilliantly  scarlet,  but  on  close  inspection  the 
rash  is  seen  to  consist  of  fine,  closely  set  red  points,  the  intervening 
skin  being  diffusely  red.  It  disappears  on  pressure,  the  anaemic  spot 
having  a  slightly  yellowish  tint.  Not  infrequently  the  rash  is  coarsely 
punctiform,  the  intervening  skin  remaining  white ;  or  the  rash  may 
occur  in  patches ;  or  it  may  be  finely  papular ;  or  with  an  intense 
rash  there  may  be  punctate  petechiae  ;  or  sudamina  may  form.  The 
rash  persists  for  2,  3,  or  4  days,  and  then  slowly  disappears. 

The  mucous  membrane  of  the  mouth  and  throat  is  brilliantly  red 
and  more  or  less  SAVollen  ;  the  tonsils  are  reddened,  and  often  present 
a  punctate  or  membranous  exudate  (lacunar  tonsilitis).  The  tongue 
is  at  first  covered  with  a  white  fur  through  which  the  swollen  red 
papillae  project  (strawberry  tongue).  In  a  few  days  the  fur  exfoli- 
ates (raspberry  tongue).  The  pulse  is  unduly  rapid  (in  children 
from  120  to  150  or  over)  in  comparison  with  the  temperature,  and  the 
respiration  is  accelerated.    The  spleen  is  somewhat  enlarged.    Head- 


SCARLET  FEVER 


685 


ache,  restlessness,  insomnia,  and  nocturnal  delirium  are  present  in 
cases  of  notable  severity,  especially  at  the  onset,  disappearing  as  the 
rash  becomes  established.  Aside  from  the  initial  nausea  gastro- 
intestinal symptoms  are  not  common.  The  urine  is  scanty,  high- 
coloured,  and  often  slightly  albuminous.  A  few,  usually  hyaline, 
casts  are  not  uncommon.     A  leucocytosis  is  usually  present. 

In  favourable  cases  the  temperature  gradually  falls  as  the  rash 
disappears,  so  that  by  the  7th  or  8th  day  it  reaches  the  normal  (Chart 
XVIII).     At  this  period  desquamation  begins,  the  cuticle  becoming 


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Chart  XVIII. — Scarlet  fever. 


detached  in  small  scales  or  large  flakes.  Beginning  with  the 
neck  and  chest,  the  desquamation  is  usually  completed  by  the  end 
of  the  3d  or  4th  week,  extending  more  rarely  into  the  7th  or  8th 
week. 

As  scarlet  fever  varies  greatly  in  severity,  certain  clinical  types 
are  recognised,  which  differ  as  follows  from  the  cases  of  average  in- 
tensity just  described : 


686  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

(1)  Mild  Form. — The  rash  may  be  present  without  vomiting,  fever 
or  inflammation  of  the  throat ;  or  the  tonsils  may  be  inflamed  with- 
out a  rash ;  or  fever,  sore  throat,  and  strawberry  tongue  may  exist, 
and  the  rash  be  lacking.  The  presence  of  an  epidemic  or  an  indubi- 
table history  of  exposure  may  be  the  only  evidence  by  which  the 
nature  of  such  cases  may  be  surmised,  unless  the  occurrence  of  some 
characteristic  sequel,  acute  nephritis  in  particular,  throws  an  unhappy 
light  upon  the  primary  attack. 

The  following  forms  are  often  spoken  of  as  malignant : 

(2)  Anginose  Form.— In  this  variety  the  throat  symptoms  are 
prominent.  There  is  an  intense  inflammation  of  the  tonsils,  fauces, 
pharynx,  and  nasal  chambers,  with  swelling  and  an  extensive  mem- 
branous exudate.  The  cervical  glands  are  enormously  swollen,  and 
the  tissues  of  the  neck  become  the  seat  of  a  braAvny  induration.  The 
discharges  from  the  throat  and  nose  are  extremely  offensive.  There 
are  high  temperature  (105°  to  107°),  cyanosis,  stupor,  diarrhoea,  rapid, 
weak,  and  irregular  pulse,  and  the  child  dies  of  an  acute  toxagmia, 
sometimes  within  24  hours.  If  death  does  not  ensue,  at  such  an  early 
period,  abscesses  and  sloughing  ot  the  tonsils  and  cervical  tissues  may 
take  place,  and  be  further  complicated  by  pneumonia  and  profound 
exhaustion. 

(3)  Hemorrhagic  Form. — The  rash  is  petechial,  the  spots  steadily 
developing  into  large  ecchymoses ;  and  there  may  be  hemorrhages 
from  the  mucous  surfaces,  particularly  hasmaturia  and  epistaxis. 
The  patient  may  die  on  the  2d  or  3d  day. 

(4)  Atactic  (Malignant)  Form. — The  onset  is  sudden  and  intense, 
with  chill  or  convulsion,  and  vomiting.  The  fever  is  higli  (107°  to 
108°),  and  there  is  headache,  restlessness,  and  delirium,  soon  followed 
by  coma.  Death  may  take  place  within  24  or  36  hours,  before  the 
rash  has  had  time  to  appear. 

Complications  and  Sequelae. — Nephritis  of  varying  degrees 
of  severity,  occurring  during  the  2d  or  3d,  rarely  the  4th,  week  of 
the  disease,  is  usually  recovered  from,  but  may  be  fatal  from  acute 
uraemia  or  oedema  of  glottis.  Endocarditis,  pericarditis,  and  myo- 
carditis are  not  uncommon.  Pneumonia,  pleurisy  (often  purulent). 
Otitis  media  (frequent  and  serious),  sometimes  followed  by  mas- 
toiditis, necrosis,  labyrinthine  disease,  thrombosis  of  the  lateral  sinus, 
meningitis,  or  cerebral  abscess.  Arthritis  (scarlatinal  "  rheuma- 
tism "),  Adenitis  (of  the  submaxillary  or  cervical  glands),  leading 
in  severe  cases  to  suppuration,  and  in  rare  instances  to  chronic  en- 
largement. Chorea  occasionally  occurs,  with  arthritis  and  endocar- 
ditis ;  and  convulsions,  hemiplegia,  and  spinal  paralysis,  and  throm- 
bosis of  the  cerebral  veins  have  been  noted  very  infrequently.     Can- 


SCARLET  FEVER  687 

crum  oris,  single  or  double  phlegmasia  alba  dolens,  symmetrical 
gangrene  of  the  extremities,  and  perforation  of  the  soft  palate  are 
very  rare  complications. 

Differential  Diagnosis. — In  the  majority  of  cases  the  sudden 
onset,  high  fever,  extraordinarily  rapid  pulse,  strawberry  tongue,  and 
the  early  appearance  of  the  rash  render  a  diagnosis  of  scarlet  fever 
easily  made.     The  following  conditions  may  require  differentiation : 

(1)  Acute  Follicular  (Lacunar)  Tonsilitis.— The  onset  of  this  dis- 
ease may  be  quite  indistinguishable  from  that  of  scarlet  fever,  but  the 
appearance  of  the  rash  upon  the  2d  day  will  declare  the  presence  of 
the  latter. 

(2)  Diphtheria. — In  certain  cases  of  this  disease  there  may  be  an 
erythema,  but  the  rash  is  darker,  generally  confined  to  the  trunk, 
and  disappears  earlier.  The  onset  is  less  abrupt,  there  is  usually  a 
more  marked  degree  of  prostration,  and  a  culture  from  the  throat 
reveals  the  Klebs-Loeffler  bacillus.  Xevertheless,  if  the  two  diseases 
coexist,  it  may  be  quite  impossible  to  affirm  the  fact. 

(3)  Rubella. — The  face  in  this  disease  may  strikingly  resemble 
that  of  scarlet  fever,  but  the  rash  is  not  punctif orm,  the  fever  is  slight, 
the  pulse  is  not  so  rapid — in  short,  the  mildness  of  the  constitutional 
symptoms  will  usually  decide  against  scarlet  fever. 

(4)  Measles. — In  this  disease  the  sore  throat  is  usually  absent ;  so 
also  is  a  leucocytosis.  The  papular  and  blotchy  character  of  the  rash 
and  its  darker  tint,  its  abundance  upon  the  face,  its  later  appearance 
(3d  or  4th  day  of  the  disease),  and  the  prodromal  coryza  and  catar- 
rhal symptoms  will  declare  for  measles. 

(5)  Acute  Exfoliating  Dermatitis. — This  disease  may  furnish  a 
very  faithful  clinical  picture  of  mild  scarlet  fever.  The  vomiting, 
relatively  rapid  pulse,  strawberry  tongue,  sore  throat,  ear  complica- 
tions, and  nephritis  of  scarlet  fever  are,  however,  absent ;  and  recur- 
rent attacks  are  not  uncommon.  I  consider  it  a  good  clinical  rule 
to  label  as  scarlet  fever  every  case  presenting  a  scarlatinous  rash  plus 
an  exudate,  punctate  or  membranous,  upon  the  tonsils. 

(6)  Drug  Eruptions. — Quinine,  belladonna,  potassium  iodide, 
copaiba,  and  certain  foods  (lobsters,  crabs)  may  cause  an  intense 
diffuse  scarlatiniform  erythema,  but  the  sudden  onset  and  rapid 
pulse  of  scarlet  fever  is  lacking  and  the  temperature  is  normal. 

Prognosis. — Uncomplicated  cases  of  moderate  severity  usually 
recover ;  severe  and  malignant  forms  are  apt  to  prove  fatal.  The 
mortality  varies  with  the  epidemic  from  5  to  30  per  cent,  mainly 
in  children  under  6  years  of  age.  Hemorrhages,  severe  throat 
symptoms,  oedema  of  the  larynx,  early  delirium  and  subsultus,  and 
hyperpyrexia  are  unpromising  events. 


€88 


DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 


XIII.  MEASLES  (RUBEOLA) 
Symptoms. — After  an  incubation  of  from  7  to  18  days  (usu- 
ally 14)  the  disease  begins  with  chilliness,  sneezing,  lachrymation, 
coryza,  drowsiness,  and,  in  24  hours,  cough.  There  is  usually  red- 
ness of  the  eyes  and  lachrymation.  Headache,  nausea,  and  vomiting 
may  also  be  present.  The  temperature  rises  steadily  for  the  first  2 
days,  and  may  then  remit  to  rise  again  with  the  appearance  of  the 
rash  (Chart  XIX). 

The  exanthem  appears  on  the  4th  day,  first  upon  the  face,  as 
small,  red,  flattened  papules  which  grow  larger  and  invade  the  trunk 
and  extremities.    The  countenance  has  a  mottled,  swollen  appearance, 

which,  with  the  red- 
dened and  photophobic 
eyes,  aif ords  a  very  char- 
acteristic facies.  The 
blotchy  character  of  the 
rash  is  best  seen  upon 
the  trunk.  The  erup- 
tion, except  in  severe 
cases,  is  distinctly  dis- 
crete and  disappears 
upon  pressure.  The  ex- 
anthem can  be  seen  upon 
the  mucous  surfaces  of 
the  mouth  and  throat. 
Koplik's  spots  (page 
221)  may  be  observed  as 
a  forerunner  of  the  rash. 
The  general  symptoms 
do  not  lessen  until  the 
6th  day,  at  which  time 
the  fever  generally  falls 
by  crisis,  and  the  catar- 
rhal symptoms  slowly  disappear.  The  rash  lasts  until  the  6th  or  7th 
day  and  then  gradually  fades.  Desquamation  occurs  in  the  form  of 
fine,  branny,  almost  unnoticeable  scales. 

The  form  of  this  disease  known  as  hemorrhagic  or  "black"  mea- 
sles, occurring  in  bad  hygienic  surroundings,  may  be  grave  and  fatal. 
The  constitutional  symptoms  are  more  violent,  there  is  marked  pros- 
tration, the  rash  becomes  petechial,  and  there  are  hemorrhages 
from  the  mucous  membranes.  Death  results  from  an  overwhelming 
toxaemia.     Irregular  cases  in  which  the  rash  is  present  by  the  2d 


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Chart  XIX. — Measles. 


MEASLES— ROTHELN  6$^ 

day,  or  on  the  other  hand  is  delayed  until  the  6th  day,  or  in  which 
the  prodromal  symptoms  are  present  but  the  rash  fails  to  appear^ 
are  not  uncommon  during  an  epidemic. 

Complications  and  Sequelas. — Catarrhal  pneumonia  from, 
extension  of  the  bronchitis  which  is  a  part  of  the  disease,  and  lobar 
pneumonia  (less  common) ;  laryngitis  (not  infrequent)  ;  otitis  (fre- 
quent), diarrhoea  (frequent).  Rarer  complications  are  tuberculosis, 
cancrum  oris,  stomatitis,  vulvitis,  and  paraplegia  or  hemiplegia  due 
to  myelitis  or  neuritis. 

Diagnosis. — (1)  Buhella.  —  Prodromata,  fever,  and  catarrhal 
symptoms  are  much  milder,  the  rash  appears  earlier  (1st  or  2d  day) 
and  is  more  evenly  distributed  than  in  measles. 

(2)  Scarlet  Fever. — In  this  disease  the  onset  is  more  sudden,  the 
fever  is  higher  and  does  not  exhibit  the  pre-eruptive  remission,  the 
sore  throat  is  more  marked,  and  the  rash  is  usually  a  bright-red 
and  uniform  erythema,  contrasting  with  the  blotchy  exanthem  of 
measles. 

Prognosis. — The  mortality  is  variable.  Ordinary,  uncompli- 
cated cases  recover ;  pulmonary  complications  in  weakly  or  tuber- 
culous children  are  responsible  for  a  considerable  number  of  fatal 
cases. 

XIV.    RUBELLA   (ROTHELN) 

Symptoms. — After  an  incubation  of  10  or  12  days,  "  German. 
measles  "  begins  with  slight  sore  throat,  slight  fever  (100°),  chilliness^ 
headache,  coryza,  and  some  aching  in  back  and  legs.  These  symp- 
toms are  often  remarkable  for  their  mildness,  and  the  rash  is  fre- 
quently the  first  evidence  of  illness. 

The  rash  appears  on  the  1st  or  2d  day,  first  on  the  face,  whence 
it  spreads  over  the  trunk  and  the  remainder  of  the  body  within  the 
next  24  hours.  It  consists  of  slightly  elevated,  rounded,  or  oval, 
pale-red,  and  usually  discrete  spots ;  occasionally  the  rash  is  of  a 
brighter  red  or  pink  tint  and  diffuse,  resembling  the  rash  of  scarlet 
fever.  It  persists  for  from  3  to  5  days,  often  leaving  a  slight  pig- 
mentation of  the  skin,  and  may  be  followed  by  a  moderate  branny 
desquamation.  The  glands,  especially  the  cervical  and  posterior 
auricular,  are  swollen.  In  occasional  cases  the  temperature  may 
rise  to  103°  and  the  constitutional  symptoms  be  well  marked. 

Complications. — Bronchitis,  pneumonia,  gastro-intestinal  ca- 
tarrh, albuminuria,  and  jaundice  may  occur,  but  complications  of 
any  kind  are  infrequent. 

Differential  Diagnosis. — (1)  Measles. — From  measles,  rubella 
is  to  be  distinguished  mainly  by  the  mildness  of  the  symptoms  in  the 


690  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

latter.  As  the  symptomatology  is  in  many  respects  exactly  similar 
it  may  be  well-nigh  impossible  to  discriminate  between  light  measles 
and  severe  rubella.  A  rose-red  tint  of  the  rash  and  prompt  swelling 
of  the  cervical  and  especially  of  the  posterior  auricular  glands,  point 
to  the  latter. 

(2)  Scarlet  Fever. — The  more  sudden  onset,  the  initial  vomiting, 
the  erythematous  character  of  the  rash,  the  longer  duration  and 
severer  course  of  the  disease  will  serve  to  separate  it  from  rubella. 

(3)  Urticaria. — The  characteristic  wheals,  intense  itching,  and 
usual  absence  of  catarrhal  symptoms  will  discriminate  this  disease 
from  rubella. 

XV.     DIPHTHERIA 

Symptoms. — The  period  of  incubation  of  this  disease  (Klebs- 
Loeffler  bacillus)  varies  from  2  to  10  days ;  usually  2  or  3.  The 
onset  is  with  fever  (102°  to  104°),  chilliness,  headache,  and  pain  in 
the  back  and  limbs.  A  convulsion  may  occur  in  infants  or  very 
young  children.  Albuminuria  is  common.  There  is  nothing  dis- 
tinctive in  the  initial  symptoms.  According  to  the  site  of  the  spe- 
cific inflammation  the  following  forms  of  diphtheria  are  recognised : 

(1)  Pharyngeal  Diphtheria. — Sore  throat,  dysphagia,  swollen  and 
tender  glands  in  the  neck,  and  stiffness  of  the  cervical  tissues  become 
manifest.  The  tonsils  are  swollen  and  covered  with  grayish  or  yel- 
lowish white  membrane,  which  is  usually  adherent,  and  leaves  a  bleed- 
ing surface  when  forcibly  stripped  off.  By  the  2d  or  3d  day  the 
membrane  extends  to  the  faucial  pillars,  perhaps  also  to  the  uvula 
and  the  posterior  pharyngeal  wall.  In  favourable  cases  the  symp- 
toms subside  and  the  throat  becomes  clear  of  membrane  by  the  10th 
day.  The  membrane  may  be  punctate  and  confined  to  the  tonsils 
(lacunar  or  tonsillar  diphtheria),  simulating  in  every  respect  an 
ordinary  follicular  tonsilitis ;  or  there  may  be  a  soft  non-membranous 
exudate  upon  the  tonsils  alone ;  or  the  case  may  be  so  extremely 
mild  that  membrane  or  exudate  does  not  appear,  the  throat  present- 
ing only  the  redness  of  an  ordinary  catarrhal  inflammation. 

(2)  Laryngeal  Diphtheria. — Membranous  croup  is  in  the  large 
majority  of  cases  laryngeal  diphtheria ;  in  a  small  minority  a  strep- 
tococcus inflammation.  It  is  usually  secondary,  by  extension  from 
the  pharynx,  occasionally  primary.  A  croupy  cough,  hoarseness,  or 
aphonia,  and,  above  all,  evidences  of  progressive  laryngeal  stenosis, 
constitute  the  leading  symptoms.  As  the  narrowing  of  the  glottic 
opening  proceeds  the  breathing  becomes  stridulous,  and  dyspnoea  and 
cyanosis  become  manifest.  The  supraclavicular,  episternal,  inter- 
costal, and  epigastric  spaces  are  deeply  retracted  with  inspiration  and 


DIPHTHERIA  691 

"bulge  with  expiration.  The  child  is  excessively  restless,  the  nostrils 
work  violently,  and  the  sterno-mastoids  become  prominent  during 
inspiration.  Shreds  of  membrane  may  be  coughed  up.  If  the  steno- 
sis is  not  relieved  the  child  passes  into  a  semicomatose  state  and 
finally  dies.  The  fever  is  usually  slight  and  the  general  condition  of 
the  child  is  good.  The  membrane  may  extend  into  the  trachea  and 
the  bronchial  tubes. 

(3)  JVasal  Diphtheria. — This  may  be  primary,  but  is,  as  a  rule,  see- 
ondary  by  extension  from  the  pharynx. 

The  general  symptoms  are  generally,  but  not  invariably,  severe ; 
high  fever,  prostration,  and  extensive  swelling  of  the  cervical  glands. 
There  is  an  offensive,  often  bloody,  discharge  from  the  nostrils,  or  an 
«pistaxis,  and  the  orifices  of  the  nose  and  upper  lip  are  excoriated. 
The  membrane  may  usually  be  found  by  inspection.  In  certain  cases, 
■as  yet  somewhat  inexplicable,  there  may  be  thick  membranes  in  the 
nose  containing  diphtheria  bacilli,  but  constitutional  symptoms  are 
absent  and  the  disease  is  quite  harmless  (fibrinous  rhinitis). 

(4)  Miscellaneous  Sites  of  Diphtheria. — If  a  wound  or  an  ulcer- 
ated or  excoriated  surface  becomes  infected,  a  pseudo-membrane  may 
form  at  the  point  of  lodgment  of  the  germs.  Diphtheria  of  the  con- 
junctiva may  occur  primarily,  or  by  extension  from  the  nose ;  of  the 
external  ear,  from  the  discharge  of  a  diphtherial  otitis  media  ;  of  the 
mouth  and  lips,  by  extension ;  of  wounds,  ulcers,  and  the  genitals,  by 
-direct  infection  from  contaminated  hands,  instruments,  or  dressings. 

Variations  in  Intensity. — The  case  may  be  mild,  with  slight 
fever  and  little  if  any  prostration.  In  severe  cases  attended  by  ex- 
tensive and  intense  local  changes,  the  prostration  is  extreme,  the 
temperature  is  subnormal,  the  face  is  ashy,  the  pulse  rapid  and  fee- 
ble. In  malignant  diphtheria  the  general  symptoms  are  grave  from 
the  very  onset  of  the  disease.  The  fever  is  high,  the  prostration 
extreme,  the  pulse  rapid  and  weak,  and  death  occurs  in  2  or  3  days 
from  the  excessive  toxaemia.  In  such  cases  the  diphtheritic  lesions 
in  the  nose  and  pharynx  are  usually  of  an  aggravated  type,  and  there 
maybe  subcutaneous  ecchymoses. 

Complications  and  Sequelae.— Broncho-pneumonia  and  pul- 
monary collapse  are  notably  frequent ;  rarely  pulmonary  gangrene. 
Acute  nephritis  is  common  ;  so  also  is  otitis  media.  Epistaxis  may 
be  serious.  Endocarditis  and  heart  failure  (usually  due  to  a  neuritis 
of  the  cardiac  nerves)  are  not  very  rare. 

Among  the  sequeJce,  aside  from  chronic  catarrh  of  the  nasopharynx 
and  anaemia,  by  far  the  most  important  and  characteristic  is  diph- 
theritic paralysis.  It  occurs  in  10  to  15  per  cent  of  the  cases,  and 
<;omes  on  during  convalescence  (2d,  3d,  or  4th  week).     It  is  as  char- 


692  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

acteristic  of  diphtheria  as  nephritis  is  of  scarlet  fever.  Like  the  lat- 
ter, it  may  follow  the  mildest  case  of  the  disease  and  perhaps  be  the 
first  symptom  indicating  the  nature  of  the  primary  sore  throat. 

Diphtheritic  paralysis  is  a  toxic  neuritis,  general  or  local,  and 
according  to  the  particular  nerves  involved  the  symptoms  may  show 
a  great  variety.  The  most  common  form  is  that  affecting  the  palate 
and  pharynx,  and  is  indicated  by  the  nasal  character  of  the  voice, 
regurgitation  of  fluids  through  the  nose,  and  dysphagia,  with  which 
there  often  coexists  a  moderate  weakness  of  the  legs.  Kext  in  fre- 
quency the  ocular  muscles  are  involved,  causing  ptosis,  strabismus, 
and  loss  of  accommodative  power.  The  special  nerves  of  taste  or 
hearing  may  be  involved.  There  may  be  a  multiple  neuritis  affect- 
ing both  legs  (paraplegia),  with  absent  tendon  reflexes,  although  the 
last  sign  does  not  of  necessity  imply  a  neuritis  ;  or  the  extensors  of 
the  feet ;  or  one  or  both  arms  ;  or  all  four  extremities  ;  or  the  face  ; 
or  the  respiratory  muscles  (diaphragm  in  particular)  ;  or  the  cardiac 
nerves.  The  abnormally  rapid  or  slow  pulse,  dilated  heart,  and  the 
occasional  advent  of  dangerous  or  fatal  syncope,  met  with  either  at 
the  acme  of  the  disease  or  during  convalescence,  result  in  all  prob- 
ability from  an  involvement  of  the  cardiac  nerves,  less  commonly 
from  an  infectious  myocarditis. 

Differential  Diagnosis. — The  only  absolute  proof  of  the  exist- 
ence of  diphtheria  is  the  presence  of  the  Klebs-Loeffler  bacillus.  In 
the  severer  forms  of  anginal  diphtheria,  where  the  exudate  is  not  con- 
fined to  the  tonsils  but  spreads  to  the  pillars  of  the  fauces,  soft  pal- 
ate, or  pharynx,  the  clinical  diagnosis  is  readily  made ;  but  when  the 
picture  and  the  course  of  the  disease  is  exactly  that  of  a  follicular 
tonsilitis,  or  the  membrane  is  absent  as  in  the  milder  forms  of 
diphtheria,  a  reliable  diagnosis  can  be  made  only  by  a  bacteriological 
or  microscopical  examination  of  the  exudate.  The  membranous 
anginas  occurring  in  scarlet  fever,  measles,  pertussis,  and  scarlet 
fever,  and  usually  due  to  the  streptococcus,  can  not  be  differentiated 
from  true  diphtheria  except  by  proving  the  absence  of  the  Klebs- 
Loeffler  bacillus.  These  forms  of  membranous  sore  throat  are  very 
appropriately  qualified  as  diphtheroid. 

For  making  cultures  in  suspected  cases  of  diphtheria  the  Depart- 
ment of  Health  of  Kew  York  city  furnishes  an  outfit  (free)  consist- 
ing of  a  box  in  which  there  are  2  test  tubes,  one  containing  a  steril- 
ized cotton  swab,  the  other  a  slant  of  coagulated  blood  serum.  Both 
are  plugged  with  sterilized  cotton.  The  directions  which  accompany 
the  outfit  are  as  follows  : 

"  The  patient  should  be  placed  in  the  best  light  attainable,  and,, 
if  a  child,  properly  held.     In  cases  where  it  is  possible  to  get  a  good 


DIPHTHERIA— ERYSIPELAS  693 

view  of  the  throat,  depress  the  tongue  and  rub  the  cotton  swab 
gently,  but  freely,  against  any  visible  pseudo-membrane  or  exudate. 

"In  other  cases,  including  those 'in  which  the  exudate  is  confined 
to  the  larynx,  open  the  mouth  and  pass  the  swab  back  till  it  reaches 
the  pharynx,  and  then  rub  it  freely  against  the  mucous  membrane. 
Without  laying  the  swab  down,  withdraw  the  cotton  plug  from  the 
culture  tube,  insert  the  swab,  and  rub  that  portion  which  has  touched 
the  exudate  gently  back  and  forth  along  the  surface  of  the  blood 
serum.  Do  not  break  the  surface  of  the  blood  serum,  for  it  is  a  sur- 
face growth  of  bacteria  that  is  desired.  Then  replace  the  swab  in  its 
own  tube,  plug  both  tubes,  fill  out  inclosed  blank,  and  return  the 
whole  outfit  at  once  to  the  station  from  which  it  was  obtained.  Do 
not  use  tubes  which  are  contaminated,  or  in  which  the  contents  have 
liquefied  or  dried  up.  Do  not  make  culture  within  two  hours  after 
any  antiseptic  wash  or  spray  has  been  used  in  the  patient's  throat." 

Prognosis. — The  mortality  varies  from  10  to  50  per  cent,  and 
the  prognosis  should  be  guarded.  In  moderately  severe  cases  of 
pharyngeal  diphtheria  recovery  may  be  expected ;  if  the  nose  is 
involved  the  gravity  increases ;  and  laryngeal  diphtheria  (membra- 
nous croup)  is  a  very  fatal  disease.  The  antitoxine  treatment  has 
produced  a  notable  diminution  in  the  mortality. 

XVI.    ERYSIPELAS 

Symptoms. — This  disease — due  to  infection  by  the  Streptococcus 
pyogenes — has  a  period  of  incubation  varying  from  3  to  7  days.  The 
form  usually  seen  by  the  internalist  is  that  which  affects  the  face  and 
head.  The  attack  begins  more  or  less  suddenly  with  a  chill  or  chilli- 
ness, followed  by  a  rapid  rise  of  temperature  (103°  to  105°).  In  previ- 
ously strong  and  healthy  persons  the  constitutional  depression  may 
be  slight;  but  in  the  old  or  debilitated,  or  in  chronic  alcoholics, 
there  may  be  great  prostration,  dry  tongue,  feeble  pulse,  and 
delirium. 

Coincident  with,  or  a  little  later  than,  the  onset  of  the  general 
symptoms  a  reddened  spot  is  to  be  seen,  usually  on  the  bridge  of 
the  nose  or  upon  one  of  the  alae,  less  frequently  upon  other  parts 
of  the  face,  or  the  ear,  or  head.  This  rapidly  extends,  the  skin 
becomes  swollen,  red,  and  tense,  and  is  often  studded  with  vesicles 
or  small  bullae,  especially  on  the  eyelids,  ears,  and  forehead.  The 
pain  is  burning  and  tensive.  The  inflammatory  area  has  a  well- 
defined,  somewhat  raised  margin,  and,  as  it  extends,  the  areas  first 
attacked  become  somewhat  lighter  in  colour  and  less  swollen. 
When  the  greater  portion  of  the  face  is  involved  the  eyes  are  nearly 
or  quite  closed,  the  nose  is  bulbous,  the  lips  and  ears  are  thickened 
46 


694  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

and  edematous.  The  cervical  glands  are  enlarged.  Small  cutaneous 
abscesses  are  common  on  the  neck,  cheeks,  and  forehead,  and  there 
may  be  extensive  suppuration  under  the  scalp.  The  mucous  mem- 
brane of  the  mouth  and  throat  is  reddened,  and  in  rare  cases  the 
inflammation  may  extend  to  the  larynx  and  cause  oedema.  Leuco- 
cytosis  is  present,  and  the  urine  is  often  albuminous. 

The  fever  continues  high  with  slight  remissions  for  6  or  7  days, 
and  usually  terminates  by  crisis.  The  local  redness  and  swelling 
subside,  and  desquamation  follows.  In  the  wandering  form  of  the 
disease  {E.  migrans  or  ambulatis)  the  inflammation  disappears  from 
one  part  and  appears  in  another,  the  temperature  runs  an  irregular 
course,  and  the  patient  may  exhibit  the  symptoms  of  the  typhoid 
status. 

Complications  and  Sequelae. — Actual  meningitis,  as  proved 
by  autopsy,  rarely  occurs,  the  meningeal  symptoms  (delirium,  coma) 
arising  from  the  fever  or  the  toxaemia.  Pericarditis,  pleurisy,  acute 
nephritis  (occasional),  pneumonia  (occasional),  otitis  media.  Septi- 
caemia, pyaemia,  and  ulcerative  endocarditis  are  not  uncommon. 
Articular  rheumatism  is  a  relatively  frequent  complication  (Anders). 

Differential  Diagnosis. — The  mode  of  onset,  the  fever,  and 
the  swollen,  well-defined  edge  of  the  erysipelatous  inflammation  ren- 
der the  diagnosis  easy  in  a  developed  case. 

(1)  Acute  Eczema. — The  absence  of  fever,  the  lack  of  a  definite 
border  or  of  marked  swelling,  and  the  presence  of  intense  pruritus 
will  declare  the  disease  to  be  an  acute  eczema. 

(2)  Erythema. — The  absence  of  fever,  swelling,  or  local  heat 
separates  erythema  from  erysipelas. 

Prognosis. — The  mortality  varies  from  4  to  7  per  cent.  In 
healthy  adults  recovery  is  the  rule.  In  persons  over  60,  in  chronic 
topers,  or  in  the  debilitated,  the  prognosis  is  serious ;  and  erysipelas 
of  the  navel  in  the  newborn  is  usually  fatal.  Death  occurs  from 
exhaustion  or  toxaemia. 

XVII.    TOXvCMIA,    SEPTIOEMIA,  AND    PYAEMIA 

Definitions. — {a)  Toxcemia  results  from  the  introduction  into 
the  system  of  toxines  formed  by  micro-organisms,  mainly  by  those 
which  are  pathogenic.  Saprmmia  is  a  toxsemia  due  to  the  absorp- 
tion of  toxines  formed  by  the  bacteria  of  putrefaction.  In  either 
case  the  organisms  develop  at  some  local  site,  whence  the  poisonous 
substances  are  absorbed — e.  g.,  the  throat  in  diphtheria,  or  a  moist 
gangrene  of  the  leg. 

(b)  Septicmmia  (bacteraemia)  is  a  condition  in  which  there  is  an 
incursion  of  pathogenic  germs  into  the  blood  and  tissues  of  the  body 


TOXAEMIA— SEPTIC^MLA.  695 

in  general,  with  or  without  a  discoverable  avenue  of  entrance,  but  in 
which  there  are  no  foci  of  suppuration. 

(c)  Pymmia  is  a  septicaemia  due  to  pyogenic  organisms,  plus  one 
or  more  foci  of  suppuration. 

Causes  and  Symptoms.— («)  Toxaemia. — (1)  Causes. — This 
condition  attends  the  invasion  of  many  of  the  infectious  diseases, 
especially  erysipelas,  diphtheria,  tetanus,  and  pneumonia,  in  which 
the  pathogenic  germ  lodges  and  multiplies  in  some  special  local- 
ity. The  constitutional  symptoms  are  due  to  the  absorption  of 
the  toxines  manufactured  at  the  site  of  infection  and  not  to  the 
entrance  of  the  germ  into  the  blood.  At  a  later  period  the  patho- 
genic organisms  may  invade  the  blood  and  tissues,  and  the  condition 
then  becomes  a  septicaemia.  Of  the  form  of  toxaemia  known  as  sap- 
raemia  (absorption  of  the  products  of  putrefaction)  the  most  com- 
mon examples  are  moist  gangrene  of  the  extremities,  gangrene  of 
the  lungs  or  other  portions  of  the  body ;  auto-intoxication  from  the 
intestinal  tract ;  the  ingestion  of  tyrotoxicon  or  other  ptomaines 
resulting  from  the  decomposition  of  meat,  milk,  or  cheese ;  the 
inhalation  of  the  gases  of  putrefaction  (causing  nausea,  fever,  and 
diarrhoea) ;  or  absorption  from  a  retained  and  offensive  placenta. 

(3)  Symptoms  of  Toxwmia. — General  malaise,  prostration,  rest- 
lessness, headache,  chill,  and  fever.  Of  these  the  last  is  the  most 
constant.  The  symptoms  referable  to  the  heart  (rapid,  weak  pulse) 
and  the  nervous  system  constitute  the  best  criteria  of  the  severity  of 
the  toxaemia.     There  is  usually  a  leucocytosis. 

{h)  Septicaemia. — (1)  Causes. — The  septicaemic  condition  may 
originate  from  a  recognisable  focus  of  infection,  as  in  autopsy 
wounds,  puerperal  septicaemia,  anthrax,  pneumonia,  gonorrhoea,  and 
typhoid  fever,  a  general  infection  resulting  from  what  was  originally 
a  local  process.  In  the  majority  of  cases  the  septicaemia  is  due  to 
the  streptococcus  or  staphylococcus ;  but  there  are  often  combined 
or  mixed  infections — e.  g.,  the  septicaemia  may  be  caused  by  the 
simultaneous  presence  of  the  Streptococcus  pyogenes  and  the  Bacillus 
typhosus,  the  Diplococcus  pneumonim,  the  Bacillus  tuberculosis,  or 
the  Klebs-LoefiQer  bacillus. 

In  other  cases  the  local  focus  of  infection  is  not  recognisable 
during  life  and  perhaps  not  at  autopsy  (cryptogenetic  septicasmia). 
Generally  in  these  cases  the  patient  is  already  ill  of  some  acute  or 
chronic  malady ;  but  in  a  certain  proportion  the  infection  occurs  in 
those  who  are  in  good  health.  Of  the  germs  causing  the  infection 
the  Streptococciis  pyogenes  is  the  most  common,  next  the  Staphylo- 
coccus pyogenes,  the  pneumococcus,  the  Bacillus  proteus,  and  the 
Bacillus  pyocyaneics. 


696  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Here  also  may  be  considered  certain  local  or  general  infections 
occurring  very  frequently  as  secondary  or  intercurrent  events  in 
chronic  diseases,  especially  in  chronic  nephritis,  arteriosclerosis, 
chronic  valvular  disease,  cirrhosis  of  the  liver,  Hodgkin's  disease, 
leucaemia,  chronic  tuberculosis,  and  other  chronic  maladies.  Because 
of  the  fact  that  these  infections  are  apt  to  close  the  scene  they  are 
spoken  of  as  "  terminal.  "  The  micro-organisms  found  in  the  ter- 
minal infections  are,  in  addition  to  those  previously  mentioned,  the 
gonococcus,  the  gas  bacillus,  and  the  Bacillus  tuberculosis.  The 
local  affections  to  which  they  give  rise  are  acute  meningitis,  pericar- 
ditis, endocarditis,  or  pleurisy ;  acute  miliary  tuberculosis  of  the  peri- 
tonaeum or  pleura ;  and  entero-colitis. 

(2)  Symptoms  of  Septiccemia. — When  septicaemia  starts  from  a 
local  infective  focus,  whence  the  micro-organisms  enter  the  blood, 
the  symptoms  of  the  invasion  may  begin  on  the  2d,  3d,  or  4th  day, 
rarely  later.  At  the  onset  there  is  usually  chilliness  rather  than  rigour, 
with  fever,  moderate  at  first,  but  which  rises  and  tends  to  become  of 
the  continued  type,  with  decided  daily  remissions.  There  is  head- 
ache, anorexia,  prostration,  delirium,  or  marked  apathy.  The  pulse 
is  rapid,  small,  and  compressible.  The  tongvie  shows  a  marginal  red- 
ness, and  may  become  dry  and  brown  ;  there  may  be  nausea,  vomit- 
ing, and  diarrhoea;  and  the  spleen  may  be  palpably  swollen.  Pe- 
techial spots  are  not  uncommon ;  slight  toxaemic  jaundice  usually 
develops ;  and  scarlatinif  orm  rashes  or  herpes  may  appear.  The 
urine  frequently  contains  albumin,  leucocytes,  red  cells,  and  tube 
casts.  If  the  septicaemia  is  cryptogenetic,  and  especially  if  it  is  due 
to  the  presence  of  the  streptococcus,  the  fever  is  high,  irregular,  with 
recurrent  slight  chills,  and  of  a  more  decided  septic  cast. 

(c)  PysBinia. — (1)  Causes. — Pyaemia  is  a  septicaemia  complicated 
by  multiple  abscesses  arising  from  an  original  focus  of  suppuration. 
The  abscesses,  primary  or  secondary,  may  be  seated  in  any  part  or 
organ  of  the  body.  The  organisms  most  commonly  causing  suppura- 
tion are  the  streptococcus  and  staphylococcus,  although  other  germs 
may  be  pyogenic,  viz.,  the  pneumococcus,  the  Bacillus  typhosus,  the 
Bacillus  coli  communis,  Pfeiffer's  bacillus  (of  influenza),  the  Bacillus 
proteus,  the  Bacillus  pyocyaneus,  and  probably  the  gas  bacillus. 

The  vessels  in  the  neighbourhood  of  the  original  suppurative 
focus  become  inflamed,  with  the  formation  of  thrombi ;  in  the  ma- 
jority of  cases  the  veins  are  involved  (phlebitis),  less  commonly  the 
arteries  (arteritis).  From  these  infected  thrombi  particles  of  varying 
size  become  detached,  and  are  carried  as  emboli  by  the  blood  stream 
to  various  parts  or  organs,  where  they  become  impacted.  Instead 
of  causing  simple  infarctions,  as  do  non-infected  emboli,  they  give 


PYEMIA 


69Y 


rise  to  new  foci  of  suppuration  because  of  the  masses  of  pyogenic 
organisms  conveyed  by  them.  The  veins  are  the  usual  channels  by 
which  the  septic  emboli  are  transmitted  to  various  parts  of  the 
body ;  particles  from  an  arterial  thrombus  are  arrested  in  the  capil- 
lary areas  in  which  the  branches  of  the  thrombosed  artery  terminate. 

The  sites  of  the  secondary  (metastatic,  embolic)  abscesses  vary 
according  to  the  vascular  area  in  which  the  original  suppurative  focus 
is  situated ;  thus,  if  it  lies  in  the  intestines,  multiple  metastatic  ab- 
scesses are  found  in  the  liver,  the  septic  particles  being  conveyed  by 
the  portal  system  of  veins ;  if  in  the  skin,  muscles,  or  bones,  the  em- 
bolic abscesses  are  found  in  the  lungs  ;  or  if  the  emboli  are  very  small 
they  may  pass  through  the  pulmonary  circulation  and  lodge  in  the 
kidney,  spleen,  and  joints  ;  or  may  be  detained  in  the  heart  and  pro- 
duce an  ulcerative  endocarditis,  furnishing  septic  particles  which, 
travelling  in  the  arterial  stream,  become  the  cause  of  abscesses  in 
various  parts  of  the  body. 

(2)  Symptoms  of  Pycemia. — A  severe  chill  or  rigour  usually  marks 
the  onset  of  the  disease,  the  temperature  rapidly  rises  to  103°  or  104° 


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Chart  XX. — Irregular  chills  and  fever  in  pyaemia  due  ta  gangrene  of  lung  following  an 

inhalation  pneumonia. 


or  over,  and  is  followed  by  a  remission,  or  perhaps  an  intermission, 
with  profuse  sweating.  The  chills,  high  fever,  and  sweating  recur 
at  irregular  intervals  (Chart  XX),  the  temperature  curve  in  the  mean- 
time showing  a  slightly  elevated  and  remitting  line.  There  are  ano- 
rexia, nausea,  and  vomiting.  In  the  acute  cases  there  is  rapid  ema- 
ciation, and  as  the  dieases  advances  prostration  becomes  marked,  the 


698  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

skin  is  moderately  jaundiced,  the  pulse  is  rapid  and  feeble,  and  the 
dry,  brown  tongue,  delirium,  coma,  and  other  symptoms  of  the  typhoid 
status  develop.  In  chronic  cases  the  fever  is  irregular,  and  the  chills 
recur  at  long  intervals.     There  is  a  leucocytosis. 

In  the  majority  of  cases  local  symptoms,  due  to  multiple  meta- 
static inflammations,  become  manifest  sooner  or  later,  as  follows :  In 
the  lungs,  dyspnoea,  cough,  perhaps  purulent  or  rusty  expectoration, 
and  the  physical  signs  of  consolidation,  cavity,  or  pleural  effusion ; 
in  the  splee7i,  enlargement  of  the  organ,  with  pain,  tenderness  (peri- 
splenitis), and  perhaps  splenic  friction  sounds  on  auscultation;  in 
the  liver,  symptoms  are  slight,  liver  may  be  enlarged  and  tender, 
perhaps  with  friction  sounds  (perihepatitis) ;  in  the  heart,  endocar- 
ditis, perhaps  ulcerative  {q.  v.) ;  in  the  Mdneys,  the  urinary  evidences 
of  multiple  renal  abscesses  or  infarcts,  see  (8)  (c),  page  646 ;  in  the 
joints,  pain,  redness,  fluctuation. 

Diagnosis  of  Pyaemia. — The  cardinal  symptoms  are  the 
irregular  chills,  fever,  and  sweats,  together  with  the  discovery  of  a 
primary  suppurative  focus.  Of  the  latter  the  most  common  are : 
Suppurating  wounds,  surgical  or  accidental ;  childbirth ;  prostatic 
abscess,  chronic  ulcerative  cystitis,  gonorrhoea,  chancroids,  and  bubo ; 
appendicitis,  suppurating  hemorrhoids,  or  intestinal  ulceration,  per- 
haps with  a  pylephlebitis;  suppurative  mastoiditis  resulting  from 
an  acute  or  chronic  otitis  media ;  osteomyelitis,  or  septic  arthritis. 
Ulcerative  endocarditis,  while  usually  secondary,  may  be  the  primary 
cause  of  pyaemia.  In  doubtful  cases  of  pyaemia  or  septicaemia,  espe- 
cially of  the  cryptogenetic  form,  a  most  careful  search  is  to  be  made 
for  a  wound,  abrasion,  or  local  lesion  in  any  part  of  the  body.  An 
examination  of  stained  blood  films  may  possibly  result  in  the  dis- 
covery of  pyogenic  organisms. 

Differential  Diagnosis  of  Pyaemia. — As  compared  with 
septicaemia,  pyaemia  exhibits  recurring  chills,  deeply  remitting  fever, 
and  sweats,  with  great  prostration,  rapid  wasting,  moderate  icterus, 
and  evidences  of  embolic  abscesses ;  while  in  septicaemia  there 
is  usually  but  a  single  chill,  the  fever  is  of  the  continued  type, 
sweats  are  uncommon,  the  jaundice  is  much  lighter,  and  there  are 
no  metastatic  abscesses.  Moreover,  in  septicaemia,  delirium  and 
coma  are  early  symptoms  ;  in  pyaemia  they  become  manifest  later  in 
the  disease. 

(rt)  Diseases  Simulated  by  Pyaemia. — (1)  Jfrt^anV;.— Because  of 
the  chills,  fever,  and  sweats,  pyaemia  may  be  mistaken  for  an  inter- 
mittent malarial  fever,  but  the  finding  of  the  plasmodium  and  the 
prompt  effect  of  quinine  in  the  latter  offer  ready  means  of  differ- 
entiation. 


PYEMIA— YELLOW  FEVER  699 

(2)  Typhoid  Fever. — The  more  chronic  cases  of  pyaemia  in  which 
there  is  an  irregular  fever  with  delirium,  prostration,  diarrhoea,  and 
a  swollen  spleen,  may  simulate  typhoid  fever,  but  the  presence  of 
rose  spots,  the  absence  of  leucocytosis,  and  the  finding  of  a  positive 
Widal  test  will  declare  for  the  latter. 

{h)  Diseases  wMch  may  simulate  PyaBmia. — Among  these  are 
pyelitis  (especially  if  due  to  renal  calculus) ;  renal  tuberculosis ; 
empyema  ;  beginning  pulmonary  tuberculosis  ;  abscess  of  the  liver ; 
lodgment  of  a  gallstone  in  the  common  duct ;  Hodgkin's  disease ; 
grave  anaemia ;  and  swiftly  advancing  malignant  disease. 

Prognosis  of  PysBinia  and  Septicaemia. — The  prognosis 
varies  with  the  cause.  If  the  latter  is  removable  before  serious 
inroads  have  been  made  upon  the  strength,  or  if  irremediable  com- 
plications have  not  occurred,  recovery  takes  place.  Otherwise,  espe- 
cially in  pyaemia,  the  prognosis  is  always  grave. 

XVm.    YELLOW  FEVER 

Symptoms. — Whether  this  disease  is  due  to  the  Bacillus  icte- 
roides  (Sanarelli)  is  still  in  dispute.  The  stage  of  incubation  varies 
from  1  day  to  2  weeks,  usually  3  or  4  days. 

(1)  First  Stage. — Onset  sudden,  with  chilliness  and  a  rapid  rise 
of  temperature  (100°  to  106°),  accompanied  by  headache  and  intense 
pain  in  the  back  and  limbs.  Sore  throat,  a  furred  tongue,  and  epi- 
gastric tenderness  are  present ;  nausea  and  vomiting  are  usually 
persistent.  Constipation  generally  exists.  The  pulse  is  remark- 
able for  its  slowness  in  comparison  with  the  temperature  (75  :  103°), 
and  may  become  less  frequent  as  the  temperature  rises.  Albu- 
minuria, which  may  be  transient,  occurs  early  in  the  disease — i.  e., 
on  the  2d  or  3d  day.  The  facies  is  said  to  be  quite  characteristic. 
The  face  is  flushed,  the  eyes  are  redly  injected  and  intolerant  of 
light,  and  the  eyelids  and  lips  slightly  swollen.  Careful  Inspection 
shows,  even  on  the  first  day,  a  subicteric  tint.  The  fever  keeps 
high,  with  slight  variations,  for  from  1  to  3  days,  and  then  falls,  with 
an  amelioration  of  the  symptoms,  and  the  patient  enters  upon  the 

(2)  Stage  of  Remission. — This  lasts  from  a  few  hours  to  a  day, 
and  in  favourable  cases  marks  the  beginning  of  convalescence. 
More  commonly  tlie  fever  rises  again  and  the  patient  passes  into  the 

(3)  Second  Stage. — The  skin  becomes  yellow  or  almost  bronzed. 
The  vomiting  persists,  may  be  projectile  and  painful,  and  in  severe 
cases  the  vomitus  contains  dark  blood  (black  vomit) ;  or  the  blood 
may  be  bright  and  unaltered.  The  stools  may  be  tarry,  and  there 
may  be  bleeding  from  the  nose  and  gums,  as  Avell  as  petechial  spots 
on  the  skin.     The  urine  is  scanty,  containing  blood,  albumin,  and 


700  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

casts;  or  there  may  be  complete  suppression,  giving  rise  to  ursemic 
coma  or  convulsions.  The  tongue  is  dry  and  brown,  or  raw  and  fis- 
sured. Unless  ursemic  dulness  is  manifested  the  mind  usually 
remains  unclouded.  Great  prostration,  or  even  collapse,  with  cold 
skin  and  extremities,  is  present.  In  favourable  cases  the  secondary 
fever,  after  lasting  from  1  to  3  days,  falls  by  lysis  ;  in  bad  cases  the 
temperature  goes  rapidly  upward  to  a  higher  point  than  in  the  first 
stage  and  death  soon  follows. 

The  entire  duration  of  the  disease  is  about  one  week.  Conva- 
lescence may  be  hindered  by  a  relapse  (not  common),  diarrhoea,  paro- 
titis, or  abscesses. 

Differential  Diagnosis. — The  cardinal  symptoms  of  yellow 
fever  are  the  facies,  the  reduction  of  the  pulse  rate  although  the 
temperature  remains  high  or  rising,  and  the  early  albuminuria.  It 
is  quite  possible  that  a  serum  test  will  be  worked  out  for  yellow  fever 
comparable  to  that  of  Widal  for  typhoid  fever. 

Very  mild  cases  (slight  fever  for  24  to  48  hours)  can  not  be  recog- 
nised unless  an  epidemic  is  prevailing ;  and  the  early  cases  of  an 
outbreak  are  apt  to  present  difiiculties  in  diagnosis.  The  intensity 
of  the  disease  varies  from  mild^  to  severe  (prostration,  vomiting,, 
hemorrhages),  to  malignant^  in  which  a  fatal  result  occurs  in  2  or  3 
days  from  the  virulence  of  the  poison.  The  disease  is  to  be  dis- 
criminated from 

(1)  Dengue. — See  page  672. 

(2)  Malarial  Fever. — In  the  aestivo-autumnal  variety  of  this  dis- 
ease, which  is  the  only  form  likely  to  be  confused  with  yellow  fever, 
jaundice  rarely  appears  until  the  4th  or  5th  day ;  albumin  is  very 
seldom  found  as  early  as  the  2d  day ;  black  vomit  is  very  rare  y 
hsematuria  is  much  more  common ;  the  spleen  is  usually  enlarged ; 
and  the  characteristic  crescentic  forms  of  the  plasmodium  may  be 
found  in  the  blood. 

Prognosis. — The  mortality  varies  from  15  to  85  per  cent,  show- 
ing a  wide  range  in  the  virulence  of  different  epidemics.  An  ini- 
tial fever  exceeding  104°  is  of  bad  omen ;  so  also  is  black  vomit ;. 
while  anuria,  delirium,  coma,  and  convulsions  usually  mean  death. 
On  the  other  hand,  moderate  fever,  slight  jaundice,  an  ample  flow  of 
urine,  and  freedom  from  hemorrhages  offer  a  favourable  prognosis. 
When  death  occurs  it  is  generally  from  exhaustion  or  uraemia. 

XIX.    DYSENTERY 

Four  varieties  of  this  disease  are  recognised.  All  of  these  have 
as  a  symptom  frequent,  usually  mucous  and  bloody,  stools ;  and  in. 
the  acute  forms  abdominal  griping  and  severe  tenesmus. 


DYSENTERY  701 

Varieties  and  Symptoms.— (1)  Catarrhal  Dysentery.— Usu- 
ally after  1  or  2  days  of  a  painless  moderate  diarrhoea,  griping  and 
colicky  abdominal  pains  are  manifest.  The  stools  become  frequent, 
and  are  expelled  with  severe  straining  and  tenesmus.  The  desire  to 
defecate  is  unremitting,  and  there  is  a  constant  and  distressing  feel- 
ing of  rectal  fulness,  pressure,  and  bearing  down.  The  stools  are  at 
first  partly  fascal,  but  soon  come  to  consist  purely  of  small  amounts 
(I  oz.)  of  gelatinous  mucus,  muco-pus,  and  blood,  varying  in  num- 
ber from  15  to  200  in  24  hours.  In  mild  cases  there  is  slight  fever ; 
in  the  severer  forms  the  temperature  may  reach  102°  or  103°.  The 
tongue  is  at  first  furred,  later  becoming  red  and  smooth  ;  thirst  is 
excessive ;  nausea  and  vomiting  are  not  usually  present ;  and  the 
abdomen  is  often  flat  and  resistant.  In  severe  cases  there  is  marked 
prostration,  with  a  frequent  pulse,  and  rapid  emaciation. 

If  the  case  is  of  moderate  severity,  in  7  or  8  days  the  stools  become 
less  frequent  and  less  bloody,  the  mucus  diminishes,  brownish  shreds 
of  necrosed  mucous  membrane  may  be  found,  faecal  matter  makes  its 
appearance,  and  the  stools  gradually  assume  a  normal  character. 
While  the  milder  forms  of  the  disease  terminate  in  1  week,  the 
severer  types  endure  for  at  least  4  weeks  before  convalescence  is 
established. 

(2)  Amoebic  (Tropical)  Dysentery. — The  invasion  may  be  sudden, 
usually  gradual,  beginning  with  a  moderate  diarrhoea.  There  is 
slight  fever  (which  may  be  entirely  absent),  nausea  and  vomiting 
are  uncommon,  and  abdominal  griping  and  tenesmus  present  only  at 
the  onset.  The  stools  are  at  first  mucous  and  bloody,  but  later 
become  fluid  and  yellowish  gray,  containing  mucus  and  at  times 
blood,  and  vary  from  6  to  12  in  24  hours.  The  diarrhoea  is  some- 
what characteristic  in  that  it,  although  persistent,  alternately  remits 
and  relapses  at  irregular  intervals.  There  is  a  steady  loss  of  strength 
and  weight.  If  complications  do  not  occur,  the  disease  lasts  from  6 
to  12  weeks ;  convalescence  is  slow  because  of  weakness  and  anaemia, 
relapses  are  frequent,  and  the  disease  is  prone  to  become  chronic. 

(3)  Diphtheritic  Dysentery. — This  form  of  the  disease,  in  which 
there  may  be  necrosis  and  ulceration  of  the  mucosa  of  the  colon, 
with  the  formation  of  a  more  or  less  marked  croupous  exudate  or 
pseudo-membrane,  is  not  uncommon.  It  may  be  primary  or  sec- 
ondary. 

In  the  rare  primary  cases  the  disease  is  usually  acute  and  of  sud- 
den onset,  with  extreme  prostration,  delirium,  abdominal  pain,  ten- 
derness and  distention,  frequent  stools,  and  high  fever.  This  condi- 
tion may  be  mistaken  for  typhoid  fever. 

The  secondary  form  is  more  frequent,  and  is  found  as  an  inter- 


702  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

current  and  often  terminal  event  in  chronic  nephritis,  chronic  car^ 
diac  disease,  pulmonary  tuberculosis,  and  in  various  cachexise,  as  well 
as  in  certain  acute  ailments,  especially  typhoid  fever  and  pneumonia. 
The  intestinal  symptoms  are  slight,  simply  a  moderate  diarrhoea.  The 
stools  vary  from  3  to  4  daily,  are  often  copious  and  weakening,  and 
at  first  may  contain  a  little  mucus  and  blood.  There  is  little,  if  any, 
tormina  or  tenesmus. 

(4)  Chronic  Dysentery. — Usually  a  sequel  of  an  acute  attack, 
except  in  the  amoebic  variety,  which,  from  its  beginning,  may  be 
subacute  and  tend  to  chronicity.  The  symptoms  are  not  especially 
characteristic.  The  stools,  varying  from  4  to  12  or  more  in  34 
hours,  may  be  fluid  and  frothy,  or  semifluid,  yellowish  or  brown, 
occasionally  containing  mucus  and  undigested  food,  rarely  blood, 
pus,  or  necrotic  shreds ;  constipation  may  alternate  with  diarrhoea ; 
and  acute  exacerbations  are  not  uncommon.  Except  during  the 
exacerbations  tormina  and  tenesmus  are  rarely  present.  There  is 
usually  tenderness  along  the  course  of  the  colon,  often  flatulence ; 
the  tongue  is  red  and  glazed,  or  dry  and  fissured;  and  the  loss  of 
flesh  and  the  anaemia  are  extreme. 

Complications  and  Sequelae. — Hepatic  abscess  {q.  v.),  per- 
haps with  a  secondary  abscess  of  the  lung,  is  the  most  frequent  and 
gravest  complication,  occurring  as  a  rule  only  in  the  amoebic  variety 
and  in  the  tropics  (20  per  cent).  In  cases  of  amoebic  dysentery  in 
this  country  its  frequency  does  not  exceed  3  per  cent.  Local  peri- 
tonitis by  extension  may  occur,  or  an  ulcer  may  perforate,  causing, 
according  to  its  location,  perityphlitis,  or  periproctitis.  There  may 
be  during  long-continued  and  severe  cases,  or  as  sequelae,  pleurisy, 
pericarditis,  endocarditis,  painful  and  swollen  joints,  pylephlebitis, 
oedema  (due  to  anaemia),  chronic  nephritis,  and  paraplegia  (due  to 
neuritis).  The  debility  of  chronic  dysentery  predisposes  to  tubercu- 
losis and  pneumonia,  and  occasionally  to  corneal  ulceration.  Any 
form  of  dysentery  may  leave  the  patient  with  impaired  digestion 
and  a  liability  to  diarrhoea.     Dysentery  and  malaria  may  coexist. 

Differential  Diagnosis. — In  catarrhal  dysentery  the  cardinal 
symptoms  are  the  frequent  stools,  composed  of  blood  and  mucus, 
and  the  tenesmus.  In  ammhic  dysentery  the  course  of  the  disease 
is  characteristically  slow,  irregular,  and  chronic,  presenting  remis- 
sions and  exacerbations;  the  pathognomonic  test  is  the  finding  of 
the  amoebae  in  the  stools,  or  in  the  sputum  if  an  hepatic  abscess  has 
perforated  into  the  lung.  The  existence  of  the  secondary  dipJitlieritic 
variety  may  be  suspected,  but  the  diagnosis  is  generally  made  at 
autopsy.  The  primary  acute  diphtheritic  variety  is  not  seldom  mis- 
taken for  typhoid  fever  (see  (4)  following).     Chronic  dysentery  is 


DYSENTERY— CHOLERA  ASIATICA  703 

difficult  to  distinguish  from  chronic  diarrhoea,  but  the  dysenteric 
character  of  the  symptoms  (tormina,  tenesmus,  bloody  and  mucoid 
stools)  in  the  initial  attack,  and  during  the  exacerbations  as  well, 
may  establish  the  diagnosis. 

Dysentery  is  to  be  separated  from  : 

(1)  DiarrhoBa. — The  absence  of  tenesmus  and  stools  composed 
purely  of  mucus  and  blood  are  sufficient  for  the  discrimination. 

(2)  Local  Affections  of  the  Rectum.— Cancer  or  syphilitic  disease 
of  the  rectum,  or  inflamed  and  strangulated  hemorrhoids,  may  cause 
tenesmus  and  bloody,  mucoid  discharges,  but  the  history  and  a 
physical  examination  of  the  rectum  will,  as  a  rule,  readily  determine 
the  cause  of  the  symptoms. 

(3)  Intussusception. — In  this  condition,  although  defecation  may 
be  frequent  and  tenesmic,  there  is  usually  persistent  and  increasing 
vomiting,  the  stools  are  bloody  rather  than  mucoid,  laxatives  are  not 
effectual,  fever  is  not  an  early  symptom,  and  examination  of  the 
abdomen  may  reveal  a  tumour. 

(4)  Typhoid  Fever. — In  this  disease  the  fever  does  not  rise  so 
rapidly  and  to  such  a  height  as  in  primary  diphtheritic  dysentery ; 
the  intestinal  symptoms  are  less ;  and  the  stools  are  rarely  bloody. 
Moreover,  in  dysentery  the  spleen  is  not  enlarged,  the  rose  rash  is 
absent,  and  a  positive  Widal  reaction  is  not  obtained. 

Prognosis. — In  the  catarrhal  form  recovery  is  the  rule.  In  the 
amcehic  form  the  mortality  varies ;  in  epidemics  during  campaigns  in 
the  tropics  it  rises  to  70  or  80  per  cent,  while  occasional  cases  in 
civil  life  and  temperate  zones  give  a  death  rate  of  5  or  6  per  cent 
only.  In  the  diphtheritic  forms  the  prognosis  for  life  is  unfavour- 
able. In  dysentery  death  usually  results  from  exhaustion.  The 
symptoms  which  justify  a  bad  prognosis  are  a  dry  tongue,  feeble  and 
rapid  pulse,  delirium,  stupor,  and  evidences  of  collapse. 

XX.    CHOLERA    ASIATICA 

Symptoms. — This  disease — due  to  the  comma  bacillus — ^has  an 
incubation  period  of  from  2  to  5  days. 

(1)  Stage  of  Invasion.— Commonly  there  is,  during  this  period, 
slight  diarrhoea,  and  colicky  abdominal  pain,  with  headache,  mental 
depression,  perhaps  nausea  and  vomiting.  These  symptoms  may 
progress  no  further  (cholerine),  but  usually  the  two  other  stages  of 
the  disease  supervene,  viz.,  collapse,  and  reaction. 

(2)  Stage  of  Collapse. — This  may  come  on  without  prodromata, 
but  ordinarily  an  existing  looseness  of  the  bowels  is  suddenly  suc- 
ceeded by  frequent  copious  stools,  which  soon  lose  their  faecal  charac- 
ter and  become  liquid,  serous,  or  "  rice-water  "  discharges,  usually 


704  DIAGNOSIS,   DIRECT   AND  DIFFERENTIAL 

passing  without  pain,  sometimes  with  tormina  and  tenesmus.  Per- 
sistent and  severe  vomiting  soon  appears.  The  vomitus  is  copious, 
and  becomes  serous,  like  the  stools.  Thirst  is  excessive,  the  tongue 
is  furred  and  dry,  and  recurring  and  severely  painful  cramps  in  the 
legs  and  feet  constitute  an  early  symptom.  The  patient  becomes 
rapidly  exhausted  or  collapsed.  The  skin  is  cold,  shrivelled,  and 
wet;  the  lips  and  finger  tips  are  profoundly  cyanotic,  the  face  is 
gray,  pallid,  and  pinched,  the  eyeballs  recede,  and  the  cheeks  become 
sunken.  While  the  internal  temperature  (by  rectum)  may  be  ele- 
vated (102°  to  104°),  the  axillary  or  mouth  temperature  may  drop 
to  95°  or  below.  The  voice  is  husky  or  whispering,  and  there  may 
be^  mental  dulness  merging  into  stupor  and  coma,  although  con- 
sciousness is  often  preserved  to  the  close.  The  pulse  becomes  feeble, 
running  or,  in  bad  cases,  imperceptible  at  the  wrist.  The  urine  is 
scanty,  albuminous,  and  contains  tube  casts ;  complete  suppression 
may  occur.  This  stage  lasts  from  a  few  hours  to  2  days.  If  death 
does  not  occur  during  the  collapse,  the  disease  passes  into  the 

(3)  Stage  of  Reaction. — The  skin  becomes  warm,  the  flow  of  urine 
is  re-established,  vomiting  ceases,  the  stools  become  less  frequent 
and  more  faecal  in  character,  the  pulse  strengthens,  the  fever  departs, 
and  in  favourable  cases  convalescence  begins. 

Varieties  and  Terminations. — The  attack  may  be  mild 
(cholerine),  with  nausea,  griping,  copious  stools,  and  cramps,  but  with 
very  slight  collapse  symptoms,  recovery  occurring  before  the  graver 
conditions  develop.  In  the  severest  cases  the  patient  is  overwhelmed 
and  dies  in  a  few  hours,  before  the  onset  of  diarrhoea  (cholera  sicca), 
or  perishes  just  before  the  stage  of  collapse.  The  stage  of  reaction 
and  apparent  convalescence  may  be  interrupted  by  a  relapse,  during 
which  death  occurs ;  or  the  symptoms  may  merge  into  those  of 
cholera  typhoid — i.  e.,  fever,  dry,  brown  tongue,  feeble  and  rapid 
pulse,  delirium,  coma,  and  death.  There  may  be  erythematous, 
macular,  or  purpuric  rashes. 

Complications  and  Sequelae. — Acute  nephritis,  anuria,  and 
uraemia ;  pneumonia  and  pleurisy ;  diphtheritic  inflammations  of  the 
mucous  membranes  (colon,  pharynx,  genitals)  are  not  uncommon ; 
suppurative  parotitis  (not  uncommon)  ;  ulceration  of  the  cornea ; 
abscesses  in  various  parts,  erysipelas,  local  gangrene  (rare) ;  and, 
during  convalescence,  muscular  cramps  in  arms  and  legs. 

Differential  Diagnosis. — During  an  epidemic  the  diagnosis  is 
readily  made.  Sporadic  cases  may  be  mistaken  for  cholera  morbus 
(or  nostras),  which  in  the  severest  form  may  present  exactly  the  same 
symptoms  as  Asiatic  cholera.  A  positive  differentiation  is  possible 
only  by  the   microscope    and    cultures,   whereby   the   presence   or 


CHOLERA— BUBONIC  PLAGUE— MALARIA  706 

absence  of  the  comma  bacillus  is  ascertained.  Attacks  resembling 
Asiatic  cholera  may  arise  from  poisoning  by  arsenic,  bichloride  of 
mercury,  antimony,  or  other  metals,  but  the  history  and,  if  sus- 
pected, the  chemical  tests  of  the  stomach  contents  usually  serve  for 
differentiation. 

Prognosis. — The  mortality  varies  from  20  to  80  per  cent,  but 
the  prognosis  must  always  be  guarded.  The  chronically  debilitated, 
the  alcoholic,  the  very  old,  and  the  very  young  show  a  large  mor- 
tality. 

XXI.  BUBONIC    PLAGUE 

Sjnnptoms. — This  disease — caused  by  the  Bacillus  pestis — has 
an  incubation  period  varying  from  2  to  5  days. 

The  initial  symptoms  are  headache,  backache,  muscular  stiffness, 
vertigo,  mental  depression  and  uneasiness,  rapid  respiration,  and 
perhaps  epistaxis  or  haemoptysis.  .  In  24  hours,  more  or  less,  there 
is  chilliness  or  a  chill,  and  the  temperature  rises  to  104°  to  106°, 
with  delirium,  great  thirst,  dry,  brown  tongue,  and  oftentimes  nausea 
and  vomiting.  Ecchymoses  and  petechial  spots  are  very  commonly 
present.  About  the  3d  to  the  5th  day  the  inguinal  glands  become 
swollen  (buboes),  less  commonly  the  axillary,  cervical,  and  popliteal, 
and  may  either  undergo  resolution  or  proceed  to  suppuration  (fa- 
vourable) or  gangrene  (rare).  Carbuncles  may  appear,  especially  on 
the  legs,  gluteal  regions,  or  back.  In  the  severest  cases  haematenie- 
sis,  intestinal  hemorrhages,  and  haematuria  may  occur. 

Varieties. — There  are  3  varieties :  the  mild  form^  with  slight 
fever  and  constitutional  symptoms  (rarely  fatal) ;  the  ordinary 
bubonic  forin,  with  glandular  swellings  and  severe  disturbance  (may 
recover) ;  and  the  malignant  form^  usually  without  glandular  enlarge- 
ments, the  poison  localizing  itself  in  the  lungs,  kidneys,  brain,  stom- 
ach, or  intestines,  or  acting  as  a  general  toxaemic  agent  without 
localization  (almost  always  fatal).  The  mortality  is  enormous,  70  to 
95  per  cent. 

XXII.  MALARIAL    FEVER 

I.  Vaeieties  an"d  Symptoms. — Four  varieties  of  malarial  poi- 
soning are  recognised :  intermittent  malarial  fever,  remittent  mala- 
rial fever,  pernicious  malarial  fever,  and  the  malarial  cachexia.  For 
a  description  of  the  life  history  and  the  method  of  detection  of  the 
causative  organism  {Plasmodium  malarim),  see  page  587. 

Intermittent  Malarial  Fever.— (a)  Symptoms.— A  paroxysm 
of  intermittent  fever  may  be  divided  into  3  parts,  chill,  fever,  and 
sweating. 


706  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

(I)  The  Chill. — Premonitory  symptoms  are  headache,  languor, 
yawning,  gastric  unease,  perhaps  nausea  and  vomiting.  The  patient 
begins  to  feel  cold,  and  soon  shivers  and  shakes  more  or  less  vio- 
lently, the  teeth  chatter,  and  the  face  and  finger  nails  are  cyanotic. 
Although  the  skin  is  cool  and  pallid,  the  thermometer  in  the  mouth 
or  rectum  may  rise  to  105°  or  106°.  The  pulse  is  rapid,  small  and 
hard.     In  from  10  minutes  to  1  hour  the  cold  stage  is  succeeded  by : 

(3)  The  Fever^  or  Hot  Stage. — The  coldness  disappears,  the  skin 
becomes  excessively  hot  and  reddened,  the  face  is  flushed,  the  eyes 
injected,  there  is  a  throbbing  headache  and,  possibly,  active  delir- 
ium. The  pulse  is  full  and  bounding.  The  fever  may  reach  its 
maximum  during  the  chill,  and  in  any  case  does  not  continue  to  rise 
very  rapidly.     In  from  3  to  6  hours  the  fever  falls  by  crisis. 

(3)  Siveating  Stage. — As  the  temperature  descends  the  patient 
begins  to  sweat,  slightly  or  profusely,  first  about  the  head  and  neck, 
finally  from  head  to  feet ;  the  headache  disappears ;  and  in  2  or  3 
hours  he  feels  comfortable  and  may  fall  asleep. 

The  duration  of  the  entire  paroxysm  varies  as  a  rule  from  8  to 
13  hours. 

Types  of  Intermittency.— (See  Charts  II  and  III,  page  103.) 

(1)  Tertian. — When  1  group  of  the  tertian  parasites  is  present 
the  paroxysm  is  tertian — i.  e.,  recurs  every  other  day ;  with  3  groups 
it  is  quotidian,  recurring  every  day — i.  e.,  double  tertian.  In  the 
Northern  and  Middle  States  the  double  tertian  is  the  type  most 
commonly  encountered. 

(3)  Quartan. — When  1  group  of  the  quartan  parasite  is  present 
the  paroxysm  occurs  every  4th  day  (quartan  type);  with  3  groups 
the  paroxysms  occur  3  days  in  succession,  the  3d  day  none  ;  with  3 
groups,  daily  or  quotidian  paroxysms  occur  as  in  the  double  tertian. 

iEstivo-autumnal  Fevers. — Symptoms. — (1)  Of  Remittent 
Malarial  Fever. — This  type  of  fever  is  caused  by  the  aestivo-autumnal 
parasite  which  may  not  only  occur  in  ill-defined  and  multiple  groups, 
but  has  as  well  an  uncertain  and  probably  varying  period  of  develop- 
ment. Consequently  the  type  of  the  fever  is  often  very  irregular. 
The  paroxysms  may  be  of  an  intermittent  quotidian  periodicity,  but 
are  longer  (30  hours)  than  with  the  tertian  or  quartan  infection,  and 
exhibit  a  tendency  to  anticipate — i.  e.,  the  intervals  between  the 
paroxysms  grow  shorter.  Chill  is  often  absent,  and  the  fever  rises 
and  falls  more  slowly.  In  the  severer  forms  of  aestivo-autumnal  fever 
the  paroxysms  lengthen,  each  one  treading  closely  upon  the  heels  of 
that  which  precedes  it,  until  the  fever  becomes  almost  continuous 
(103°  to  103°),  with  slight  remissions.  Sharp  intercurrent  paroxysms 
of  fever  (105°  to  106°),  perhaps  with  chills,  may  occur. 


MALARIAL  FEVER  707 

In  a  case  of  average  severity  the  Ist  day  of  the  disease  begins 
with  a  chill  or  chilliness,  followed  by  fever,  which  remits  with 
sweating  usually  in  the  early  morning  of  the  2d  day,  to  be  followed 
by  another  paroxysm  in  the  afternoon.  The  face  is  flushed,  the 
pulse  full  and  bounding  but  seldom  dicrotic,  the  tongue  is  furred, 
moderate  jaundice  is  often  present,  there  is  a  bronchitis,  and  slight 
delirium  may  become  manifest.  In  the  mildest  cases-  the  symptoms 
are  light,  and  the  fever  ceases  in  about  7  days ;  in  others  it  lasts 
from  10  days  to  2  weeks ;  in  the  severest  attacks  the  temperature  is 
almost  continuously  high,  and  the  disease  may  be  protracted  for  3 
or  4  weeks  (especially  if  quinine  is  not  given),  simulating  typhoid 
fever ;  or  the  characters  of  the  pernicious  form  may  appear, 

(2)  Symptoms  of  Pernicious  Malarial  Fever. — This  type  of  mala- 
rial fever  is  also,  like  the  remittent  form,  due  to  the  aestivo -autumnal 
parasite.  It  is  rare  in  the  temperate  zone.  The  symptoms  of  the 
various  forms  are  due  to  a  more  or  less  overwhelming  toxaemia. 
Three  varieties  of  the  pernicious  form  are  recognised :  algid,  coma- 
tose, and  haemorrhagic. 

Algid  Form. — Sudden  onset  of  vomiting,  often  purging  or  choleri- 
form  diarrhoea,  great  prostration  or  symptoms  of  collapse,  coldness, 
perhaps  with  no  distinct  chill,  and  a  normal  or  even  subnormal  tem- 
perature, are  the  symptoms  of  the  algid  form.  There  is  oliguria, 
sometimes  anuria.  After  persisting  for  several  days,  with  slight 
rises  of  temperature,  the  patient  may  die  from  profound  exhaus- 
tion. 

Comatose  Form. — The  disease  begins  abruptly,  with  high  fever, 
and  either  active  delirium  or  a  rapidly  developing  coma.  The 
patient  may  perish  in  the  attack,  or  more  commonly  regain  con- 
sciousness in  12  to  24  hours.     Kecurrent  attacks  are  often  fatal. 

Hemorrhagic  Form. — There  may  be  cutaneous  ecchymoses,  epis- 
taxis,  bleeding  from  the  gums,  haematemesis,  intestinal  hemorrhage, 
metrorrhagia,  and  haematuria.  Jaundice  is  very  frequent.  The 
hemorrhagic  cases  often  begin  with  a  severe  chill,  followed  by  high 
fever,  and  perhaps  delirium.  The  urine  may  contain  albumin  and 
casts — granular,  epithelial,  and  blood.  Anuria  and  uraemia  may 
occur.  Haematuria  is  the  most  common  of  the  hemorrhagic  features 
of  malaria,  sometimes  reaching  epidemic  dimensions,  and  not  infre- 
quently causing  death.  It  is  mainly  a  haemoglobinuria  (p.  636).  The 
hsemoglobinuria  may  be  preceded  by  a  severe  chill,  fever,  and  sweat ; 
or  a  mild  malarial  paroxysm ;  or  occur  without  notable  fever.  It 
may  be  intermittent ;  or  continuous,  with  remissions. 

Malarial  Cachexia. — In  the  majority  of  cases  this  condition 
is  a  legacy  from  repeated  attacks  of  some  variety  of  the  acute  malarial 


708  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

fevers ;  repeated  either  from  reinfection  or  from  lack  of  proper  and 
energetic  treatment.  In  excessively  malarial  regions  the  preceding 
febrile  paroxysms  may  have  been  slight. 

Symptoms. — The  cardinal  symptoms  are  anaemia  and  enlargement 
of  the  spleen,  sometimes  also  of  the  liver.  The  patient  is  pale  and 
thin,  the  face  is  of  a  dirty  yellow  tint,  sallow  and  cachectic.  There 
may  be  no  fever,  or  the  temperature  vary  irregularly  from  99.5°  to 
103".  The  red  cells  may  sink  to  but  1,000,000  to  the  cubic  milli- 
metre. The  spleen  is  greatly  enlarged  and  indurated.  Dyspnoea, 
palpitation,  oedema  of  the  feet  and  ankles,  headaches,  and  neuralgias 
are  common  because  of  the  anaemia.  Chronic  gastro-intestinal 
catarrh,  vertigo,  insomnia,  tremor,  paraplegia  (excessively  rare), 
slight  bronchitis,  and  painful  stiffness  of  the  muscles  and  joints 
may  be  present.  Hemorrhages  (retinal,  haematuria,  haematemesis, 
etc.)  may  occur. 

II.  Complications  of  Malarial  Fever. — Anders  states  that 
complications  occur  in  about  10  per  cent  of  malarial  cases.  They 
are,  in  order  of  freqiiency,  enteritis,  nephritis,  rheumatism,  typhoid 
fever  (but  8  times  in  1780  cases),  lobar  pneumonia,  jaundice,  and 
dysentery. 

III.  Differential  Diagnosis  of  Malarial  Fever. — The  only 
indubitable  proof  of  the  presence  of  malaria  lies  in  the  discovery  of 
its  parasite  in  the  blood.  There  is  no  doubt  that  the  term  "  malaria  " 
has  been  and  is  used  to  cover  a  multitude  of  diagnostic  sins,  an  eva- 
sion which  is  perhaps  pardonable  in  view  of  the  technical  skill  and 
experience  which  is  requisite  to  give  value  to  a  negative  result  of  a 
blood  examination  for  the  plasmodium.  It  is  a  good  practical  rule 
to  suspect  malaria,  but  to  be  extremely  chary  in  making  a  positive 
diagnosis  unless  the  symptoms  are  absolutely  typical,  and  perhaps 
not  even  then  without  the  finding  of  the  haematozoon.  That  an 
intermittent  fever  is  not  malarial  may  be  affirmed  with  an  almost 
absolute  certainty  if  it  does  not  promptly  cease  when  quinine  is 
given  in  sufficient  quantity  (20  to  30  grains  daily). 

The  characters  of  the  blood  in  malaria  are  worthy  of  special 
notice.  Owing  to  the  fact  that  the  red  corpuscles  are  the  hosts  of 
the  Plasmodia  there  is  an  extensive  destruction  of  haemoglobin  and 
a  diminution  in  the  number  of  the  red  cells,  with  consequent 
anaemia — the  extent  of  the  latter  depending  upon  the  duration  and 
continuity  of  the  malarial  poisoning.  The  rapid  supervention  of 
anaemia  is,  indeed,  very  characteristic  of  this  disease.  The  leuco- 
cytes are  as  a  rule  diminished  in  number  and  some  are  pigmented. 
In  certain  cases  the  blood  has  the  characters  of  pernicious  anaemia 
(p.  595).     The  great  frequency  of  herpes  in  malaria  is  notable. 


MALARIAL  FEVER  709 

Differential  Diagnosis  of  Intermittent  Fever. — It  is  of 

great  importance  to  bear  in  mind  that  various  conditions  are  accom- 
panied by  an  intermittent  fever.  The  simple  remembrance  of  this  fact 
will  in  many  cases  prevent  mistakes  in  diagnosis.  Intermittent  fever 
requires  differentiation  mainly  from  the  following  conditions  : 

(1)  Tuberculosis. — The  chills  and  intermittent  fever  sometimes 
present  in  beginning  pulmonary  tuberculosis  are  not  arrested  by 
quinine,  the  plasmodium  is  absent,  and  the  physical  signs  or  the 
finding  of  the  tubercle  bacillus  will  serve  for  differentiation. 

(2)  Pymmia  or  Concealed  Suppurations. — In  this  disease  the  chills, 
fever,  and  sweats  occur  at  irregular  intervals ;  there  is  more  prostra- 
tion, a  marked  leucocytosis  exists,  the  malarial  organism  is  not  found, 
and  recurrences  are  not  prevented  by  quinine.  Moreover,  there  is 
often  some  local  lesion  which  will  indicate  the  pyaemic  nature  of  the 
intermittent  pyrexia. 

(3)  Pyelitis. — This  may  closely  simulate  intermittent  fever,  but 
the  presence  of  pyuria,  leucocytosis,  and  perhaps  of  lumbar  pain  and 
tenderness  and  swelling  of  the  kidney,  together  with  the  results  of 
the  blood  examination  and  the  therapeutic  test,  will  declare  the  pye- 
litic  origin  of  the  fever. 

(4)  Ulcerative  Endocarditis. — In  addition  to  the  history,  clinical 
symptoms,  and  physical  signs,  the  blood  examination  shows  the 
absence  of  the  plasmodium  and  the  presence  of  a  leucocytosis,  and 
quinine  does  not  arrest  the  chill  and  fever. 

(5)  Gallstones. — The  chill  and  intermittent  pyrexia  sometimes 
associated  with  cholelithiasis  may  usually  be  distinguished  from  ma- 
laria by  the  history,  the  characteristic  hepatic  colic,  the  tender  and 
perhaps  palpable  gall  bladder,  the  frequent  jaundice,  and  the  abseiice 
of  the  Plasmodium.  , 

Differential  Diagnosis  of  Remittent  Fever  is  to  be  made 
from  t}^hoid  fever  (p.  665),  and  of  Pernicious  Malarial  Fever 
from  yellow  fever  (p.  700).  The  algid  form  of  pernicious  malaria 
may  resemble  Asiatic  cholera,  but  the  absence  of  an  epidemic,  the 
finding  of  the  plasmodium,  and  finally,  in  suspected  cases,  the  non- 
discovery  of  the  comma  bacillus  in  the  stools,  will  exclude  the  latter. 

IV.  Prognosis  of  Malarial  Fever. — In  intermittent  fever,  al- 
ways favourable  with  proper  treatment ;  in  remittent  fever,  usually 
favourable  with  proper  treatment,  but  death  may  occur  in  very  severe 
cases  from  exhaustion,  or  haematuria,  anuria,  and  uraemia ;  in  per- 
nicious malarial  fever  the  mortality  runs  from  20  to  25  per  cent. 


47 


710  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 


XXm.    RHEUMATIC    FEVER 

Symptoms. — (1)  Acute  Rheumatic  Fever. — There  are  wide  varia- 
tions in  the  intensity  of  the  symptoms.  The  attack  may  be  preceded 
by  malaise,  indefinite  joint  pains,  and  sore  throat,  especially  tonsilli- 
tis. In  the  majority  of  cases  the  onset  is  sudden,  with  slight  chilli- 
ness, rapid  rise  in  temperature  (rarely  over  103°),  and  coincident 
joint  symptoms.  The  affected  articulations,  usually  the  wrists,  elbows, 
ankles,  or  knees,  become  swollen,  hot,  reddened,  tender,  and  excess- 
ively painful  upon  movement.  Generally  2  or  more  joints  are  in- 
volved, the  inflammation  leaving  one  and  simultaneously  appearing 
in  another.  Rarely  one  joint  alone  is  affected.  Xo  joint  is  exempt  in 
severe  cases,  but  ordinarily  the  vertebral,  sterno-clavicular,  and  pha- 
langeal articulations  escape.  The  swelling  affects  mainly  the  peri- 
articular tissues,  and  there  is  rarely  evidence  of  much  fluid  in  the 
joint.  The  muscles  in  severe  cases  may  be  tender  and  rigid,  and  the 
tendinous  sheaths  of  the  wrists  and  ankles  may  be  involved  and 
cause  considerable  swelling.  Profuse  sweats,  at  first  acid,  are  char- 
acteristic ;  the  urine  is  scanty,  loaded  with  urates,  and  may  contain 
albumin ;  the  bowels  are  constipated,  and  the  tongue  is  heavily 
furred.  Sudamina  and  a  red  miliary  eruption  are  of  frequent  occur- 
rence. Anaemia  develops  very  rapidly,  and  there  is  a  marked  leucocy- 
tosis.  The  fever  is  very  irregular,  rising  and  falling  in  correspond- 
ence with  the  severity  and  extent  of  the  joint  inflammations.  Free 
sweating  lowers  the  temperature. 

The  duration  of  the  disease  varies  from  a  few  days  to  6  or  8 
weeks.  In  the  protracted  cases  short  periods  of  improvement  alter- 
nate with  relapses. 

(2)  Subacute  Rheumatism. — This  resenables  the  acute  form,  except 
that  all  the  symptoms  are  of  a  milder  character;  the  fever  does  not 
exceed  101°,  the  joint  inflammations  are  less  intense,  and  not  so 
many  articulations  are  involved.  The  subacute  cases  are  often  pro- 
tracted for  weeks  or  months,  and  may  ultimately  merge  into  a  chronic 
type  of  the  disease. 

Complications  and  Sequelae. — The  most  common  and  impor- 
tant complication  is  an  endocarditis  (rarely  of  the  ulcerative  form), 
the  frequency  of  which  is  variously  estimated  at  from  25  to  40  per 
cent,  or  even  more,  of  all  cases.  The  liability  increases  in  propor- 
tion to  the  number  of  attacks.  The  valve  most  frequently  affected 
is  the  mitral,  and  the  importance  and  seriousness  of  this  complica- 
tion depends  upon  the  progressive  sclerotic  and  deforming  changes 
of  the  valve  segments  which  it  initiates.  Pericarditis,  fibrinous, 
serofibrinous,  or  purulent  (in  children),  sometimes  attended  by  de- 


RHEUMATIC  FEVER  YH 

lirium,  may  .occur,  so  also  may  myocarditis.  Other  complications  are 
pneumonia,  pleurisy ;  hyperpyrexia  (106°  to  110°),  with  or  without  de- 
lirium, and  attended  by  great  prostration,  rapid  and  feeble  pulse,  and 
final  stupor ;  cerebral  complications — e.  g.,  delirium  with  or  without 
hyperpyrexia  or  pericarditis,  convulsions  (not  common),  coma  (urae- 
mic,  hyperpyrexia!,  toxaemic),  chorea,  and  very  rarely  meningitis. 
Small  firm,  painless,  and  rapidly  developing  subcutaneous  nodules, 
attached  to  the  tendons  and  fasciae,  especially  of  the  fingers,  wrists, 
back  of  elbow,  patellae,  and  malleoli,  are  sometimes  found  in  the 
course  of  the  disease  or  during  convalescence.  They  may  last  for 
weeks  or  months.  Urticaria,  purpura,  erythema  nodosum,  and  ex- 
tensive ecchymoses  may  be  present. 

Differential  Diagnosis. — The  cardinal  symptoms  of  rheu- 
matic fever  are  the  sudden  onset  of  a  polyarthritis,  flitting  from 
joint  to  joint,  with  fever  and  sweats,  and  the  rapid  occurrence  of 
anaemia.  Ordinarily  the  diagnosis  is  readily  made,  but  in  some  in- 
stances the  following  affections  require  to  be  differentiated.  (See 
also  page  93.)  In  children  the  arthritic  symptoms  may  be  very 
slight,  while  endocarditis,  which  is  much  more  common  than  in 
adults,  may  in  consequence  of  the  lightness  of  the  other  symptoms 
be  entirely  overlooked. 

(1)  PycBmia  with  Suppurative  Arthritis. — The  irregular  chills 
and  fever,  the  greater  prostration,  the  slight  jaundice,  the  fact  that 
the  joint  symptoms  do  not  shift  from  one  articulation  to  another, 
and  that  the  joint  as  a  rule  proceeds  to  suppuration,  together  with 
the  finding  of  a  purulent  focus,  are  in  favour  of  pyaemia.  The  acute 
arthritis  of  nursing  infants  (usually  pyaemic,  or  due  to  gonorrhoea! 
ophthalmia  or  vaginitis)  is  generally  limited  to  one  joint  (knee  or 
hip),  and  rapidly  passes  to  suppuration.  Acute  osteomyelitis  is  usu- 
ally located  in  the  epiphysis  of  the  bone  rather  than  in  the  joint, 
and  the  greater  severity  of  both  local  and  constitutional  symptoms 
will  aid  in  separating  it  from  rheumatism. 

(2)  Gonorrhceal  Rheumatism  {Arthritis). — This  is  frequently  mon- 
articular (often  involving  the  knee)  from  the  beginning,  the  consti- 
tutional symptoms  are  generally  not  pronounced  in  comparison  with 
the  local  signs,  it  is  very  intractable,  and  there  is  a  history  of  an 
immediately  preceding  gonorrhoea. 

(3)  Gout. — In  typical  cases  of  this  disease  the  involvement  of  the 
great  toe  and  the  absence  of  decided  fever  and  sweats  will  differen- 
tiate it  from  rheumatism.  But  when,  as  is  not  uncommon,  several 
of  the  joints  are  affected,  it  may  be  very  difficult  to  make  a  positive 
diagnosis.  Gout  usually  occurs  later  in  life  than  rheumatic  fever, 
and  tophi  may  be  found. 


712 


DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 


Prognosis. — Favourable  with  regard  to  life,  but  a  certain  num- 
ber of  cases  become  chronic,  and  endocarditis  often  lays  the  founda- 
tion for  subsequent  irremediable  valvular  disease. 

XXIV.    LOBAR    PNEUMONIA 

In  a  very  large  proportion  of  cases  of  lobar  pneumonia  the  Diplo- 
coccus  pneumonim  (or  lanceolatus)  is  present ;  in  a  small  number, 
other  organisms,  especially  the  streptococcus,  are  found. 

Symptoms  and  Physical  Sign^s. — Typical  Cases. — In  a 
typical  case  the  onset  is  abrupt,  with  a  severe  and  often  prolonged 
chill,  followed  by  headache,  general  aching,  and  a  rapid  rise  of  tem- 
perature to  104°  or  105°.  Very  soon  a  short,  dry,  restrained,  and 
distressing  cough  sets  in,  with  a  sharp,  stabbing  pain  near  the  nipple 

or  in  the  axilla  of  the 
affected  side.  The  respi- 
rations become  rapid  (30 
to  60  in  adults,  80  or  over 
in  infants),  with  an  expir- 
atory grunt,  and  the  alaB 
of  the  nose  dilate  with 
each  inspiration.  The 
face  is  flushed,  and  there 
is  often  a  circumscribed 
redness  upon  the  cheek 
of  the  affected  side.  The 
expectoration  becomes 
rusty  or  blood-stained, 
and  is  excessively  thick 
and  tenacious.  The  pulse 
is  rapid  (100  to  120),  full, 
and  bounding,  and  the 
normal  pulse-respiration 
ratio  of  1  to  4  becomes 
1  to  3,  1  to  2,  or  even  1 
to  1.  Herpes  labialis  is  more  frequent  in  pneumonia  than  in  any 
other  disease  (12  to  40  per  cent  of  all  cases).  The  tongue  is  furred, 
there  may  be  nausea  and  vomiting,  the  bowels  are  usually  consti- 
pated, and  tympanites  is  not  uncommon.  There  is  in  most  cases  a 
leucocytosis  (12,000  to  50,000).  The  urine  is  scanty,  high  coloured, 
and  often  contains  a  trace  of  albumin.  A  great  diminution  or  entire 
absence  of  the  chlorides  is  a  striking  feature.  The  fever  having 
risen  to  its  maximum,  usually  within  the  first  24  hours,  continues 
high,  with  remissions,  until  the  5th  to  the  10th  day,  when  in  typical 


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Chabt  XXI.— Pneumonia  (lobar)  with  pseudo-crisis 

and  true  crisis. 


LOBAR  PNEUMONIA  713 

cases  it  falls  in  a  few  hours  (5  to  12)  by  crisis  to  normal  or  below 
(97°  to  96°),  with  a  corresponding  drop  in  the  pulse  and  respiration 
(Chart  XXI). 

The  physical  signs  are  modified  by  the  stage  of  the  disease  (en- 
gorgement, red  hepatization,  gray  hepatization). 

(1)  Inspection. — Increased  (compensatory)  motion  of  the  unaf- 
fected side  may  be  observed,  and  confirmed  by  palpation  and  men- 
suration, after  the  disease  is  well  established ;  so  also  may  the  excess- 
ive action  of  the  accessory  muscles  of  respiration. 

(2)  Palpation. — Atter  consolidation  has  occurred,  unless  the  bron- 
chial tubes  are  filled  with  thick  secretion  or  fibrinous  exudate  (which 
may  perhaps  be  removed  by  coughing)  or  pleural  effusion  is  present, 
the  vocal  fremitus  over  the  affected  portion  of  the  lung  is  increased, 
and  a  friction  fremitus  also  may  be  felt. 

(3)  Percussion. — In  the  first  stage  the  note  may  be  somewhat 
high-pitched,  perhaps  hyper-resonant  (Skodaic  resonance),  and  a 
similar  note  may  be  elicited  from  healthy  lung  lying  above  an  area 
of  consolidation.  Wintrich's  change  of  sound  (p.  407)  may  be  found 
with  pneumonia  of  the  apex.  Under  similar  circumstances  the  note 
may  have  a  cracked-pot  quality.  If  the  consolidation  is  deep-seated 
the  resonance  may  simply  be  impaired.  Ordinarily  there  is  marked 
dulness  over  the  solidified  portion  of  the  lung. 

(4)  Anscultation. — In  the  early  stage  the  breath  sounds  are  often 
weak,  and  at  the  end  of  inspiration  the  crepitant  rale  may  be  heard. 
As  engorgement  merges  into  consolidation  the  breath  sounds  become 
broncho-vesicular,  and  finally  intensely  and  typically  bronchial.  If 
the  larger  bronchi  are  plugged,  bronchial  breathing  may  be  absent, 
sometimes  temporarily.  The  voice  sounds,  both  spoken  and  whis- 
pered, are  transmitted  with  great  distinctness,  but  this  also  may  be 
prevented  by  filling  of  the  bronchi. 

During  the  2d  stage  friction  sounds  are  often  heard,  but  no  rales 
may  be  present.  During  the  3d  or  resolving  stage  small  moist  crepi- 
tations {rale  redux),  later  mixed  with  moist  rales  of  all  sizes,  become 
audible. 

Special  Symptoms  and  their  Variations.  —  (1)  The 
patient  often  lies  on  the  affected  side.  Orthopncea  is  not  very 
frequent. 

(2)  The  fever  may  be  very  slight  or  entirely  absent  in  old  persons 
and  chronic  alcoholics.  I  have  seen  cases  of  intense  pneumonic 
infection  with  a  temperature  not  exceeding  100°.  In  a  few  cases  the 
crisis  occurs  on  the  3d  day.  The  termination  may  be  by  lysis,  espe- 
cially in  children ;  and  in  delayed  resolution  the  febrile  movement 
may  last  for  weeks.     A  pseudo-crisis  2  or  3  days  previous  to  the  final 


714  DIAGNOSIS,   DIRECT   AND   DIFFERENTIAL 

fall  is  not  uncommon.     A  rise  just  before  and  just  after  the  true 
crisis  (precritieal  and  post-critical)  is  occasionally  seen. 

(3)  Cough  and  expectoration  are  not  seldom  absent  or  very  slight 
in  infants,  old  people,  topers,  and  those  already  ill  with  some  acute 
infectious,  or  serious  chronic,  illness.  If  violent  cough  persists  after 
the  crisis,  a  pleural  effusion  is  to  be  suspected.  The  sputum  may  be 
bright-red,  rusty,  bright  yellow,  or,  in  adynamic  and  typhoid  cases,  of 
a  dark-brown  colour  (prune-Juice).  It  is  always  very  glutinous  and 
clinging.     Haemoptysis  is  an  uncommon  early  event. 

(4)  Pain  is  absent  if  the  pleura  is  not  involved,  as  in  pneumonia 
affecting  only  the  centre  of  the  lung,  and  is  absent  or  slight  in  apical 
consolidation.  In  children  the  pain  is  almost  always  referred  to  the 
abdomen.  Abdominal  and  epigastric  pain  is  not  rare  in  adults,  often 
exceptionally  severe,  and  is  generally  due  to  involvement  of  the  dia- 
phragmatic pleura  in  pneumonia  of  the  lower  lobes. 

(5)  Tympanites  is  not  uncommon,  and  may  be  so  excessive,  in 
conjunction  with  abdominal  pain,  as  to  suggest  peritonitis  or  appen- 
dicitis.    The  spleen  is  generally  swollen,  occasionally  also  the  liver. 

(6)  The  jo?^fee  in  severe  cases  may  be  dicrotic  ;  or  small  and  rapid; 
or  full  but  soft  ("  gaseous  "),  and  followed  by  serious  cardiac  weak- 
ness. Because  of  the  obstruction  to  the  pulmonary  circulation  the 
right  heart  may  have  an  excessive  amount  of  work  thrown  upon  it, 
and  the  character  of  the  pulse  is  no  indication  of  the  manner  in 
which  the  right  ventricle  is  standing  the  strain.  A  better  criterion 
is  the  character  of  the  pulmonary  second  sound.  If  this  is  accentu- 
ated the  lesser  circulation  is  being  maintained  ;  a  disappearance  or 
weakening  of  this  sound  is  significant  of  right  heart  weakness  and 
dilatation.  An  absent  leucocytosiSy  if  persistent,  is  a  bad  prognostic 
omen,  except  in  very  mild  cases. 

(7)  Symptoms  referable  to  the  nervous  system  are  common.  In 
children  convulsions  frequently  initiate  the  disease ;  and,  also  usu- 
ally in  children,  the  symptoms  may  closely  resemble  those  of  menin- 
gitis and  the  pneumonia  be  undiscovered.  Delirium  occurs  in  the 
adynamic  cases  and  may  be  active  or  maniacal,  especially  in  drunk- 
ards.    Deafness,  not  dependent  on  otitis,  is  not  infrequent. 

Clinical  Vaeieties  of  Pisteumoxia. — The  variations  which  are 
of  more  or  less  clinical  importance  depend  in  part  upon  the  location 
and  extent  of  the  pulmonary  lesions,  but  mainly  upon  differences  in 
the  virulence  of  the  infective  agent  and  the  resisting  power  of  the 
individual. 

(1)  Pneumococcus  Toxmmia  {or  Septicemia). — Under  this  heading 
are  embraced  the  cases  which  have  been  called  adynamic,  low,  or 
typhoid  pneumonia.     The  clinical  picture  is  that  of  a  more  or  less 


LOBAR  PNEUMONIA  715 

profound  and  sudden  blood-poisoning,  with  symptoms  indicating  the 
involvement  of  the  nervous  mechanisms  which  preside  over  the  most 
important  functions  of  the  organism.  The  physical  signs  are  often 
well  marked,  but  may  be  slight.  There  is  delirium  or  stupor,  early 
severe  prostration  and  cyanosis,  and  often  slight  jaundice.  The 
tongue  is  dry  and  brown,  the  pulse  and  respiration  are  usually  rapid, 
tlie  expectoration  prune-juice  or  very  bloody,  the  fever  may  or  may 
not  be  high,  and  subsultus  and  carphologia  may  be  present.  The 
spleen  is  often  palpable,  and  nausea,  vomiting,  tympanites,  and  occa- 
sionally diarrhoea  may  be  present.  This  form  of  the  disease  may  be 
a  mixed  infection  (pneumococcus  plus  streptococcus).  It  occurs 
especially  in  drunkards  and  persons  debilitated  from  previous  dis- 
ease. Rare  cases  are  those  in  which  the  toxaemia  is  so  sudden  and 
overwhelming  that  death  may  occur  in  from  24  to  48  hours. 

(2)  Latent  Pneumonia. — The  characteristic  symptoms  are  hidden 
— indeed,  may  be  altogether  absent.  The  pulse  is  weak,  not  neces- 
sarily rapid,  and  the  pulse-respiration  ratio  may  deviate  little,  if  at 
all,  from  the  normal.  Cough  and  expectoration  may  be  absent. 
There  may  be  delirium.  In  spite  of  the  paucity  of  symptoms  there 
are  some  points  which  Avill  lead  to  an  exploration  of  the  chest : 
1.  Old  age  or  chronic  alcoholism.  2.  A  curious  and  at  first  inexpli- 
cable muscular  weakness.  3.  Patient  inspection  discloses  a  trifling 
amount  of  dyspnoea,  manifested  by  an  abnormal  increase  of  respi- 
ration after  moderate  exertion  such  as  turning  in  bed,  or  slight 
breathlessness  in  talking.  4.  A  trace  of  cyanosis  in  the  lips  and 
finger  nails. 

(3)  Abortive  {or  Larval)  Form. — Cases  of  pneumonia  are  encoun- 
tered whose  duration  is  so  short  that  they  deserve  the  term  abortive. 
These  are  seen  particularly  in  children,  although  they  occur  not  infre- 
quently during  epidemics  of  pneumonia  in  military  camps,  hospitals, 
and  iails.  They  differ  from  the  ordinary  form  of  pneumonia  only  in 
duration  and  rapidity  of  convalescence.  In  the  shortest  personal 
case  there  was  unmistakable  consolidation  within  12  hours  after  its 
onset,  and  defervescence  took  place  at  the  end  of  48  hours  (Chart  I, 
page  7).     The  termination  is  by  a  rapid  crisis. 

(4)  Obstructive  Form.— This  term  was  popularized  by  A.  H.  Smith. 
It  is  applied  to  cases  in  which  there  is  great  obstruction  to  the  pas- 
sage of  blood  through  the  lungs,  arising  from  the  extent  of  the  con- 
solidation or  from  the  existence  of  intense  pulmonary  congestion, 
with  more  or  less  oedema.  Unusual  strain  is  thus  put  upon  the 
right  ventricle,  which  is  unable  to  propel  the  blood  with  normal 
velocity  through  the  pulmonary  circulation.  The  right  auricle  and 
ventricle  are  overdistended,  while  the  aorta  and  its  branches  are 


716  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

underfilled.  The  superficial  veins  are  also  empty,  having  passed  the 
major  portion  of  their  contents  into  the  large  venous  trunks. 

A  certain  amount  of  pulmonary  obstruction  is  an  element  in 
every  case  of  pneumonia,  but  in  this  form  it  is  a  predominant  factor. 
The  amount  of  obstruction  is  measured  in  great  part  by  the  pul- 
monary second  sound.  If  the  obstruction  is  marked  and  the  power 
of  the  right  ventricular  systole  is  adequate,  the  pulmonary  arterial 
tension  will  be  increased  and  the  closure  sound  of  the  pulmonary 
valve  loud  and  accentuated.  It  is  further  obvious  that  this  accen- 
tuation of  the  pulmonary  second  sound  will  cease  under  two  condi- 
tions, viz.,  lessening  of  the  pulmonary  obstruction,  or  decrease  in 
the  power  of  the  right  heart.  Whether  it  is  due  to  the  former  or 
the  latter  cause  must  be  determined  by  the  general  condition  of  the 
patient,  and  the  evidence  of  lessened  or  increased  rapidity  and  ease 
of  breathing. 

Extensive  involvement  of  lung  tissue,  some  dulness  and  numerous 
rales  over  the  uninvaded  portion  of  the  lungs,  marked  cyanosis,  rapid 
and  embarrassed  breathing,  together  with  a  pulmonary  second  sound 
at  first  accentuated,  later  becoming  extinct,  with  progressive  increase 
of  the  unfavourable  symptoms,  constitute  the  clinical  picture  of  the 
obstructive  form  of  pneumonia. 

(5)  With  Nervous  Sym2)toms  Predominating. — This  form  of  pneu- 
monia, simulating  meningitis,  occurs  mainly  in  children,  and  at  one 
time  was  thought  to  be  associated  especially  with  pneumonia  of  the 
apex.  It  sets  in  with  headache,  high  fever,  delirium,  convulsions, 
tremor  of  the  muscles,  and  perhaps  cervical  retraction.  The  chest 
symptoms  may  be  so  overshadowed  by  the  meningeal,  that  it  is  an 
excellent  rule  to  consider  head  symptoms  in  a  child  as  demanding 
an  examination  of  the  chest.  The  possible  existence  of  true  menin- 
geal inflammation  as  a  not  uncommon  complication  requires  some 
reservations,  but  it  occurs  at  the  height,  or  toward  the  close,  of 
pneumonia,  whereas  the  pseudo-meningitis  initiates  the  disease. 

Pneumonia  occurring  in  chronic  alcoliolics  may  at  first  glance  be 
quite  unsuspected,  the  symptom  group  being  that  of  delirium  tre- 
mens. An  increased  pulse,  respiration,  and  temperature  will  usually 
prevent  misinterpretation,  although  in  a  considerable  proportion  of 
cases  there  is  no  pain,  cough,  or  sputum,  and  the  respiration  rate 
may  be  normal. 

(6)  With  Gastro-intestinal  Symptoms. — In  children,  vomiting  and 
diarrhoea  may  be  so  marked  and  persistent  as  to  divert  attention 
from  the  chest.     This  rarely  happens  with  adults. 

(7)  With  Marked  Peritoneal  or  Abdominal  Symptoms. — In  some 
eases  there  are  violent  abdominal  pain  with  constipation  and  great 


LOBAR  PNEUMONIA  Y17 

meteorism,  simulating  intestinal  obstruction ;  or  vomiting,  abdominal 
tenderness,  marked  tympanites,  and  rigidity  of  the  abdominal  mus- 
cles— symptoms  identical  with  those  of  peritonitis. 

An  involvement  of  the  diaphragmatic  pleura  will  account  for 
the  pain.  This  pain  may  be  felt  in  the  hypochondriac,  umbilical, 
and  lumbar  regions.  It  may  also  in  part  explain  the  rigidity  of  the 
abdominal  muscles,  the  latter  contracting  to  limit  the  movements  of 
the  diaphragm.  It  is  somewhat  significant  that  the  pneumonia  in 
these  cases  almost  invariably  involves  the  lower  lobe  or  lobes.  It  is 
also  possible  that  there  may  be  an  actual  peritonitis  by  extension, 
although  this  is  a  rare  complication  in  pneumonia.  In  other  in- 
stances the  subsequent  course  of  the  disease  justifies  the  diagnosis  of 
a  *pneumo-typhoid,  the  pulmonary  inflammation,  as  an  initial  event, 
coexisting  with  unusually  violent  abdominal  symptoms. 

(8)  With  Delayed  Appearance  of  Physical  Signs. — These  are  ex- 
tremely perplexing  cases  when  encountered,  unless  the  rusty  spu- 
tum is  present,  and  are  not  very  rare.  The  physical  signs  may 
not  be  manifest  until  the  5th  day,  or  even  until  the  8th  day,  of  the 
rational  symptoms.  The  old  explanation  is  doubtless  correct,  viz., 
that  the  consolidation  begins  centrally  and  spreads  slowly  to  the 
periphery. 

(9)  Secondary  or  Intercurrent  Pneumonia. — The  pneumonia  which 
occurs  during  the  course  of  certain  acute  infections  may  be  latent. 
The  respiration  rate  may  be  only  slightly  increased,  cough  absent, 
and  the  physical  signs  of  consolidation  often  lacking.  The  percus- 
sion note,  usually  over  one  of  the  bases,  may  be  slightly  dulled,  the 
breath  sounds  feeble  and  accompanied  by  a  few  moist  or  crackling 
rales.  This  form  of  pneumonia  occurs  most  frequently  in  typhoid 
fever,  typhus  fever,  diphtheria,  influenza,  and  the  bubonic  plague. 

(10)  Terminal  Pneumonia. — Patients  who  are  very  ill  and  soon 
to  die  of  some  chronic  disease,  especially  diabetes,  chronic  nephritis, 
arteriosclerosis,  cardiac  disease,  or  pulmonary  tuberculosis,  may  have 
a  pneumonia  which  is  practically  latent  and  is  usually  discovered 
post  mortem.  The  respirations  may  be  a  little  more  rapid  than 
normal  and  the  temperature  slightly  raised. 

(11)  Pneumonia  as  Modified  by  Age. — In  the  old  the  disease  is 
often  latent,  without  chill,  and  with  slight  cough  or  expectoration. 
The  general  prostration  is  notable,  while  the  physical  signs  are 
obscure  and  indefinite. 

In  infants  and  young  children  the  cerebral  symptoms  are  often 
prominent ;  an  initial  convulsion  is  not  uncommon,  and  may  be  fol- 
lowed by  stupor  or  coma.  Pneumonia  of  the  apex  is  more  frequent 
than  in  adults,  and  rusty  sputum  is  seldom  seen. 


718  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

(13)  Post-operative  and  Ether  Pneumonia. — The  majority  of  cases 
of  pneumonia  following  etherization  or  operation  are  broncho-pneu- 
monic and  not  lobar.  When  the  lobar  form  occurs  it  does  not  differ 
in  any  respect  from  the  cases  met  with  in  medical  practice.  In  a 
number  of  instances  seen  by  request  in  the  surgical  wards,  the  pneu- 
mococcus  was  always  found  in  the  sputum. 

(13)  Streptococcus  Pneumonia. — This  form  of  pneumonia  is  said 
(Dexny)  to  be  characterized  by  special  involvement  of  the  upper  lobe, 
a  tendency  for  the  inflammation  to  wander,  a  protracted  and  irregu- 
lar fever  with  long-delayed  resolution,  and  is  finally  determined  by 
finding  streptococci  in  the  sputum, 

(14)  Epidemic  Pneumo?iia. — Pneumonia  may  assume  the  propor- 
tions of  an  epidemic.  The  mortality  is  greater,  and  each  outbreak 
may  be  characterized  by  a  predominance  of  some  one  of  the  special 
types  which  have  been  described  (cerebral,  septicaemic,  etc.). 

(15)  Variations  in  Localization. — The  lower  lobe  of  the  right  lung 
is  the  most  frequent  seat  of  the  disease,  and  when  the  pneumonia  is 
double,  both  lower  lobes  are  those  usually  involved.  Pneumonia  of 
the  apex  is  most  common  in  children.  Wandering,  creeping,  or 
migratory  pneumonia  is  a  variety  in  which  there  is  a  steady  advance 
of  consolidation  from  lobe  to  lobe.  It  can  be  readily  followed  by  the 
resulting  physical  signs  and  recurring  elevation  of  pulse,  respiration, 
and  temperature,  and  is  apt  to  be  protracted.  Massive  pyie^imoniu, 
in  which  not  only  the  air  cells  but  the  bronchi  of  one  or  more  lobes 
are  filled  with  exudate,  is  a  rare  variety.  Because  of  the  filling  of 
the  bronchi  the  physical  signs  are  almost  exactly  those  of  pleurisy 
with  effusion.  Central  pneumonia  is  not  uncommon.  The  consoli- 
dation begins  in  the  centre  of  a  lobe,  or  at  the  root  of  the  lung.  The 
rational  symptoms  of  pneumonia  may  be  present  for  several  days 
before  the  physical  signs  are  rendered  distinctive  by  the  advance  of 
the  consolidation  to  the  surface.  See  also  (8)  preceding.  Indeed, 
resolution  may  take  place  without  the  development  of  more  than 
barely  satisfactory  signs. 

Here  may  be  included  cases  of  which  I  have  seen  several  exam- 
ples— limited  or  incomplete  hepatization.  The  main  points  of  these 
cases  are :  a  moderately  sudden  onset,  with  chilliness  but  no  marked 
chill,  slight  cough,  slight  non-localized  pain  in  chest,  pulse-respira- 
tion ratio  of  3  :  5,  temperature  fluctuating  irregularly  between  100.5° 
and  102.5°,  duration  3  to  4  weeks.  A  cursory  examination  of  the  chest 
is  usually  negative,  but  if  a  minute  search  is  made,  a  single  strip  or 
patch  of  dulness  and  bronchial  breathing  will  be  found,  usually  in 
the  right  axillary  region,  corresponding  to  the  adjacent  borders  of  the 
middle  and  upper  lobes,  but  not  at  any  time  involving  the  entire  lobe. 


LOBAR  PNEUMONIA  719 

(16)  Acute  Pulmonary  Congestion. — This  may  be  seen  in  numerou8 
cases  of  epidemic  influenza,  especially  in  children.  Strictly  speaking 
it  does  not  belong  in  this  classification,  because  intense  congestion 
is  the  first  and  last  of  the  process,  pneumonia  not  developing.  Clin- 
ically its  onset  is  sudden,  temperature  high,  pulse-respiration  ratio 
eminently  pneumonic.  There  is  no  perceptible  alteration  of  the 
percussion  note,  and  the  respiratory  murmur  is  normal  except  for  a 
very  moderate  harshness  over  both  sides  of  the  chest.  The  crepitant 
rale  is  occasionally  heard.  It  subsides  either  with  or  without  treat- 
ment in  12  to  24  hours.  It  is  very  apt  to  come  on  at  night,  and  to 
subside  by  morning.  There  may  be  a  recurrence  on  1  or  2  subse- 
quent nights.  As  this  condition  is  undistinguishable  from  the  first 
stage  of  pneumonia,  the  physician  frequently  receives  praise  to  which 
he  is  not  entitled. 

Termixatioxs,  Relapses,  axd  Recuerexces.— (1)  Delayed 
Besolution. — It  is  well  known  that  in  many  cases  the  physical  signs 
of  consolidation  persist  for  a  varying  period,  even  for  2  or  3  weeks, 
with  normal  or  nearly  normal  pulse,  respiration,  and  temperature. 
Such  cases  do  not  come  under  this  heading.  The  delayed  resolution 
may  follow  an  apparently  typical  frank  pneumonia,  but  is  more  com- 
monly a  sequel  to  the  septicaemic,  latent,  or  incomplete  forms.  It  is 
attended  by  a  remittent,  almost  suppurative,  temperature  curve ;  not, 
however,  with  such  wide  excursions  as  may  attend  the  latter.  The 
pulse  and  respiration  remain  unduly  rapid,  8  or  10  weeks  elapsing 
before  resolution  is  complete. 

(2)  Abscess,  gangrene,  and  chronic  interstitial  pneumonia  are  rare 
terminations.  (3)  Recurrences  are  common ;  3d  or  4th  attacks  are 
not  infrequent ;  and  cases  have  been  reported  in  which  the  recur- 
rences numbered  from  8  to  10  or  more.  (4)  Relapses  are  rare,  and 
the  cases  in  which,  after  the  temperature  has  been  normal  for  1  or 
2  days,  an  apparent  2d  attack  runs  its  course,  are  probably  instances 
of  an  irregular  delayed  resolution  (Osler). 

CoMPLiCATioxs. — (1)  Pleurisy  and  Empyema. — Aside  from  the 
common  inflammation  of  that  portion  of  the  pleura  which  covers  the 
surface  of  a  consolidated  area,  there  are  cases  in  which  the  pleurisy 
is  so  severe  and  extensive  that  it  rivals  or  surpasses  the  pneumonic 
element — pleuro-pneumonia.  The  effusion  may  be  large,  and  is 
unusually  rich  in  fibrin.  Xot  infrequently  the  fluid  is  purulent, 
even  though  the  pneumonia  has  been  slight. 

As  pleurisy,  serous  or  purulent,  is  by  no  means  a  rare  sequel  of 
pneumonia,  and  is  not  seldom  overlooked,  the  possibility  of  its  occur- 
rence during  convalescence  should  be  borne  in  mind.  A  slight,  per- 
sistent, and  irregular  rise  of  temperature,  after  it  has  been  normal 


720  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

for  several  days,  with  dulness,  absent  or  weak  respiration  and  voice 
sounds,  at  the  base,  without  rales,  will  constitute  grounds  of  suspi- 
cion. A  persistent  leucocytosis  is  important  and  suggestive.  Whether 
these  signs  are  due  to  thickening  of  the  pleura  or  to  effusion  may  be 
ascertained  by  puncture. 

(2)  Endocarditis. — The  ulcerative  or  malignant  form  of  endocar- 
ditis originates,  in  from  15  to  25  per  cent  of  cases,  from  a  pneumonia. 
It  affects  mainly  the  left  heart.  The  symptoms  of  ulcerative  endo- 
carditis are  uncertain  and  sometimes  absent.  If  the  fever  is  irregu- 
lar and  prolonged,  and  chills,  fever,  and  sweats  occur,  it  is  suspi- 
cious ;  if  evidences  of  septic  embolism  become  manifest  and,  in  addi- 
tion, meningitis  occurs,  together  with  the  development  of  a  loud 
diastolic  murmur  not  previously  present,  the  diagnosis  of  ulcerative 
endocarditis  is  quite  certain. 

(3)  Pericarditis. — This  is  not  so  frequent  as  endocarditis,  and 
occurs  particularly  in  the  double  or  left-side  pneumonia  of  children. 
It  is  usually  fibrinous,  sometimes  serous,  rarely  purulent.  Praecor- 
dial  pain,  increased  dyspnoea,  and  weak  pulse  may  declare  its  exist- 
ence. The  physical  signs  of  pericardial  effusion  may  then  be  found. 
It  is  often  overlooked  or  latent. 

(4)  Meningitis. — This  very  serious  and  fatal  complication  is  for- 
tunately rare,  and  when  found  is  often  associated  with  ulcerative 
endocarditis.  Its  existence  is  usually  not  recognised  if,  as  is  so 
often  the  case,  it  affects  the  convexity.  If  basilar,  intense  head- 
ache, marked  cervical  retraction,  delirium,  stupor,  and  coma  will 
announce  its  presence. 

(5)  Jaundice. — Toxaemic  icterus  is  very  common  in  some  epi- 
demics. 

(6)  Other  Complications. — These  are :  nephritis  (rare),  parotitis 
(occasional),  peritonitis  (rare),  otitis  media  in  children  (not  infre- 
quent), peripheral  neuritis  (rare),  diphtheritic  colitis  with  diarrhoea 
(not  uncommon),  venous  thrombosis  in  protracted  cases  (occasional), 
embolism  of  the  femoral  or  other  large  artery  (rare),  and  cerebral 
embolism  with  aphasia  and  hemiplegia  (rare).  Pneumonia  may 
occur  in  a  malarial  subject,  or  malaria  be  manifest  during  the 
course  of  a  pneumonia.  The  existence  of  the  malaria  is  to  be 
decided  by  the  blood  examination.  Pneumonia  not  infrequently 
occurs  in  phthisical  subjects.  Kheumatic  fever  may  precede  an 
attack  of  pneumonia ;  or  rheumatism  may  occur  during  an  attack, 
although  the  redness,  swelling,  and  pain  in  one  or  more  joints  which 
sometimes  occurs,  either  at  the  height  of  the  disease  or  after 
the  crisis,  may  proceed  to  suppuration,  and  the  pneumococcus 
has  been  found  in  the  pus  from  the  diseased  joint.      The   articu- 


LOBAR  PNEUMONIA  721 

lar  complications  are  often  accompanied  by  pleurisy  or  endocar- 
ditis. 

Differential  Diagnosis. — As  a  rule  the  diagnosis  is  readily 
made.  Frank,  typical  cases  present  extremely  distinctive  and  unmis- 
takable symptoms.  It  may  be  overlooked  in  the  very  old  or  the 
very  young,  and  in  chronic  alcoholics ;  so  also  with  secondary,  ter- 
minal, central,  or  incomplete  pneumonias. 

Certain  diseases  may  simulate  lobar  pneumonia,  or  the  latter  may 
simulate  other  diseases. 

Diseases  Simulating  Lobar  Pneumonia. — (1)  Acute  Pul- 
monary Congestion. — This  may  simulate  a  beginning  pneumonia 
(page  719). 

(2)  Hypostatic  Congestion. — This  develops  in  long-continued 
fevers,  or  diseases  requiring  a  prolonged  dorsal  recumbent  posture 
and  attended  by  a  weak  heart.  There  is  slight  dulness  at  both 
bases,  with  a  few  moist  crackling  rales  at  the  end  of  deep  inspira- 
tion, with  perhaps  some  harshness  of  the  breath  sounds.  It  can 
usually  be  distinguished  from  pneumonia  by  the  absence  of  rusty 
sputum  or  of  a  rise  in  temperature,  and  is  bilateral.  Similar  signs 
may,  however,  announce  a  secondary  or  terminal  double  pneumonia. 

(3)  Pulmonary  (Edema. — In  this  condition,  usually  in  connection 
with  nephritis  or  cardiac  valvular  disease,  there  is  sudden  dyspnoea, 
cough,  and  expectoration,  but  it  may  be  distinguished  from  pneu- 
monia by  the  absence  of  fever,  the  presence  of  weak  breath  sounds 
and  numerous  fine  and  coarse  moist  rales  on  both  sides  of  the  chest, 
and  the  absence  of  marked  dulness  and  bronchial  respiration.  The 
sputum  in  cEdema  is  fluid,  frothy,  and  not  rusty. 

(4)  Acute  Bronchitis. — In  children  this  may  simulate  pneumonia, 
but  there  is  no  chill  or  convulsion,  the  respiration  is  not  so  rapid 
nor  the  fever  so  high  as  in  pneumonia,  dry  and  moist  rales  are  heard 
over  both  chests,  and  there  is  no  dulness  or  bronchial  breathing. 

(5)  Pulmonary  Infarctions  {or  Apoplexy). — These  occur  in  con- 
nection with  pyaemic  or  local  septic  processes,  attended  by  throm- 
bosis ;  or  in  chronic  disease  of  the  heart.  There  is  more  or  less 
sudden  dyspnoea,  cough,  and  expectoration,  but  the  sputum  is  fluid 
and  often  very  bloody  (resembling  a  small  haemoptysis)  rather  than 
tenacious  and  rusty,  and  may  be  expectorated  once  or  twice  only. 
If  the  infarct  is  large,  signs  of  a  circumscribed  consolidation,  usu- 
ally in  one  of  the  lower  lobes,  may  be  manifest,  but  there  is  less 
fever  than  in  pneumonia.  If  the  embolus  causing  the  infarct  is 
septic,  a  true  localized  pneumonia  may  develop,  usually  terminating 
in  abscess  or  gangrene.  The  sputum  becomes  rusty,  and  on  exami- 
nation the  streptococcus,  or,  as  in  a  case  of  my  own,  the  staphylo- 


722  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

coccus  (from  an  ulcerative  cystitis)  may  be  found  by  cultural  tests, 
instead  of  the  pneumococcus. 

(6)  Bronclio-pneumonia. — This  disease  is  usually  preceded  by 
bronchitis,  or  an  acute  infection  (e.  g.,  measles) ;  dyspnoea  and  cya- 
nosis are  well  marked ;  the  sputum  is  thick,  and  streaked  with  blood 
rather  than  rusty ;  the  fever  is  irregular,  does  not  terminate  by  crisis, 
and  may  last  for  weeks.  The  physical  signs  are  those  of  a  diffuse 
bronchitis,  dry  and  moist  rales  over  both  chests ;  the  evidences  of 
consolidation  (dulness,  broncho-vesicular  or  bronchial  breathing)  are 
often  indefinite,  and  when  well  marked  are  usually  limited  to  a  ver- 
tical strip  on  each  side  of  the  spine,  whereas  in  lobar  pneumonia 
they  are  quite  as  well,  and  indeed  often  more  distinctly,  perceived 
over  the  lateral  aspect  of  the  chest. 

(7)  Acute  Pneumonic  Phthisis. — The  onset,  symptoms,  and  phys- 
ical signs  of  this  disease  may  exactly  resemble  those  of  lobar  pneu- 
monia until  the  8th  or  10th  day,  when  the  fever  continues,  the  patient 
grows  worse  instead  of  better,  and  ultimately  the  signs  of  softening 
gradually  develop,  the  expectoration  becomes  muco-purulent  and 
greenish,  and  contains  tubercle  bacilli  and  elastic  tissue.  A  differen- 
tial diagnosis  is  impossible  until  sufficient  time  has  elapsed  for  the 
appearance  of  the  distinctive  symptoms.  The  evidences  of  this  dis- 
ease as  contrasted  with  lobar  pneumonia  may  be  summarized  as  fol- 
lows :  Tuberculous  family  or  personal  history,  recurring  chills  and 
sweats  common,  fever  more  often  distinctly  remittent,  more  rapid 
loss  of  flesh,  herpes  labialis  not  present,  crisis  absent,  usually  affects 
one  apex  and  extends  downward  ;  opposite  apex  often  involved ;  dis- 
ease continues  with  unabated  severity  beyond  the  10th  day,  evi- 
dences of  softening  (gurgling  rales,  cavernous,  or  amphoric  breathing, 
etc.)  occur,  and  elastic  tissue  and  tubercle  bacilli  appear  in  sputum, 
which  is  abundant,  purulent,  and  green. 

(8)  Pneumo-typhus. — See  pages  656  and  665. 

(9)  Pleurisy  luith  Effusion. — Mistakes  rarely  occur  except  in 
children.  The  onset  of  pleurisy  is  not  so  sudden,  there  is  usually 
chilliness  rather  than  a  rigour,  the  fever  is  not  so  high  and  declines 
by  slow  lysis,  the  cough  is  frequent  and  dry,  with  scanty  or  absent 
expectoration,  and  the  general  prostration  is  comparatively  slight. 
Herpes  is  absent  or  rare.  The  physical  signs  differ  materially.  In 
pleurisy  the  affected  side  is  distended,  vocal  fremitus  is  absent  (not 
increased),  there  is  flatness,  with  a  marked  sense  of  resistance,  rather 
than  dulness,  and  the  line  of  flatness  may  change  position  as  the  pa- 
tient moves.  Auscultation  shows  absent  or  diminished  voice  sounds 
or  egophony ;  absent  or  diminished  respiratory  murmur,  or  distant 
bronchial  breathing,  and  usually  an  absence  of  rales.     There  is  evi- 


LOBAR  PNEUMONIA— TUBERCULOSIS  723 

dence  of  displacement  of  the  heart  or  the  liver.     Finally,  puncture 
will  afford  positive  proof  of  the  presence  of  fluid. 

Diseases  Simulated  by  Lobar  Pneumonia. — (1)  Gastro- 
intestinal Disturbance. — A  routine  examination  of  the  chest  in  chil- 
dren will  do  away  with  any  mistake  of  this  kind. 

(2)  Delirium  Tremens. — Make  a  routine  examination  of  the  chest. 

(3)  Meningitis. — Usually  as  in  (1)  preceding.  If,  however,  the 
pneumonia  is  complicated  by  meningitis,  the  symptoms  of  the  latter 
usually  occur  at  the  height,  or  toward  the  end,  of  the  disease,  whereas 
the  simulated  meningeal  symptoms  are  present  from  the  onset.  In 
true  meningitis  the  presence  of  marked  cervical  retraction,  Kernig's 
sign  (page  283),  exaggerated  reflexes,  hyperaesthesia,  strabismus,  paral- 
ysis and  other  pressure  signs,  and  perhaps  lumbar  puncture  will 
serve  to  determine  its  existence. 

(4)  Cerebrospinal  Fever. — See  page  674. 

(5)  Typhoid  Fever. — In  pneumonia  with  rapid  supervention  of 
the  symptoms  of  the  typhoid  status,  a  differential  diagnosis  may  be 
quite  impossible  if  the  case  is  not  seen  from  the  outset,  unless  the  rose 
spots  appear,  or  a  positive  Widal  reaction  is  obtained. 

Prognosis  of  Lobar  Pxeumoxia. — The  disease  is  very  fatal  in 
drunkards,  and  in  people  of  60  years  or  over  (60  to  80  per  cent). 
The  younger  the  patient  (except  in  infants  under  1  year)  the  better 
the  prognosis.  Meningitis  as  a  complication  is  always  fatal ;  endocar- 
ditis adds  much  to  the  gravity.  Toxaemic  or  septicaemic  ("  typhoid  ") 
symptoms  are  especially  unfavourable,  so  also  are  hyperpyrexia  (105° 
or  over),  great  dyspnoea,  marked  cyanosis,  rapid  spread  of  consolida- 
tion from  one  lobe  to  another,  or  involvement  of  both  lungs,  and 
steadily  increasing  rapidity  and  weakness  of  the  heart  with  pulmo- 
nary oedema. 

XXV.     TUBERCULOSIS 

I.  Acute  Gexeral  (Disseminated)  Tuberculosis 

Acute  miliary  tuberculosis  results  in  many  cases  from  the  rupture 
into  a  vein  of  a  tuberculous  nodule,  after  which  the  bacilli  are  carried 
by  the  blood  stream  to  various  organs  of  the  body.  Whatever  its 
origin,  the  condition  is  usually  at  first  an  acute  generalized  infection, 
and  may  so  remain ;  but  later  in  its  course  the  infection  may  be  pre- 
dominantly localized  either  in  the  meninges  (most  common)  or  the 
lungs ;  or  it  may  be  thus  localized  from  the  onset.  Three  varieties 
are  recognised,  as  follows  : 

General  or  Typhoid  Form.— (1)  Symptoms.— The  general 
symptoms  are  those  of  an  infectious  disease  without  localizing  symp- 
toms, closely  resembling  typhoid  fever.     Malaise,  weakness,  chilliness. 


Y24  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

and  fever,  sometimes  occurring  rather  abruptly,  initiate  the  disease. 
Epistaxis  is  uncommon.  The  fever  is  irregular,  and  is  often  the 
first  notable  symptom.  It  rises  in  the  evening  (often  to  103°  or  104°) 
with  decided  morning  remissions,  or  it  may  be  of  the  inverse  type ; 
occasionally  the  temperature  may  be  nearly  normal  for  several  days, 
and  rise  again ;  in  exceptional  cases  it  may  be  normal  or  subnormal. 
As  the  disease  advances  the  pulse  becomes  rapid  and  feeble  (rarely 
dicrotic),  the  face  is  flushed,  the  tongue  dry  and  brown.  Moderate 
bronchitis  and  somewhat  hurried  respiration  are  common.  There  are 
prostration,  mental  dulness,  mild  delirium  or  stupor,  and,  occasion- 
ally, diarrhoea.  The  spleen  is  somewhat  enlarged ;  the  urine  is  scanty, 
high  coloured,  often  with  a  trace  of  albumin,  and  the  diazo-reaction 
may  be  present ;  a  reddish  eruption,  or  toward  the  end  petechia, 
may  appear.    There  may  be  a  moderate  leucocytosis.    Jaundice  is  rare. 

(3)  Differential  Diagnosis. — Acute  general  miliary  tuberculosis 
so  closely  simulates  typhoid  fever  that  the  most  acute  diagnostician 
may  be  at  a  loss  to  decide  which  is  present  until  the  lapse  of  time 
permits  the  finding  of  some  distinctive  symptoms.  The  differential 
points  are  given  elsewhere.     (See  page  666.) 

Acute  Tuberculous  Meningitis. — This  may  occur  as  a  local- 
ization of  a  general  miliary  tuberculosis,  or  the  meningeal  symptoms 
may  be  so  pronounced  that  it  should  be  classed  as  a  meningitis  rather 
than  a  general  infection. 

(1)  Symptoms. — The  onset  may  be  abrupt.  More  commonly  after 
an  illness  (measles,  pertussis),  a  fall,  or  indefinite  failure  of  health, 
the  patient  (usually  a  child)  loses  appetite,  flesh,  and  strength,  and 
may  become  irritable  and  peevish.  In  a  week  or  so  the  initial  or 
irritative  stage  comes  on,  manifested  by  headache  (often  intense), 
nausea  and  vomiting,  chilliness,  and  fever.  If  the  onset  is  sudden, 
convulsions,  coma,  or  delirium  may  occur.  Light  and  noise  aggra- 
vate the  headache,  which  is  so  severe  that  the  child  cries  out  sud- 
denly (hydrocephalic  cry)  or  screams  continuously.  The  pulse  is  at 
first  rapid,  becoming  slow  and  irregular ;  the  respirations  are  usually 
unaltered.  Constipation  is  the  rule.  Sleep  is  restless,  and  disturbed 
by  starting  or  waking  in  alarm ;  muscular  twitchings  are  common ; 
vertigo  and  cutaneous  hyperaesthesia  are  often  manifest ;  cervical  re- 
traction is  frequently  observed,  and  the  pupils  are  usually  contracted. 
During  the  first  stage  the  fever  may  rise  to  102°  or  103°.  Leucocy- 
tosis is  usually  present  throughout. 

The  symptoms  slowly  shift  into  those  of  the  paralytic  (or  pres- 
sure) stage.  The  child  becomes  dull  and  apathetic,  and  is  delirious 
if  disturbed ;  the  vomiting  may  persist,  but  more  commonly  lessens ; 
the  bowels  are  obstinately  constipated,  and  the  abdomen  becomes 


TUBERCULOSIS  725 

scaphoid.  The  pupils  are  unequal  or  dilated ;  the  respiration  sighing 
or  irregular ;  the  pulse  slow  and  intermittent,  or  irregular.  The 
tache  cerehrale  can  be  produced.  Convulsions  are  not  infrequent, 
and  nystagmus,  strabismus,  ptosis,  or  optic  neuritis  (blindness)  may 
become  manifest,  and  deafness  may  develop.  Cervical  retraction  or 
spasm,  and  various  forms  of  paralysis  (hemiplegia,  monoplegia),  are 
common.  Gradually  a  typhoid  state  ensues,  with  dry  tongue,  diar- 
rhoea, rapid  pulse,  and  involuntary  passage  of  urine  and  faeces. 
Cheyne-Stokes  respiration  is  not  uncommon.  The  eyes  are  partly 
open  and  the  eyeballs  rolled  upward.  The  temperature  varies,  rising 
and  declining  at  short  intervals.  In  some  cases  a  rise  to  106°  or  107°, 
followed  by  a  sudden  fall  to  normal  or  below,  heralds  the  fatal  ending. 

The  duration  of  the  disease,  which  is  probably  always  fatal,  varies 
from  2  to  4  weeks. 

(2)  Differential  Diagnosis. — To  distinguish  tuberculous  menin- 
gitis from  the  other  meningitides  may  be  difficult  unless  some  pre- 
existing tuberculous  focus  (lungs,  glands,  bones)  can  be  found,  or 
choroidal  tubercles  are  discovered  by  the  ophthalmoscope.  Lumbar 
puncture  may  afford  a  fluid  containing  tubercle  bacilli.  If  the  fluid 
obtained  is  free  from  any  variety  of  micro-organism  it  also  argues 
for  a  tuberculous  affection.  The  onset  in  the  tuberculous  form  is 
slower  and  the  fever  is  not  so  high  as  in  the  suppurative  variety, 
and  in  the  latter  there  is  a  marked  leucocytosis,  which  is  slight  or 
absent  in  the  former. 

Acute  Miliary  Tuberculosis  of  the  Lungs. — (1)  Symp- 
toms.— When  the  general  infection  is  pre-eminently  localized  in  the 
lungs  the  onset  may  be  sudden.  More  commonly,  to  the  symptoms 
of  the  general  infection  are  added  cough,  rapid  breathing  (even  to 
60  per  minute),  and  perhaps  pleuritic  pain.  The  expectoration  is 
muco-purulent,  and  may  be  rusty  or  streaked  with  blood.  Dyspnoea 
and  cyanosis  are  marked  and  much  more  severe  than  would  be  ex- 
pected from  the  physical  signs,  which  are  those  of  a  bronchitis  of 
the  smaller  tubes.  The  percussion  note  is  usually  normal  or  hyper- 
resonant,  especially  over  the  front  of  the  chest.  If  old  tuberculous 
foci  or  broncho-pneumonic  patches  are  present,  especially  in  children, 
there  may  be  slight  dulness  at  the  bases.  On  auscultation,  fine  or 
coarse,  dry  or  moist  rales  are  heard,  and  occasionally  fine,  soft  pleural 
frictions  or  rubbing  sounds.  The  respiration  may  be  either  weak  or 
bronchial  over  the  areas  of  localized  dulness,  if  such  be  present.  The 
spleen  is  swollen  in  the  very  acute  cases.  The  pulse  is  rapid  and 
weak.  The  fever  runs  from  102°  to  103°.  The  duration  of  the 
disease  varies,  according  to  its  intensity,  from  10  or  12  days  to  weeks 
or  months. 
48 


726  DIAGNOSIS,  DIRECT  AND   DIFP^ERENTIAL 

(2)  Diagnosis. — The  folloAving  circumstances  point  to  the  tuber- 
culous nature  of  the  disease  :  Dyspnoea,  cyanosis,  and  diffuse  bron- 
chitis in  adults;  the  presence  of  tubercles  in  the  choroid;  the  oc- 
currence of  meningeal  symptoms  ;  the  occasional  finding  of  tubercle 
bacilli  in  the  sputum ;  a  history  of  cough,  or  tuberculous  disease 
of  glands,  bones,  or  lungs ;  and  in  children  a  recent  attack  of  per- 
tussis or  measles. 

II.  Acute  Pulmonary  Phthisis 

Two  varieties  are  recognised  : 

Pneumonic  Form. — Clinically  the  symptoms  are  those  of  lobar 
pneumonia.  The  duration  of  the  disease,  which  is  always  fatal, 
varies  from  2  to  6  weeks,  but  may  in  rare  instances  be  protracted 
to  3  or  4  months.  The  differential  diagtiosis  is  from  lobar  pneu- 
monia (page  722). 

Broncho-pneumonic  Form. — (a)  Symptoms. — Eepeated  chills, 
rapid  pulse  and  respiration,  high  and  irregular  fever,  and  perhaps 
haemoptysis,  initiate  the  "  galloping  "  form  of  phthisis.  Xight  sweats 
and  rapid  loss  of  flesh  and  strength  ensue.  A  muco-purulent  sputum, 
at  first  scanty,  later  profuse,  appears,  containing  elastic  tissue  and 
tubercle  bacilli.  The  physical  signs  are  at  first  indefinite,  or  are 
those  of  a  diffuse  bronchitis,  but,  shortly,  areas  of  slight  or  marked 
dulness,  with  harsh  broncho-vesicular  or  bronchial  respiration  and 
numerous  moist  and  crackling  rales  will  be  found,  usually  first  at 
the  apices.  These  signs  maybe  either  unilateral  or  bilateral,  more 
commonly  the  latter.  Subsequently  the  evidences  of  softening  and 
cavity  formation  supervene.  If  the  disease  is  very  acute  the  patient 
may  develop  typhoid  symptoms  and  die  in  3  weeks ;  more  commonly 
the  duration  is  from  6  or  8  weeks  to  2  or  3  months ;  occasionally  the 
acute  symptoms  subside  and  the  case  becomes  one  of  chronic  phthisis. 
The  fatal  broncho-pneumonia  following  measles  and  pertussis  is,  in 
the  majority  of  instances,  tuberculous,  and  an  example  of  this  form 
of  acute  phthisis. 

(b)  Differential  Diagnosis. — (1)  Broncho-pneumonia. — A  personal 
or  family  tuberculous  history,  progressive  emaciation,  the  finding  of 
tubercle  bacilli  in  the  sputum,  and  the  eventual  occurrence  of  signs 
of  softening  will  declare  for  tuberculosis. 

(2)  Typhoid  Fever. — Typhoid  fever  with  extensive  bronchitis  may 
be  confused  with  this  form  of  phthisis,  but  the  presence  of  the  rose 
spots,  meteorism,  and  positive  Widal  reaction,  with  absence  of  tuber- 
cle bacilli  in  the  sputum  or  of  signs  of  cavity  formation,  will  exclude 
phthisis. 


TUBERCULOSIS  727 


III.  Chronic  Pulmonary  Phthisis 

The  onset  of  chronic  phthisis  is  gradual,  except  in  the  few  cases, 
previously  described,  of  general  miliary  tuberculosis  with  pulmonary 
localization,  or  acute  pulmonary  phthisis,  which  become  protracted 
and  merge  into  the  chronic  form.  Owing  to  the  immense  thera- 
peutic value  of  an  early  diagnosis  it  is  best  to  describe  the  disease  as 
in  two  stages,  viz.,  initial  or  incipient,  and  advanced. 

Incipient  Phthisis. — (1)  Symptoms. — In  the  majority  of  cases 
there  is  a  gradually  increasing  sense  of  languor  or  weakness,  with 
some  loss  of  flesh  and  pallor  of  the  face,  unaccustomed  shortness  of 
breath  on  slight  exertion,  chilly  feelings,  loss  of  appetite,  perhaps 
some  pleuritic  pain,  and  digestive  disturbance.  Then  slight  fever 
and  moderate  night  sweats  may  occur.  There  may  or  may  not  be 
slight  cough  and  expectoration,  and  physical  examination  of  the 
chest  may  be  either  practically  negative  or  reveal  signs  of  disease 
which  are  just  sufficiently  marked  to  be  recognisable. 

The  onset  and  manner  of  invasion  may  vary.  The  initial  symp- 
tom in  many  instances  is  an  hwrnoptysis,  an  occurrence  which  should 
be  considered  indicative  of  tuberculosis  unless  subsequently  proved 
to  be  otherwise,  with  which  physical  signs  may  coexist  or,  perhaps, 
not  become  manifest  for  weeks  or  months  after.  Gastro-intestinal 
symptoms^  such  as  epigastric  distress,  acidity,  eructations,  flatulence, 
or  vomiting,  may  be  so  prominent  as  to  overshadow  the  pulmonary 
disease.  The  gastric  disturbances  are  sometimes  associated  with 
anwmia  and  its  symptoms  in  the  young.  Such  cases  are  very  com- 
mon and  are  often  misdiagnosed.  A  regularly  intermittent  fever^ 
with  chills  and  sweats,  is  not  uncommon,  and  frequently  leads  to  a 
mistaken  initial  diagnosis  of  malaria.  Pleurisy  with  effusion,  or  a 
dry  pleurisy  at  one  apex,  occur  not  infrequently  as  early  symptoms, 
followed  at  varying  intervals  by  evidence  of  pulmonary  involvement. 
Most  commonly  bronchitis^  following  exposure,  and  occurring  in  per- 
sons who  have  catarrh  of  the  nasopharynx  or  who  have  suffered 
from  repeated  colds,  initiates  the  disease.  The  cough  continues  and 
the  physical  signs  of  a  localized  bronchitis  at  one  apex  are  found. 
In  some  instances  the  presence  of  tuherculons  lymph  glands  antedates 
the  pulmonary  disease,  which  is  often  latent.  In  other  cases  the 
earliest  symptoms  relate  to  the  larynx.  Finally,  the  disease  may  be 
latent  and  progress  even  to  cavity  formation  before  the  occurrence 
of  symptoms  (perhaps  haemoptysis)  sufficiently  marked  to  attract 
attention ;  or  it  may  be  quite  overshadowed  by  the  presence  of  grave 
disease  elsewhere. 


728  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

(2)  Physical  Signs. — The  physical  signs  of  the  incipient  stage 
may  be  at  first  negative  or  very  indefinite,  but  sooner  or  later  become 
plainly  manifest.  Inspection  may  show  the  phthisical  chest,  with 
deficient  expansion,  either  general  or  limited  to  one  apex.  There 
may  be  impaired  resonance  or  slight  dulness  over  an  apex,  more 
commonly  the  right.  Auscultation  over  this  apex  shows  the  presence 
of  fine,  moist,  crackling  rales  at  the  end  of  inspiration.  The  breath 
sounds  are  frequently  interrupted  or  cogwheel,  and  feeble,  or  harsh 
and  broncho-vesicular,  or  the  expiration  may  be  high-pitched  and  pro- 
longed. The  voice  sounds,  especially  the  whispered  voice,  are  trans- 
mitted with  more  than  normal  intensity.  As  time  passes  and  con- 
solidation becomes  more  extensive,  perhaps  with  cavity  formation, 
the  case  enters  the  : 

Advanced  Stage. — (l)  Symptoms. — The  cough  increases  and 
may  keep  the  patient  awake  at  night.  At  times  slight,  it  may  be  so 
violent  and  paroxysmal  as  to  cause  vomiting.  The  sputum,  at  first 
mucous,  becomes  greenish-gray,  and  finally  takes  on  the  nummular 
form  (said  to  signify  cavities).  Pain  over  an  apex,  or  more  commonly 
in  the  lower  chest,  anteriorly  or  posteriorly,  perhaps  felt  only  upon 
coughing  and  due  to  pleurisy,  is  not  uncommon.  Htemoptyses  occur 
in  from  60  to  80  per  cent  of  all  cases ;  in  the  early  stages  usually  slight, 
from  erosion  or  congestion  of  the  bronchial  mucosa ;  in  the  later 
stages  often  copious,  from  erosion  of  small  vessels.  The  bursting  of 
an  aneurism  of  the  pulmonary  artery  may  cause  a  large  and  imme- 
diately fatal  haemorrhage  in  far-advanced  cases. 

The  respiration  is  quickened,  but  not  in  proportion  to  the  extent 
of  the  disease.  Marked  subjective  dyspnoea  is  not  common.  The 
pulse  is  usually  rapid,  often  running  to  120  or  130.  Anaemia,  with 
a  relatively  great  diminution  of  haemoglobin,  is  always  marked. 
Xausea,  vomiting,  anorexia,  gastric  disturbances,  and  perhaps  diar- 
rhoea, are  common.  Xight  sweats  may  be  drenching  and  frequent. 
The  loss  of  flesh  is  progressive.  In  women,  menstruation  usually 
ceases  at  an  early  period ;  rarely  it  becomes  profuse.  Pregnancy  may 
cause  a  temporary  arrest  of  the  disease.  The  urine  may  present  a 
febrile  albuminuria ;  or  if  amyloid  disease  supervenes,  polyuria  and 
tube  casts ;  or  if  renal  tuberculosis  is  present,  pyuria  or  ha?maturia. 
The  notoriously  hopeful  mental  attitude  of  the  patient  throws  an 
interesting  sidelight  upon  the  efficacy  of  "mental  healing"  in  serious 
organic  disease. 

Fever  is  not  only  the  earliest  symptom  of  the  disease,  but  con- 
stitutes the  most  reliable  index  of  its  activity  and  progress.  It  may 
be  intermittent  or  remittent.  In  some  cases,  even  with  extensive 
disease,  the  temperature  may  remain  normal,  or  perhaps  subnormal, 


TUBERCULOSIS  Y29 

for  varying  periods.  When  consolidation  is  advancing  the  inter- 
mittent and  remittent  types  may  alternate  irregularly  from  day  to 
day.  If  the  type  is  intermittent,  normal  or  below  normal  in  the 
morning  with  sweating,  rising  to  103°  to  105°  in  the  evening  with  a 
flush  upon  the  face,  it  is  usually  an  indication  of  large  cavities  and 
progressive  breaking  down  of  lung  tissue  (hectic,  septic,  or  suppura- 
tive fever). 

(2)  Physical  Signs  in  the  Advanced  Stage. — Inspection  shows  an 
unusual  prominence  of  the  clavicles,  scapula},  and  ribs.  In  many  in- 
stances the  congenital  phthisical  chest  is  seen.  The  supraclavicular 
and  infraclavicular  spaces  are  depressed,  more  so  on  the  side  of  the 
lung  which  is  most  affected,  and  on  the  same  side  there  is  deficient 
expansion.  Visibility  of  the  cardiac  impulse  over  a  large  area  (2d 
to  5th  left  interspaces)  is  indicative  of  disease  at  the  left  apex,  with 
retraction  of  that  portion  of  the  lung  which  is  normally  interposed 
between  the  heart  and  the  chest  wall.  Clubbed  fingers  are  frequent, 
and  there  may  be  yellowish-brown  patches  of  pityriasis  versicolor 
over  the  front  of  the  chest. 

Palpation  confirms  the  existence  of  deficient  expansion,  and  re- 
veals an  increase  of  vocal  fremitus  over  consolidated  portions  of  lung 
or  over  cavities.  Pleural  effusion  or  great  thickening  causes  it  to  be 
absent  or  diminished. 

Percussion  should  be  practiced  upon  the  supraclavicular  and  in- 
fraclavicular, supraspinous,  and  interscapular  spaces,  in  the  last  on  a 
level  with  the  fifth  dorsal  spine  in  particular,  always  comparing  both 
sides.  Normally  the  note  over  the  right  apex  is  a  little  higher 
pitched  than  that  over  the  left.  More  or  less  marked  dulness  in- 
dicates consolidation.  If  the  dulness  is  very  slight  it  is  most  easily 
determined  at  the  end  of  inspiration.  Dulness  of  a  "  wooden  "  qual- 
ity usually  indicates  extensive  fibrosis  of  the  lung.  Absolute  flatness 
with  retraction  of  the  chest  signifles  a  thickened  pleura  and  wide- 
spread consolidation,  or,  if  the  intercostal  spaces  are  bulging  and 
motionless,  a  large  pleural  effusion.  A  tympanitic  or  dull  tympanitic 
note  over  the  upper  part  of  the  lung  may  be  due  either  to  a  superfi- 
cial cavity,  or  to  an  area  of  consolidation  reaching  from  the  chest 
wall  to  the  main  bronchi.  In  miliary  tuberculosis,  or  numerous 
minute  spots  of  consolidation,  or  a  large  number  of  small  cavities, 
the  percussion  note  may  be  nearly  normal.  Myoidema  (page  518) 
may  be  observed. 

Auscultation  shows  the  presence  of  pleural  or  pleuro-pericardial 
friction  sounds.  According  to  the  amount  of  consolidation,  the 
breath  sounds  vary  from  prolonged  expiration,  through  broncho- 
vesicular  up  to  tubular  or  bronchial  breathing.     Jerking  or  "  cog- 


730  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

wheel "  inspiration  is  common,  but  not  always  significant.  Early  in 
the  disease  fine,  crackling,  or  subcrepitant  rales  are  heard,  especially 
toward  the  end  of  inspiration ;  at  a  later  period  fine  or  coarse  niles, 
either  moist  or  dry,  indicate  increased  secretion  due  to  the  accom- 
panying bronchitis ;  and  large  mucous  or  gurgling  rales  indicate  the 
presence  of  cavities.  A  cardio-respiratory  murmur  is  not  infrequent ; 
so  also  is  a  systolic  murmur  in  one  or  both  subclavian  arteries.  The 
voice  sounds,  both  spoken  and  whispered,  are  intensified  (bronchoph- 
ony, pectoriloquy)  over  areas  of  consolidation  or  over  cavities. 

The  presence  of  a  cavity  can  not  always  be  determined  with  cer- 
tainty, as  any  one  who  controls  his  clinical  diagnosis,  when  possible, 
by  the  results  of  the  autopsy  room,  will  freely  admit.  Several  of  the 
signs  of  a  cavity  may  be  most  accurately  imitated  by  an  area  or  shaft 
of  consolidated  lung  extending  from  chest  wall  to  main  bronchi. 
The  signs  which  usually  indicate  the  existence  of  a  cavity  are :  a 
tympanitic,  dull  tympanitic,  amphoric,  or  cracked-pot  percussion 
note,  or  Wintrich's  and  Gerhardt's  phenomena  (pages  406  and  408) ; 
bronchial,  cavernous,  or  amphoric  respiration,  whispering  pector- 
iloquy, or  amphoric  bronchophony,  and  large  gurgling  or  bubbling 
rales  which  may  have  a  ringing,  metallic,  or  amphoric  quality. 

The  duration  of  the  disease  varies  from  many  months  to  many 
years. 

Complications  of  Chronic  Phthisis. — LarjTigeal  phthisis, 
usually  secondary,  evidenced  by  aphonia  and  dysphagia ;  gangrene 
(occasional) ;  pneumonia  (not  infrequent  as  a  final  event) ;  pleurisy, 
usually  dry,  sometimes  with  serous  effusion ;  pneumothorax  or  pyo- 
pneumothorax (common);  amyloid  disease  of  the  liver,  spleen,  kid- 
neys, or  intestines ;  intestinal  tuberculosis ;  endocarditis  (not  com- 
mon), meningitis ;  peripheral  neuritis. 

Diagnosis  of  Chronic  Phthisis. — The  diagnosis  of  an  ad- 
vanced <3ase  is  readily  made  by  the  discovery  of  the  tubercle  bacilli 
in  the  sputum,  conjoined  with  the  well-marked  physical  signs.  The 
disease  is,  of  course,  most  difficult  to  discover  at  the  very  time  when 
its  recognition  is  of  the  greatest  importance,  namely,  at  the  begin- 
ning. It  is  probable  that  if  the  physician  resisted  his  lifelong  habit 
of  optimism  and  erred  in  the  opposite  direction  in  cases  of  suspected 
incipient  pulmonary  tuberculosis,  the  mortality  list  would  be  shorn 
of  a  measurable  proportion  of  its  bulk.  Phthisis  often  masquerades 
under  the  guise  of  "  malaria "  or  "  bronchitis,"  and  haemoptysis  is 
simply  "  from  the  throat."  A  gradual  and  unaccountable  loss  of 
strength  and  flesh,  with  a  slight  evening  rise  of  temperature,  even 
without  physical  signs,  should  be  treated  exactly  as  if  the  examiner 
felt  sure  that  tubercles  were  forming.     Kepeated  examinations  of  the 


TUBERCULOSIS  731 

sputum  for  bacilli  should  be  made.  The  presence  of  localized  moist 
or  crackling  rdles  at  one  apex,  especially  if  conjoined  with  slight 
dulness,  and  harsh  respiration  or  prolonged  expiration,  with  or  with- 
out the  finding  of  bacilli,  will  in  the  vast  majority  of  cases  decide  for 
tuberculosis.  So  also  with  the  discovery  of  a  dry  pleurisy  at  one  or 
the  other  apex.  It  should  be  remembered  that  while  the  disease 
usually  starts  in  the  apices,  especially  the  right,  it  may  first  appear 
in  the  lower  lobes  or  any  other  part  of  the  lung. 

(1)  Apical  Catarrh. — Rarely  there  is  a  non-tuberculous  catarrh  of 
one  apex  evidenced  by  fine  moist  rales,  mucous  sputum,  and  slight 
fever,  which  passes  away  in  a  few  weeks,  repeated  examinations  fail- 
ing to  reveal  tubercle  bacilli.  The  diagnosis  of  this  condition  should 
be  made  with  the  greatest  caution. 

(2)  Brojichiectasis. — The  chronic  cough  of  bronchitis  and  the 
physical  signs  of  cavity  (caused  by  dilatation  of  the  bronchial  tubes) 
may  be  mistaken  for  those  of  chronic  tuberculosis,  but  as  the  error 
can  arise  only  in  the  later  stages  of  phthisis,  the  discrimination  is 
readily  made  by  finding  the  bacilli  in  the  sputum. 

Prognosis  of  Chronic  Phthisis.— In  the  earliest  stages, 
with  proper  care,  the  outlook  is  not  unpromising ;  in  advanced  cases, 
almost  hopeless.  Unfavourable  symptoms  are  anorexia,  rapid  pulse, 
persistent  high  fever,  steady  loss  of  weight,  and  chronic  diarrhcea. 
Such  complications  as  involvement  of  the  larnyx,  pyopneumothorax, 
tuberculous  meningitis,  and  amyloid  disease  are  usually  forerunners 

of  the  end. 

IV.  Fibroid  Phthisis 

In  certain  cases  of  chronic  phthisis  there  is  an  extensive  forma- 
tion of  fibrous  tissue  in  one  apex  or  one  lung.  When  fully  developed 
the  clinical  condition  is  practically  the  same  as  in  chronic  interstitial 
pneumonia  (5'.  r.),  from  which  fibroid  phthisis  can  be  distinguished 
only  by  the  finding  of  tubercle  bacilli  in  the  sputum.  The  affected 
side  is  retracted  and  shrunken,  the  spine  is  laterally  curved,  and  the 
shoulder  of  the  same  side  prominent.  The  expansion  is  poor  or  ab- 
sent ;  the  percussion  note  dull  and  characteristically  wooden ;  the  heart 
is  uncovered  (if  the  left  lung  is  affected)  or  drawn  to  the  right ;  the 
breathing  at  the  base  is  weak,  absent,  or  distant  bronchial,  perhaps 
with  rales  of  all  sizes ;  the  vocal  fremitus  is  diminished.  The  diira- 
tion  of  the  disease  varies  from  10  to  20  years,  or  longer. 

V.  Tuberculosis  of  the  Serous  Membranes 
The  signs  and  symptoms  of  tuberculosis  of  the  pleura  and  the 
pericardiinn  are  the  same  as  those  of  pleurisy  {q.  v.)  or  pericarditis 
{q.  V.)  from  other  causes. 


732  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Tuberculosis  of  the  Peritonseum. — Most  common  between 
the  ages  of  20  and  40,  and  twice  as  frequent  in  women  as  in  men. 

(1)  Symptoms. — Extremely  variable.  The  disease  is  often  latent 
and  is  discovered  accidentally  during  a  coeliotomy  for  some  other 
condition ;  or  the  symptoms  resemble  those  of  a  typhoid  fever ;  or 
may  begin  acutely.  An  early  symptom  is  abdominal  discomfort  or 
pain,  localized  or  general;  and  if  the  pain  is  severe  it  is  apt  to  be 
continuous,  with  marked  remissions  of  varying  duration,  and  asso- 
ciated with  tenderness.  In  the  acute  cases  the  fever  may  rise  to 
103°  or  104° ;  in  the  more  chronic  cases  the  temperature  is  usually 
subfebrile,  or  may  be  normal,  or  even  steadily  subnormal,  for  days  at 
a  time.  The  fever  is  apt  to  rise  coincidently  with  the  attacks  of 
pain.  Effusion  into  the  peritonaium  (ascites),  which  may  be  hemor- 
rhagic, is  common,  usually  moderate,  but  may  be  so  abundant  as  to 
cause  very  considerable  distention.  Tympanites  in  varying  degree 
is  found,  especially  in  the  more  acute  cases,  but  occurs  also  in  the 
chronic  forms.  Digestive  disturbances,  anorexia,  nausea  (perhaps 
vomiting),  and  either  diarrhcea  or  constipation  may  be  present.  The 
latter  may  be  very  intractable.  The  skin  may  become  pigmented,  and 
there  is  usually  a  progressive  loss  of  flesh  and  strength.  In  addition 
to  ascites  and  meteorism  the  physical  examination  of  the  abdomen 
may  reveal  tumourlike  masses,  usually  situated  in  or  near  the  median 
line.  Coils  of  intestine  may  become  adherent,  forming  a  rounded 
mass,  which  is  tympanitic  or  dull  tympanitic  on  percussion  ;  or  por- 
tions of  the  fluid  effusion  may  become  encapsulated  by  adhesions 
forming  cystic  collections,  flat  or  dull  on  percussion  ;  or  the  omentum 
may  become  shrivelled  and  thicken  into  a  sausage-shaped  transverse 
cord ;  or  the  mesenteric  glands  are  enlarged  and  matted  together ;, 
or  indurated  masses  are  found  in  the  pelvis. 

(2)  Differential  Diagnosis. — In  the  latent  cases  a  diagnosis,  at  least 
in  the  early  stages,  may  be  difficult  or  impossible.  If  with  the  signs 
of  a  chronic  peritonitis  there  is  evidence  of  tuberculous  disease  in  the 
lung,  kidney,  testes.  Fallopian  tubes,  lymphatic  glands,  or  bones,  and 
especially  if  pleurisy  with  effusion  coexists,  the  peritonitis  is  probably 
tuberculosis.  The  ascites,  if  present,  is  to  be  distinguished  from  that 
due  to  cirrhosis  of  the  liver  by  the  presence  of  marked  abdominal 
pain,  tenderness,  and  tumourlike  masses,  and  an  irregular  fever ;  and 
the  absence  of  enlarged  spleen  and  gastric  or  intestinal  haemorrhages. 
It  may  be  extremely  difficult  or  impossible  to  decide  between  an  en- 
cysted effusion  and  an  ovarian  cyst.  In  the  latter  case  the  growth  is 
slower  and  more  clearly  defined,  there  is  little  or  no  loss  of  strength 
or  flesh,  usually  no  fever,  and  not  so  much  abdominal  pain  and  tender- 
ness.   Xo  evidence  of  past  or  present  tuberculous  lesions  can  be  founds 


TUBERCULOSIS  Y33 

Cancer  of  the  peritonaeum  may  produce  puckering  and  cording  of 
the  omentum,  and  tumourlike  masses,  as  in  tuberculous  peritonitis, 
but  the  more  rapid  progress  of  the  former  and  the  finding  of  malig- 
nant disease  (especially  visceral)  will  aid  in  differentiation.  Acute 
tuberculous  cases  can  not  be  distinguished  from  ordinary  acute  peri- 
tonitis, or  in  some  instances  from  enteritis  or  strangulated  hernia. 
Those  with  slow  onset,  abdominal  tenderness,  meteorism,  and  con- 
tinued low  fever  can  not  be  differentiated  from  typhoid  fever  except 
by  the  Widal  test,  rose  spots,  or  lapse  of  time.  The  tuberculin  test 
in  all  these  cases  may  be  of  service. 

Under  favourable  conditions  (coeliotomy  ?)  and  in  latent  and 
ascitic  cases  the  prognosis  is  better  than  was  formerly  supposed. 

VI.  Tuberculosis   of  the   Genito-urinary   Organs 

I.  Tuberculosis  of  the  Kidney. — This  is  more  common  in 
men  than  in  women  (3  to  1),  and  in  mid-life. 

(1)  Si/}7iptoms. — The  clinical  manifestations  are  those  of  a  pye- 
litis. There  is  frequent  urination,  pain  or  discomfort  over  one  or 
both  loins,  with  tenderness,  and  palpable,  though  rarely  very  marked, 
symmetrical  enlargement  of  one  or  both  kidneys.  The  urine  is  acid 
and  contains  pus,  albumin,  epithelium,  occasionally  small  caseous 
particles,  and  tubercle  bacilli.  Haematuria  may  occur.  In  advanced 
cases,  and  especially  when  both  kidneys  are  involved,  chills,  sweats, 
irregular  fever,  and  progressive  emaciation  ensue. 

(2)  Diagjiosis. — Tuberculous  pyelitis,  evidenced  by  pyuria,  may 
exist  for  many  years  without  causing  much  discomfort.  The  diag- 
nosis of  a  renal  tuberculosis  depends  (in  addition  to  the  symp- 
toms just  described)  upon  the  discovery  of  tuberculous  disease 
elsewhere  (especially  in  the  testis),  and  of  tubercle  bacilli  in  the 
urine.  Ureteral  catheterization,  when  practicable,  will  determine 
whether  one  or  both  kidneys  are  involved.  The  tuberculin  test  is 
helpful. 

(3)  Prognosis. — Usually  but  not  invariably  fatal  in  from  one  to 
three  years  after  a  diagnosis  has  been  made.  Many  recoveries  have 
occurred  after  nephrectomy  when  but  one  kidney  is  diseased. 

II.  Tuberculosis  of  Ureter,  Bladder,  and  Prostate 
Gland. — Usually  secondary  to  renal  tuberculosis.  The  symptoms 
are  those  of  a  chronic  cystitis  without  apparent  cause.  For  the 
urinary  characters  see  page  648.  There  is  apt  to  be  persistent 
fever  and  progressive  loss  of  flesh  in  well-developed  cases.  The  kid- 
neys and  testes  should  be  carefully  examined,  and  the  absence  of  a 
vesical  calculus  assured.  If  the  prostate  is  involved,  there  is  extreme 
irritability  of  the  bladder,  hard  nodules  may  be  felt  by  rectal  exam- 


734  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

ination,  and  the  passage  of  a  sound  is  excessively  painful.     The  urine 
should  be  examined  for  tubercle  bacilli. 

III.  Tuberculosis  of  the  Testis. — The  finding  of  a  tuber- 
culous testicle  is  of  much  importance  in  making  a  diagnosis  in 
suspected  renal  tuberculosis  or  tuberculous  peritonitis.  The  epi- 
didymis is  greatly  enlarged,  in  some  instances  equalling  the  gland 
itself  in  size,  and  it  may  be  painful.  Syphilis  of  the  testicle,  with 
which  tuberculosis  may  be  confounded,  affects  the  body  rather  than 
the  epididymis,  and  the  enlargement  is  more  irregular. 

IV.  Tuberculosis  of  the  Fallopian  Tubes  and  Ovaries. — 
The  symptoms  are  those  of  ordinary  salpingitis  and  ovaritis,  but 
if  occurring  in  a  weakly,  especially  unmarried,  woman,  with  a  tuber- 
culous family  history,  and  associated  with  extensive  adhesions,  ill- 
defined  abdominal  swellings,  and  continuous  slight  afternoon  fever, 
are  suspiciously  indicative  of  the  tuberculous  character  of  the  affec- 
tion.    Ultimately  it  tends  to  a  fatal  termination. 

VII.  Tuberculosis  of  the  Lymphatic  Glaj^ds  (Scrofula) 

Tuberculous  adenitis  occurs  mainly  in  children,  and  is  almost 
always  local,  involving  special  groups  of  lymph  glands  ;  very  rarely 
nearly  all  the  lymph  glands  in  the  body  are  implicated.  The 
gland  groups  most  commonly  affected  are  the  cervical  (frequent- 
ly), bronchial,  and  mesenteric,  less  frequently  the  axillary  and 
inguinal. 

Cervical  Tuberculous  Adenitis. — (1)  Symptoms. — The  sub 
maxillary  glands  are  usually  the  first  to  be  involved,  subsequently  the 
postcervical,  supraclavicular,  and  axillary  may  follow  suit,  and  the 
disease  may  extend  downward  to  the  bronchial  glands  as  well.  Both 
sides  are  usually  affected,  one  to  a  greater  degree  than  the  other. 
Unilateral  enlargement  of  the  supraclavicular  and  axillary  glands 
may  herald  the  beginning  of  a  tuberculous  pleurisy  or  pulmonary 
phthisis.  The  affected  glands  slowly  enlarge  from  the  size  of  a  bean 
to  that  of  an  English  walnut  or  a  hen's  e^gg.  They  are  smooth,  firm, 
and  at  first  separate,  but  later  the  several  tumours  coalesce  and  be- 
come matted  together,  forming  rounded  but  irregular  masses.  The 
overlying  skin  is  freely  movable,  unless  one  or  more  glands  suppurate, 
at  which  time  the  skin  becomes  adherent  and  the  abscess  (unless 
operated)  points  and  discharges,  leaving  a  persistent  sinus.  During 
rapid  growth  or  suppuration,  fever,  anasmia,  and  loss  of  flesh  become 
manifest. 

(2)  Diagnosis. — Slowly  enlarging  glands  in  a  child  are  probably 
tuberculous  if  there  exists  at  the  same  time  chronic  naso-pharyngeal 
catarrh,   enlarged  tonsils,  suppurative  otitis  media,  eczema  of  the 


TUBERCULOSIS  735 

scalp,  ear,  or  lips,  conjunctivitis  or  keratitis,  or  known  tuberculous 
disease  elsewhere. 

Tuberculosis  of  the  Tracheo-bronchial  Glands.— Usually 
occurs  in  children  and,  in  the  majorit}'  of  cases,  pulmonary  tuberculo- 
sis coexists,  although  the  glands  alone  may  be  involved. 

(1)  Symptoms. — These  are  mainly  mechanical  and  arise  from  the 
pressure  exerted  when  the  mass  of  diseased  glands  becomes  sufficiently 
large — i.  e.,  constitutes  a  mediastinal  tumour.  From  pressure  on  the 
recurrent  laryngeal  nerve  arises  a  paroxysmal  cough ;  and  dyspnoea, 
also  paroxysmal,  which  may  be  either  croupy  or  asthmatic  in  char- 
acter. Pressure  on  the  superior  vena  cava  causes  cyanosis,  puffiness, 
or  oedema  of  the  face.  Distinct  physical  signs  are  not  common. 
Anteriorly  there  may  be  dulness  over  the  first  piece  of  the  sternum  ; 
or  posteriorly  on  either  side  of  the  spine  from  the  2d  to  the  5th  dorsal 
vertebrae.  The  mass  of  glands  may  transmit  the  breath  sounds  from 
the  trachea  and  bronchi  with  such  intensity  that  they  resemble  those 
heard  over  a  cavity,  viz.,  bronchial,  cavernous,  or  amphoric  respira- 
tion. A  suppurating  gland  may  rupture  into  a  bronchus,  and  a  con- 
siderable quantity  of  pus,  blood,  and  cheesy  matter  may  be  suddenly 
expectorated. 

(2)  Diagnosis. — The  occurrence  of  paroxysmal  cough  and  dysp- 
noea, with  swelling  of  the  face,  in  a  child  who  is  suffering  from  phthi- 
sis or  other  form  of  tuberculosis,  enables  a  diagnosis.  In  the  absence 
of  evidences  of  tuberculosis  elsewhere  it  may  be  impossible  to  say 
that  the  cough  and  dyspnoea  are  due  to  tuberculous  bronchial  glands. 
The  physical  ^\g\\s>  per  se  are  not  reliable. 

Tuberculosis  of  the  Mesenteric  Glands.— Generally  these 
glands  are  involved  secondarily  to  intestinal  tuberculosis,  but  the 
infection  may  be  primary.  In  children  the  glandular  disease  may 
greatly  predominate  over  the  intestinal  lesions  {tahes  mesenterica). 
In  this  there  is  a  chronic  diarrhoea,  the  stools  are  fluid  and  offen- 
sive, the  abdomen  is  swollen  and  tympanitic,  and  if  the  flatulent  dis- 
tention can  be  relieved,  the  enlarged  glands  may  be  felt  as  small, 
firm,  rounded,  somewhat  movable  tumours,  most  commonly  lying  near 
the  navel  or  in  the  right  iliac  fossa.  There  is  moderate  fever,  marked 
anaemia,  and  great  emaciation.  Tuberculous  peritonitis  is  a  common 
coexistent  lesion. 

V^III.   Tuberculosis  of  the  Alimextart  Canal 

Tuberculosis  of  any  portion  of  the  alimentary  canal  except  the 
intestines  is  rare.  Tuberculous  ulcers — sharply  defined,  irregular, 
indurated  base,  with  yellowish  floor,  not  inclined  to  bleed — are  met 
with  on  the  lips  (very  rare) ;  on  the  tongue,  in  which  case,  in  contra- 


736  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

distinction  to  syphilis,  the  submaxillary  glands  are  not  enlarged  and 
the  iodides  do  no  good ;  on  the  tonsils,  often  associated  with  cervical 
adenitis ;  on  the  pharynx,  by  extension  from  a  laryngeal  tuberculo- 
sis ;  and  in  the  cesophagus  and  stomach.  In  accessible  ulcers  scrap- 
ings may  be  examined  for  tubercle  bacilli,  or  inoculations  made. 

Intestinal  Tuberculosis. — The  infection  is  often  primary  in 
children  (from  milk) ;  in  adults  almost  always  secondary  to  disease 
of  the  lungs.     It  occurs  in  one  half  of  all  cases  of  chronic  phthisis. 

(a)  Symptoms. — Persistent  diarrhoea,  often  alternating  with  con- 
stipation, is  a  prominent  symptom.  The  stools  are  thin,  offensive, 
and,  if  the  large  intestine  is  involved,  may  contain  mucus  and  blood. 
There  may  be  moderate  colicky  pain  and  localized  tenderness. 

{h)  Diagnosis. — A  chronic  diarrhoea  occurring  in  the  course  of 
chronic  pulmonary  phthisis  is  usually  tuberculous,  unless  due  to 
amyloid  disease  of  the  intestines,  in  which  case  evidences  of  amyloid 
disease  of  the  spleen,  liver,  or  kidneys  may  be  found.  Primary 
tuberculosis  of  the  intestines  is  recognised  with  great  difficulty. 
Anaemia,  loss  of  flesh,  fever,  the  discovery  of  enlarged  mesenteric 
glands,  and  the  finding  of  tubercle  bacilli  in  the  faeces  (in  the  absence 
of  pulmonary  disease  in  which  the  germs  may  be  swallowed)  may  lead 
to  a  diagnosis,  but  it  may  be  necessary  to  wait  for  the  development 
of  tuberculosis  in  some  other  part  of  the  body. 

Chronic  tuberculosis  localized  in  the  caecum  or  appendix  may,  in 
consequence  of  the  development  of  a  tumorous  mass,  simulate  a 
subacute,  chronic,  or  recurring  appendicitis,  or  a  carcinoma  of  the 
caecum.  The  discovery  of  tubercle  bacilli  in  the  stools  may  enable  a 
diagnosis. 

IX.    TUBEECULOSIS    OF    OtHER    OrGAXS 

Liver. — This  is  infrequent  except  in  connection  with  general 
tuberculosis  and  tuberculous  peritonitis.  In  the  last  the  perihepati- 
tis may  involve  the  portal  vessels  and  give  rise  to  ascites.  Other- 
wise there  are  no  symptoms  of  clinical  importance.  Spleen. — En- 
largement of  the  spleen  is  constant  in  acute  miliary  tuberculosis, 
because  of  its  involvement  in  the  tuberculous  infection.  Suprarenal 
Capsules. — Generally  chronic,  often  associated  with  tuberculosis  else- 
where. It  is  clinically  important  because  of  its  frequent  existence  in 
Addison's  disease  {q.  v.).  Brain  and  Spinal  Cord. — Acute  tubercu- 
lous meningitis  (page  734)  has  been  considered.  Chronic  tuberculosis 
of  the  brain  (meningo-encephalitis)  and  spinal  cord  causes  symptoms 
of  tumour  of  the  brain  {q.  v.),  or  spinal  tumour  {q.  v.),  or  spinal 
meningitis  {q.  v.).  Mammary  Gland. — Indicated  by  the  presence  of 
circumscribed  nodules  which  often  ulcerate  and  form  fistulae.     The 


TUBERCULOSIS— SYPHILIS  737 

nipple  is  retracted,  and  the  axillary  glands  are  enlarged  in  most 
cases.  Tuberculous  (cold)  abscess  may  occur.  The  diagnosis  is  to 
be  made  from  the  appearance  of  the  ulcers  and  fistulae,  the  finding 
of  tuberculous  disease  elsewhere,  and  the  demonstration,  by  the 
microscope  or  by  inoculation,  of  the  presence  of  tubercle  bacilli  in 
scrapings  from  the  ulcer  or  fistula. 

X.   Diagnosis  of  Tuberculosis 

Aside  from  the  symptoms  and  physical  signs  of  the  various  forms 
of  tuberculosis,  the  diagnosis  depends  : 

(1)  Upon  the  presence  of  the  tubercle  bacilli  in  sputum,  effusions, 
urine,  pus,  or  scrapings  from  the  lesions;  or  upon  the  results  of 
inoculation  of  these  substances  into  guinea-pigs. 

(2)  A  reaction  after  the  hypodermic  injection  of  tuberculin 
(Koch's  original).  One  milligramme  is  used  as  the  initial  dose,  but 
if  there  is  no  reaction — i.  e.,  unless  the  temperature  rises  within  10 
or  12  hours  to  102°  to  104° — a  dose  of  2  or  3  milligrammes  is  given  2 
or  3  days  subsequently. 

XXVI.    SYPHILIS 

1.  Acquired  Syphilis. — {a)  Primary  Stage. — In  from  2  to  4 
weeks  after  inoculation  the  initial  lesion  appears  as  a  small  red 
papule  which  increases  in  size,  becomes  eroded,  and  finally  forms  a 
small  ulcer  with  a  raised,  movable,  and  characteristically  gristly  or 
indurated  base — the  hard  chancre.  Usually  seated  upon  the  prepuce 
or  the  vulva,  it  may  occur  just  inside  the  urethra,  or  upon  the  finger 
(especially  in  physicians),  lip,  tongue,  or  elsewhere.  The  lymph 
glands,  by  way  of  which  the  affected  region  is  drained,  undergo  a 
painless  enlargement,  occurring  about  2  weeks  after  the  appearance 
of  the  initial  lesion. 

(b)  Secondary  Stage. — In  from  6  to  12  weeks  from  the  appearance 
of  the  primary  lesion  the  constitutional  symptoms  become  manifest. 
There  is  fever,  usually  mild  (101°)  and  continuous;  or  it  may  be 
remittent,  more  rarely  distinctly  intermittent.  There  is  weakness, 
headache,  slight  backache,  and  general  aching,  often  with  a  red- 
dened and  sore  throat.  Aiixemia  with  a  sallow  or  slightly  yellowish 
tint  of  the  skin  (syphilitic  cachexia)  is  present  and  may  develop 
quite  rapidly.  The  lymph  glands  all  over  the  body  may  become 
somewhat  enlarged  and  indurated.  SMn  eruptions  appear,  first  and 
most  commonly  the  macular  (roseolar)  syphilide,  reddish-brown 
"  coppery "  spots  occurring  especially  upon  the  anterior  aspect  of 
the  trunk  and  arms,  and  remaining  for  one  or  two  weeks.  It  may 
recur  at  a  later  period.     This  rash  when  seated  in  the  nose  and 


738  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

throat  causes  coryza  and  angina.  The  papular  syphilide,  resembling 
acne,  and  occurring  mainly  upon  the  face  and  trunk,  is  next  most 
common.  If  the  papules  suppurate,  as  they  may  in  the  severer  forms 
of  the  disease,  the  condition  may  simulate  smallpox. 

Syphilitic  psoriasis,  a  squamous  or  scaly,  copper-coloured  syphi- 
lide, occurs  especially  on  the  palms  and  soles.  Mucous  patches  (char- 
acteristic and  contagious),  well-defined  flattened  growths  with  a 
moist  surface  covered  by  a  grayish  secretion,  are  found  not  only 
upon  the  mucous  membrane  of  the  lips,  tongue,  gums,  cheeks,  and 
pharynx,  and  the  muco-cutaneous  junctions  of  the  anus,  vulva,  and 
penis,  but  also  in  the  moist  cutaneous  folds  of  the  perinaeum,  groins, 
axillae,  navel,  and  webs  of  the  toes.  The  tonsils  may  show  small 
ulcers ;  and  papillary  hypertrophy  of  the  mucous  membranes  may 
cause  soft  warty  outgrowths  or  condylomata,  especially  about  the 
anus  or  vulva.  AYhitish  spots  (leucomata)  may  be  seen  upon  the 
tongue,  particularly  in  smokers.  "White  patches  (leucoderma)  sur- 
rounded by  an  increased  deposit  of  pigment  may  occur,  especially 
on  the  neck.  Loss  of  hair,  perhaps  including  eyelashes  and  eye- 
brows (syphilitic  alopecia),  frequently  takes  place,  usually  3  or  4 
months  after  the  infection.  A  painful  periostitis,  the  pain  growing 
worse  at  night,  may  become  manifest.  It  is  usually  circumscribed 
(nodes  or  exostoses),  and  occurs  especially  upon  the  tibiae,  clavicles,, 
and  cranial  bones.  Syphilitic  onychia  or  paronychia  may  deform  or 
destroy  the  nail.  Three  to  six  months  after  the  initial  lesion  iritis 
may  develop ;  choroiditis  and  retinitis  are  rare.  Epididymitis  and 
parotitis  may  occur.     Abortion  or  miscarriage  is  common. 

(c)  Tertiary  Stage. — The  lesions  which  are  commonly  recognised 
as  tertiary  may  appear  as  early  as  6  months  from  the  occurrence  of 
the  initial  sore,  while  secondary  lesions  are  still  present ;  ordinarily  a 
latent  period  intervenes,  and  it  is  several  years  before  the  tertiary 
manifestations  begin.  The  characteristic  lesions  of  the  third  stage 
are  certain  cutaneous  lesions,  gummata  (syphilomata)  especially  of 
the  viscera,  diseases  of  the  bone,  and  amyloid  degeneration. 

(1)  Cutaneous  Manifestations. — The  tuberculous  syphilide  ap- 
pears as  small  nodules,  which  break  down,  resulting  in  well-defined, 
rounded,  and  deep  ulcers,  which  may  coalesce  with  neighbouring 
lesions,  healing  in  one  part  and  extending  at  another  (serpiginous 
ulcer),  with  a  thick,  yellowish  discharge.  After  healing,  the  cicatrix 
resembles  that  of  a  burn.  These  lesions  may  be  covered  by  a  conical 
stratified  crust  (rupia)  which  is  quite  characteristic.  Gummata 
originating  in  the  subcutaneous  tissues  may  grow  to  the  size  of  a 
walnut.  They  may  be  absorbed,  or  may  break  down,  forming  a  deep 
ulcer  and  a  deep  scar. 


SYPHILIS  Y39 

(2)  Gummata  of  the  Mucous  Membranes. — These  result  in  ulcers 
which  may  cause  deforming  scars ;  or  destroy  bone  or  cartilage,  if 
such  underlie  the  affected  mucous  membrane.  Thus  gummata  of 
the  mouth  and  nasopharynx  may  perforate  the  nasal  septum  and 
flatten  the  nose ;  or  perforate  and  partly  destroy  the  hard  and  soft 
palate ;  or  cause  the  adhesion  of  the  soft  palate  to  the  posterior  wall 
of  the  pharynx.  Gummatous  ulceration  of  the  rectum  may  result 
in  cicatricial  stricture. 

(3)  Gummata  of  the  Bones,  Periosteum^  and  Mtcscles. — The  cranial 
bones  in  particular,  less  frequently  the  long  bones,  are  subject  to 
gummous  periostitis.  The  gummata  are  at  first  hard,  but  subse- 
quently soften,  ulcerate,  and  expose  carious  bone ;  perhaps  causing 
perforation  of  the  skull  when  the  cranial  bones  are  affected.  Gum- 
mata growing  from  the  bodies  of  the  vertebrae  may  impinge  upon 
the  spinal  cord ;  and  similar  growths  may  involve  the  joints  and 
periarticular  tissues.  Diffuse  gummous  infiltration  of  the  fingers  or 
toes  constitutes  dactylitis  syphilitica. 

Circumscribed,  slightly  movable  gummata  may  occur  in  the  mus- 
cles ;  and  a  chronic  myositis  may  result  from  syphilis. 

II.  Congenital  Syphilis. — The  symptoms  of  inherited  syphilis 
may  be  present  at  birth  ;  usually  they  appear  between  4  and  8  weeks 
atter  birth. 

(1)  Symptoms  at  Birth. — The  infant  is  poorly  developed,  emaci- 
ated, and  blisters  or  bullae  (pemphigus)  are  usually  present  on  the 
wrists  and  hands,  ankles  and  feet.  The  epiphyses  of  the  long  bones 
may  be  separated  from  the  shaft  (osteochondritis) ;  the  spleen  and 
the  liver  are  enlarged ;  the  lips  and  angles  of  the  mouth  are  fissured 
and  ulcerated ;  and  there  is  a  marked  coryza  ("  snuffles  "). 

(2)  Early  Symptoms  after  Birth. — The  infant  may  be  born  plump 
and  healthy,  and  so  remain  for  from  4  to  8  weeks,  at  which  time  it 
begins  to  snuffle,  the  skin  around  the  nostrils  ulcerates,  and  the 
nasal  bones  may  become  necrosed  and  the  root  of  the  nose  flattened 
down.  The  skin  is  sallow,  and  usually  first  about  the  mouth,  arms, 
and  genitals,  erythematous,  eczematous,  macular,  or  papular  syphilides 
develop.  The  lips  and  angles  of  the  mouth  become  characteristically 
fissured  {rhagacles)  and  ulcerated.  Alopecia,  ulcerations  of  the  skin 
and  mucous  membranes,  enlargement  of  the  spleen  (of  diagnostic 
value),  enlargement  of  the  liver  (not  significant),  slight  swelling  of 
the  lymph  glands,  and  rarely  subcutaneous  and  mucous-membrane 
liaemorrhages  may  occur.  The  child  cries,  becomes  peevish,  sleep- 
less, anaemic,  and  thin. 

(3)  Late  Symptoms. — In  cases  which  recover  from  the  early  mani- 
festations, the  late  symptoms  may  appear  either  at  the  second  denti- 


740  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

tion  or  at  puberty.  The  child's  general  development  is  faiilty,  and 
even  at  the  age  of  puberty  the  patient  may  retain  the  characteristics 
of  a  much  earlier  period.  The  late  symptoms  are  interstitial  kera- 
titis or  iritis,  rapid  onset  of  deafness,  perhaps  due  to  labyrinthine  dis- 
ease, Hutchinson's  teeth  (page  224),  chronic  periostitis,  especially  of 
the  tibia  (sabre-shaped),  and  atrophy  of  the  testicles. 

III.  Visceral  Syphilis. — Syphilis  of  the  Brain  and  Cord. — 
The  symptoms  are  due  to  the  presence  of  gummata  ;  or  a  gummatous 
meningitis  or  arteritis ;  or  localized  sclerosis.  Cerebral  st/philis  pre- 
sents the  symptoms  of  brain  tumour  (</.  n),  epilepsy  (g.v.),  demen- 
tia paralytica,  or  apoplexy  {q.  v.).  Spinal  syphilis  presents  the 
symptoms  of  tumour  of  the  cord  {q.  v.),  or  chronic  spinal  meningitis 
iq.  v.). 

Syphilis  of  the  Lungs. — In  rare  cases  this  may  simulate  chronic 
phthisis,  but  the  diagnosis  is  difficult.  If  the  symptoms  and  signs 
of  chronic  phthisis,  or  of  chronic  interstitial  pneumonia  with  bron- 
chiectasis, occur  in  a  person  who  is  unquestionably  syphilitic,  and 
repeated  examinations  fail  to  reveal  the  presence  of  tubercle  bacilli, 
it  may  be  considered  syphilis  (gummata  or  fibrosis)  of  the  lungs. 
Janeway  has  called  attention  to  the  occasional  existence  of  fever  in 
tertiary  syphilis.  Prior  to  the  publication  of  his  paper  I  had  under 
my  care  a  physician  who  had  fever  (101°  to  102°),  cough,  expectora- 
tion, and  some  physical  signs  of  chronic  phthisis,  but  also  presented 
gumma  in  the  liver,  amyloid  kidneys,  profound  anaemia,  and  a  rapid 
arteriosclerosis,  with  absence  of  tubercle  bacilli  in  his  sputum. 
There  were  also  tibial  nodes,  pigmented  scars,  and  a  history  of  a 
very  persistent  sciatica.  In  this  case  I  made  a  diagnosis  of  pulmo- 
nary syphilis. 

Syphilis  of  the  Liver. — Gummata  form  in  the  substance  of  the 
liver,  and  as  a  result  of  their  absorption  the  liver  becomes  deeply 
lobulated.  A  chronic  fibrous  inflammation,  affecting  mainly  Glisson's 
capsule,  may  coexist,  causing  a  perihepatitis,  with  fibrous  bands  run- 
ning inward  along  the  portal  canals.  Amyloid  disease  of  the  liver 
may  supervene. 

(1)  Symptoms. — There  may  be  evidences  of  hepatic  cirrhosis 
(ascites,  slight  jaundice,  and  digestive  disturbances) ;  or  the  liver 
may  be  enlarged  and  irregular,  and  the  spleen  also  enlarged,  with 
polyuria,  albumin,  and  casts  (amyloid  disease) ;  or  the  gummata  may 
form  a  tumour  in  the  right  or  left  lobe  of  the  liver.  The  disease  may 
be  latent.  The  ascites  is  due  to  pressure  by  gummata,  or  contrac- 
tion of  cicatricial  tissue,  upon  the  portal  vein  or  its  branches. 

(2)  Diagnosis. — There  must  be  good  evidence  of  a  previous  syph- 
ilitic infection.     If  with  this  the  liver  is  found  (after   removing 


SYPHILIS  Y41 

ascitic  fluid  if  necessary)  to  be  enlarged,  distinctly  lobulated,  and 
irregular,  or  presents  several  rounded  prominences,  and  the  general 
health  is  not  greatly  impaired,  the  disease  is  probably  syphilitic.  The 
therapeutic  test  (potassium  iodide)  is  helpful. 

An  enlarged  amyloid  liver  with  irregular  gummata  closely  simu- 
lates cancer  of  the  liver,  but  in  the  latter  ascites  and  jaundice  are 
rare  ;  there  is  marked  cachexia ;  there  is  often  a  softening  or  depres- 
sion in  the  centres  of  the  nodules;  usually  a  history  of  a  primary 
malignant  growth  in  the  breast,  stomach,  intestines,  or  uterus,  and  it 
is  found  as  a  rule  only  after  40  years  of  age. 

Syphilis  of  the  Rectum. — Occurs  most  commonly  in  women,  and 
consists  in  the  development  of  diffuse  submucous  gummata  above 
the  internal  sphincter.  The  symptoms  are  those  of  a  slowly  pro- 
gressive narrowing  or  stricture  of  the  rectum.  The  stools  may  be 
muco-purulent  and  passed  with  straining  and  tenesmus,  simulating 
a  chronic  dysentery.  In  addition  to  the  history  or  presence  of  other 
syphilitic  lesions  the  diagnosis  depends  upon  a  rectal  examination 
which  reveals  a  firm  fibrous  ring,  differing  materially  from  the  cra- 
teriform  ulcer  of  rectal  cancer. 

Syphilis  of  the  Heart. — This  occurs  in  the  form  of  gummata  or 
chronic  fibrosis,  or  both. 

Symptoms. — A  sense  of  oppression,  palpitation,  and  extreme  irreg- 
ularity of  the  heart  action,  dyspnoea,  and  praecordial  pain  or  angi- 
nal attacks,  occurring  in  a  patient  who  is  known  to  be  the  sub- 
ject of  tertiary  syphilis,  may  enable  at  least  a  probable  diagnosis  of 
cardiac  syphilis.     Sudden  death  occurs  in  33  per  cent  of  these  cases. 

Syphilis  of  the  Arteries. — Endarteritis  and  periarteritis  may  play 
an  important  part  in  the  production  of  arteriosclerosis  {q.  v.),  aneu- 
rism {q.  r.),  and  paralytic  dementia. 

Syphilis  of  the  Kidneys. — The  usual  manifestation  of  renal  syph- 
ilis assumes  the  form  of  amyloid  degeneration  of  the  kidneys  {q.v.). 

Syphilis  of  the  Testicles. — This  may  appear  in  two  forms :  a  uni- 
form or  irregular  painless  atrophy  of  the  testicles,  usually  involving 
one  more  than  the  other,  and  gummata  of  the  testicles.  As  compared 
with  tuberculosis  of  the  testicle,  syphilitic  orchitis  presents  nodules 
mainly  in  the  body  of  the  testis,  the  epididymis  usually  escaping,  and 
tliere  is  no  tendency  to  ulceration.  Malignant  disease  of  the  testicle 
develops  more  rapidly,  is  painful,  and  may  ulcerate. 

IV.  Diagnosis  of  Syphilis. — The  tendency  to  concealment  on 
the  part  of  the  patient  is  to  be  remembered.  When  endeavouring  to 
ascertain  the  existence  of  a  previous  syphilitic  infection,  the  result 
of  which  may  explain  the  present  condition,  the  following  points  are 
to  be  determined : 
49 


Y42  DIAGNOSIS,   DIRECT   AND   DIFFERENTIAL 

Is  there  a  history  of  a  primary  sore  (genital  or  extragenital),  fol- 
lowed by  skin  rashes  (without  itching),  sore  throat,  and  alopecia  ? 

In  women,  have  there  been  frequent  abortions  or  miscarriages  ? 

In  children,  is  there  a  history  of  "  snuffles "  and  skin  rashes 
within  the  first  3  months  after  birth  ? 

Examine  nose,  mouth,  and  throat  for  lesions,  such  as  destruction 
of  nasal  septum  and  flattening  of  nose,  perforation  of  hard  or  soft 
palate,  ulcers,  mucous  patches,  etc. 

Examine  the  cutaneous  surface  for  scars  (groin,  leg) ;  the  genitals 
for  the  primary  scar  and  for  syphilitic  atrophy  or  enlargement  of  the 
testicles. 

Examine  the  bones  (especially  tibia,  clavicle,  and  cranial  bones) 
for  nodes,  or  necrosis. 

Examine  the  teeth  (for  Hutchinson's  sign) ;  the  eyes  for  iritic 
adhesions  or  interstitial  (ground-glass)  keratitis. 

Examine  the  lymph  glands  for  universal  moderate  enlargement 
and  induration. 

Remember  that  paralysis  of  single  cranial  nerves,  or  anomalous 
or  atypical  symptom  groups  (especially  in  disease  of  the  nervous 
system),  are  apt  to  be  of  syphilitic  origin  ;  also  that  visceral  syphilis 
presents  symptoms  which  usually  do  not  differ  from  those  of  non- 
syphilitic  disease,  and  that  the  diagnosis  of  their  syphilitic  origin  de- 
pends upon  the  history  of  infection  and  the  finding  of  lesions  which 
are  accessible  and  characteristic. 

XXVII.    GONORRHCEAL   RHEUMATISM 

This  form  of  systemic  infection,  manifested  mainly  by  an  arthri- 
tis, occurs  as  a  rule  during  or  toward  the  end  of  a  gonorrhoea,  but 
may  show  itself  at  any  time  in  the  course  of  a  subsequent  gleet. 

Symptoms. — These  are  variable.  There  may  be  fleeting  joint 
pains,  without  redness  or  fever ;  or  polyarticular  inflammation,  with 
fever,  redness,  and  swelling  of  the  affected  joints  ;  or  one  articulation, 
especially  the  knee  joint,  may  become  greatly  swollen  and  excessively 
painful  (rarely  suppurates),  with  but  moderate  fever;  or  the  knee 
joint  may  fill  with  fluid,  often  without  pain,  redness,  or  swelling;  or 
the  bursae  and  tendon  sheaths  in  the  vicinity  of  an  articulation  may 
become  inflamed  and  cause  thick  swelling  above  and  below  the  joint. 
Endocarditis  (sometimes  ulcerative),  pericarditis,  or  pleurisy  may 
occur,  usually  in  the  polyarthritic  form.  If  suppuration  takes  place 
(generally  in  the  knee  joint)  or  ulcerative  endocarditis  supervenes, 
the  symptoms  may  shift  into  those  of  a  pygemia. 

Diagnosis. — The  presence  of  a  recent  gonorrhoea  affords  a  direct 
clew  to  the  nature  of  the  disease ;   occurring  during  a  gleet,  the 


GONORRHCEAL   RHEUMATISM— ANTHRAX  743 

latter  may  be  overlooked  and  an  incorrect  diagnosis  result.  Com- 
pared with  rheumatic  fever  (page  711)  fewer  joints  are  affected,  the 
fever  and  constitutional  symptoms  are  less  marked,  the  disease  is  in- 
tractable and  tends  to  chronicity,  relapses  are  common,  and  anti- 
rheumatic treatment  is  of  little  or  no  service. 

XXVIII.    ANTHRAX 

This  disease,  usually  affecting  sheep  and  cattle,  and  due  to  the 
Bacillis  anthracis,  may  develop  in  man  from  accidental  inoculation. 
There  are  several  forms  of  anthrax. 

Symptoms. — (1)  Malignant  Pustule. — At  the  point  of  inoc- 
ulation (face,  hand),  1  to  3  days  after  infection,  a  small  red,  burn- 
ing papule  forms,  rapidly  developing  into  a  vesicle  containing  bloody 
serum,  which  soon  breaks,  leaving  a  dark  or  black  scab  lying  in  the 
centre  of  a  large  area  of  brawny  induration  and  oedematous  swelling. 
Eed  lines  (inflamed  lymphatic  vessels)  radiate  outward,  and  there 
are  secondary  vesicles  surrounding  the  original  pustule.  By  the 
second  day  the  constitutional  symptoms  are  severe ;  prostration, 
high  fever,  sweating,  nausea  and  vomiting,  delirium,  splenic  swell- 
ing, and  in  bad  cases  coma  and  collapse.  Death  may  occur  in 
from  5  to  8  days ;  or  the  vesicle  may  slough  off  and  convalescence 
begin. 

(2)  Anthrax  (Edema. — The  constitutional  symptoms  are  grave 
and  instead  of  the  formation  of  a  pustule  there  is  widespread  brawny 
oedema  which  may  lead  to  extensive  and  often  fatal  gangrene. 

(3)  Internal  Anthrax. — This  occurs  in  two  forms. 
Wool-sorters'  Disease. — In    this  there    is  a  sudden   onset,  with 

rigour,  fever  (102°  to  103°),  headache,  pains  in  back  and  legs,  faintness 
and  prostration.  The  pulse  is  rapid  and  weak,  and  in  bad  cases  there 
are  vomiting,  diarrhoea,  delirium,  coma,  collapse,  and  death  within  24 
hours.  In  some  instances  the  infection  manifests  itself  principally 
in  the  lungs,  affording  the  symptoms  and  signs  of  bronchitis,  or  of  a 
rapidly  spreading  septicasmic  (typhoid)  pneumonia. 

Intestinal  Form. — Sets  in  with  a  chill,  followed  by  pain  in  back 
and  legs,  nausea,  vomiting,  abdominal  pain  and  diarrhoea,  with  mod- 
erate fever ;  in  bad  cases,  cyanosis,  dyspnoea,  mucous  membrane  haem- 
orrhages, petechia,  and  toward  the  close  restlessness,  convulsions, 
and  muscular  spasms. 

Diagnosis. — The  occupation  of  the  patient  is  an  important 
diagnostic  factor.  Anthrax  occurs  in  hostlers,  butchers,  tanners, 
shepherds,  wool-sorters,  ragpickers,  weavers,  carpet  and  blanket  mak- 
ers, and  in  general  those  who  work  in  hides,  hair,  or  wool.  External 
anthrax  is  recognised  by  the  appearance  of  the  pustule.     Internal 


744  DIAGNOSIS,   DIRECT   AND  DIFFERENTIAL 

anthrax  is  diagnosed  with  great  difficulty  unless  external  anthrax 
coexists.  In  cases  suspected  because  of  the  occupation,  blood  or 
local  products,  if  such  can  be  obtained,  should  be  inoculated  into 
mice  or  guinea-pigs. 

Prognosis. — If  the  malignant  pustule  is  promptly  operated 
recovery  is  the  rule.     Internal  anthrax  is  usually  fatal. 

XXIX.    GLANDERS  (FARCY) 

This  is  a  disease  of  the  horse,  due  to  the  Bacillus  mallei,  but  may 
be  transmitted,  by  accidental  inoculation  to  man.  It  is  localized 
either  in  the  nose  {glanders)  or  beneath  the  skin  {farcy).  The 
essential  lesion  consists  of  nodules  which  break  down,  forming  ulcers 
on  mucous  membranes  and  abscesses  in  the  skin.  The  disease  may 
be  acute  or  chronic. 

Symptoms. — (1)  Acute  Glanders. — After  a  period  of  incubation 
of  3  or  4  days,  sometimes  14  days,  swelling,  redness,  and  inflamma- 
tion of  the  lymphatics  at  the  point  of  inoculation  is  observed.  At 
the  same  time  there  are  headache,  malaise,  anorexia,  fever,  and  joint 
pains.  In  two  or  three  days  nodules  form  in  the  nasal  cavities,  fol- 
lowed by  ulceration  and  a  muco-purulent  discharge.  The  nose 
swells,  and  the  cervical  glands  are  much  enlarged.  Coincidently  an 
eruption  of  red  papules  comes  out  on  the  face  and  about  the  joints, 
occasionally  over  the  trunk.  The  papules  rapidly  become  pustules 
(resembling  those  of  variola),  a  septicaemic  condition,  often  with  the 
development  of  pneumonia,  ensues,  and  the  disease  invariably  ends 
in  death  in  from  6  to  12  days. 

(2)  Chronic  Glanders. — The  symptoms  are  those  of  a  chronic 
coryza  with  recurring  ulcers.  There  may  be  weakness,  occasional 
fever,  loss  of  flesh,  and  wandering  pains  in  the  limbs. 

(3)  Acute  Farcy. — The  nose  is  not  involved,  but  with  the  general 
symptoms  of  an  acute  septicaemia  or  pyaemia,  nodular  enlargements 
(farcy  buds),  which  quickly  suppurate,  form  along  the  course  of  the 
inflamed  lymphatic  vessels.  The  joints  are  painful  and  swollen,  and 
abscesses  may  develop  in  the  muscles.  The  disease  is  usually  fatal 
in  from  12  to  15  days. 

(4)  Chronic  Farcy. — There  are  numerous  subcutaneous  nodules 
which  suppurate  and  sometimes  form  deep  ulcers.  The  lymphatics 
are  involved  slightly  if  at  all. 

Diagnosis. — The  occupation  of  the  patient  (stableman,  groom, 
hostler)  is  an  important  factor  in  the  diagnosis.  In  suspected  cases 
the  Bacillus  mallei  should  be  sought  for  in  the  discharges ;  or  a  portion 
of  the  latter,  or  of  a  culture  made  from  the  discharges,  should  be 
inoculated  into  the  peritoneal  cavity  of  a  male  guinea-pig.     In  two 


GLANDERS— ACTINOMYCOSIS— LEPROSY  745 

days,  if  the  Bacillus  mallei  is  present,  the  testes  are  greatly  swollen 
and  proceed  to  suppuration. 

Prognosis. — Acute  cases  die;  chronic  cases  have  a  mortality  of 
60  per  cent. 

XXX.   ACTINOMYCOSIS 

A  chronic  disease,  mainly  of  animals,  occasionally  of  man,  caused 
by  the  ray  fungus  {Streptothrix  actinomyces). 

Symptoms. — (1)  Actinomycosis  of  Mouth  and  Jaw. — The  lower 
jaw  is  enlarged,  or  the  side  of  the  face  is  swollen,  or  an  abscess  forms 
at  the  angle  of  the  jaw  and  discharges  pus,  which  contains  the 
organisms. 

(2)  Pulmonary  Actinomycosis. — The  symptoms  are  those  of  a 
putrid  bronchitis  {g.  v.),  pulmonary  abscess  (q.  v.),  or  a  chronic  tuber- 
culosis, with  irregular  fever,  and  offensive  sputum ;  or  an  empyema 
{q.v.)  may  result. 

(3)  Cerebral  Actinomycosis. — This  is  rare.  The  symptoms  are 
those  of  brain  tumour  {q.  v.)  or  cerebral  abscess  {q.  v.). 

(4)  Intestinal  Actinomycosis. — Gastric  disturbance,  diarrhoea,  lo- 
calized pain  or  tenderness  ;  or  symptoms  of  secondary  hepatic  abscess 
{q.  v.),  perforation  peritonitis  {q.  v.),  pericaecal  abscess  or  appendicitis 
{q.  v.),  may  result. 

Diagnosis. — To  be  made  only  by  the  discovery  of  the  parasite 
in  the  sputum  or  pus. 

XXXI.    LEPROSY 

A  chronic  disease  caused  by  the  Bacillus  leprce.  There  are  two 
clinical  varieties,  which,  however,  may  coexist  in  the  same  person. 
The  period  of  incubation  is  usually  from  3  to  5  years. 

Symptoms. — (1)  Tubercular  Leprosy. — In  the  early  stage  there 
are  slightly  elevated,  hypersesthetic  patches  of  erythema,  usually  on 
the  face,  arms,  and  knees.  The  patches  generally  become  pigmented ; 
rarely  white  and  anaesthetic.  At  a  later  period  somewhat  tender 
nodules  of  varying  size  form,  at  first  especially  on  the  face,  hands, 
and  feet,  with  thickening,  induration,  and  scaliness  of  the  skin.  The 
nodules  may  break  down  and  form  ulcers,  which,  healing,  give  rise 
to  deforming  cicatrices.  The  eyelashes  and  eyebrows  fall  out. 
Owing  to  involvement  of  the  mucous  membrane  of  the  mouth, 
throat,  and  larynx,  ozaena,  cough,  dyspnoea,  hoarseness,  or  aphonia 
may  result ;  blindness  may  ensue  from  keratitis  by  extension  from 
an  affected  conjunctiva. 

(2)  Anesthetic  Leprosy. — There  are  at  first  nerve  pains  and  areas 
of  hyperaesthesia  or  numbness.  Later  there  are  patches  of  anaes- 
thesia, which  may  be  whitish  or  scaly,  preceded  or  not  by  maculae. 


746  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

The  accessible  nerve  trunks  may  be  hard  and  nodulated  (peripheral 
neuritis),  and  trophic  disturbances  become  prominent.  Bullae  form, 
generally  upon  the  extremities,  and,  breaking,  result  in  destructive 
ulcers.  The  fingers  and  toes  may  become  contractured,  and  the  pha- 
langes undergo  necrosis  and  be  lost. 

Diagnosis. — The  dusky-red  hyperaesthetic  maculae  of  the  early 
stage,  with  the  subsequent  development  of  anaesthetic  areas,  are 
quite  characteristic;  while  in  advanced  cases  there  is  rarely  any 
doubt.  The  bacilli  may  be  found  in  a  nodule,  or  the  secretion  from 
an  ulcer,  in  suspected  cases. 

Prognosis. — Ultimately  hopeless ;  but  the  disease  is  extraordi- 
narily chronic,  lasting  from  4  to  20  or  even  30  years. 

XXXII.    TETANUS 

This  disease — caused  by  the  tetanus  hacilhis,  which  grows  in  the 
soil,  and  particularly  in  manure  —  arises  usually  by  inoculation 
through  wounds,  especially  of  the  extremities ;  but  it  may  be  idio- 
pathic. The  period  of  incubation  varies  from  1  to  2  weeks.  Acute, 
€hronic,  and  cephalic  forms  are  recognised. 

Symptoms. — (1)  Acute  Tetanus. — The  onset  may  be  abrupt, 
but  more  commonly  headache,  malaise,  and  perhaps  chilliness,  occur, 
with  slight  stiffness  of  the  neck,  or  of  the  muscles  of  the  jaw. 
Tonic  spasm  of  the  masseters  (lockjaw  or  trismus)  soon  develops, 
and  the  face  assumes  the  risus  sardonicus.  The  head  is  drawn 
back,  the  legs  rigidly  extended,  and  the  body  may  be  thrown  spas- 
modically into  a  condition  of  opisthotonos,  emprosthotonos,  or  pleu- 
rosthotonos.  The  arms  are,  as  a  rule,  little  involved.  During  the 
paroxysms  there  may  be  spasm  of  the  glottis,  dyspncea,  cyanosis,  or 
rapid  respiration,  with  sharp  pain  along  the  costal  margins.  The 
skin  is  covered  with  perspiration,  and  the  temperature  may  or  may 
not  be  moderately  elevated.  Hyperpyrexia  (108°  to  112°)  may  occur. 
The  pulse  is  usually  rapid.  The  paroxysms  of  spasm  are  excessively 
painful  and  recur  spontaneously,  or,  in  severe  cases,  as  a  result  of 
external  irritants,  and  last  a  variable  time.  The  muscles  remain 
tonically  contracted  in  the  intervals.  The  mind  is  not  affected. 
Usually  fatal  in  about  10  days.  Tetanus  may  affect  the  newborn,  the 
infection  entering  by  way  of  the  navel. 

(2)  Cephalic  Tetanus. — If  the  wound  of  inoculation  is  on  one  side 
of  the  head  or  face  there  is  trismus,  dysphagia,  and  paralysis  of  the 
facial  nerve  on  the  same  side  as  the  injury. 

(3)  Chronic  Tetanus. — The  symptoms  are  those  of  tli£  acute  form, 
but  are  milder,  interrupted  by  periods  of  relief  from  paroxysmal  and 
tonic  spasm,  and  the  course  of  the  disease  is  prolonged  for  weeks. 


TETANUS— HYDROPHOBIA  747 

Differential  Diagnosis. — The  cardinal  symptoms  are,  a  wound 
(usually),  a  period  of  incubation,  trismus,  and  rigidity  of  the 
neck. 

(1)  Hydrophobia. — In  this  there  is  a  history  of  a  bite  from  a 
rabid  animal,  mental  disturbances,  spasmodic  dysphagia  and  dyspnoea, 
and  an  absence  of  trismus  and  opisthotonos. 

(2)  Tetany. — Xo  history  of  a  wound  (except,  perhaps,  thyroidec- 
tomy). The  spasm  is  usually  limited  to  the  four  extremities,  very 
rarely  there  is  trismus,  and  the  attitude  of  the  hands  is  character- 
istic (Fig.  187,  page  518). 

(3)  Strychnine  Poisoning. — There  is  a  history  of  ingestion  of  the 
poison,  and  the  symptoms  rapidly  follow.  The  involvement  of  the 
jaw  muscles,  if  present  at  all,  comes  late,  the  spasms  occur  soon  after 
the  onset  of  the  symptoms,  and  there  is  muscular  relaxation  between 
the  paroxysms. 

Prognosis. — Traumatic  acute  cases  give  a  mortality  of  80  per 
cent ;  chronic  cases  somewhat  less ;  in  the  newborn  it  is  always 
fatal ;  in  the  idiopathic  cases  50  per  cent,  in  chronic  cephalic  cases  25 
per  cent,  may  recover. 

Promising  indications  are  a  long  incubation,  no  fever,  no  spasm 
except  in  neck  and  jaw,  and  a  chronic  course. 

XXXIII.    HYDROPHOBIA 

A  disease — due  to  an  unknown  organism — of  the  wolf,  dog,  cat, 
skunk,  cow,  and  horse.  Communicated  to  man  usually  by  bite  of  the 
dog.     Three  stages  of  the  disease  are  recognised. 

Symptoms. — (1)  Prodromal  Stage. — The  period  of  incubation 
varies  from  2  weeks  to  3  or  4  months,  usually  6  weeks  to  2  months. 
At  the  end  of  this  period  there  are  great  depression  of  spirits,  malaise, 
slight  fever,  headache,  anorexia,  insomnia,  hypersesthesia  of  the  retina 
or  the  auditory  nerve,  and  perhaps  darting  pain  or  numbness  in  the 
scar,  husky  voice,  and  slight  dysphagia. 

(2)  Stage  of  Excitement. — The  patient  is  excessively  excitable,  and 
there  is  intense  hyperaesthesia  of  the  special  senses  and  general  sensi- 
bility. The  throat  stiffens,  and  attempts  to  swallow  produce  attacks 
of  violent  spasm  affecting  the  muscles  of  the  mouth,  pharynx,  larynx, 
and  upper  chest,  with  severe  dyspnoea.  During  the  paroxysms,  which 
may  be  excited  by  the  sight  of  water  because  of  the  dread  of  a  seizure 
on  attempting  to  swallow,  or  by  bright  lights,  noises,  draughts  of  air, 
or  even  by  suggestion,  there  may  be  maniacal  delirium,  excessive  sali- 
vation, and  the  utterance  of  odd  sounds.  In  the  intervals  between 
the  seizures  the  mind  is  usually  clear,  but  delirium  or  mental  aber- 
ration may  be  present.    There  are,  in  most  cases,  slight  fever  (100°  to 


748  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

103°)  and  intense  thirst.  In  from  36  hours  to  3  days  the  symptoms 
gradually  merge  into  those  of  the 

(3)  Paralytic  Stage. — The  spasms  cease,  coma  ensues,  and  in  from 
6  to  18  hours  the  patient  dies  from  cardiac  weakness  and  final  syn- 
cope. 

Diagnosis. — This  depends  upon  the  history  of  a  bite,  the  spasm 
on  attempting  to  swallow,  the  intense  hyperaesthesia,  the  mental  dis- 
turbance, and  the  final  paralysis. 

Lyssophobia  (pseudo-hydrophobia)  is  a  condition  developing  in 
nervous  or  hysterical  persons  within  a  few  months  after  having  been 
bitten  by  a  dog.  There  are  mental  irritability,  despondency,  a  fear 
of  becoming  rabic,  and  emotional  seizures,  during  which  the  patient 
alleges  an  inability  to  swallow ;  but  there  is  no  fever,  no  increase  in 
severity,  the  course  of  the  disease  is  prolonged,  and  recovery  almost 
invariably  occurs. 

Prognosis. — When  fully  established  the  disease  is  always  fatal. 
Preventive  measures  (immediate  cauterization,  Pasteur's  treatment) 
are  of  great  importance. 

XXXIV.    BERI-BERI 

An  epidemic  multiple  neuritis.     Four  forms  are  recognised. 

Symptoms. — (1)  Rudimentary  Form. — This  begins  with  a  feel- 
ing of  weakness  in  the  extremities,  with  paraesthesias  and  some  anaes- 
thesia in  the  legs,  sometimes  with  slight  oedema  and  muscular  ten- 
derness ;  moderate  dyspnoea,  palpitation,  and  abdominal  uneasiness 
may  be  present.  These  symptoms  last  from  a  few  days  to  several 
months  and  then  pass  away.     Eecurrences  are  common. 

(2)  Paralytic  or  Atrophic  Form. — This  begins  as  does  (1)  preced- 
ing, but  the  muscles  of  the  extremities  (sometimes  of  the  face)  soon 
become  painful,  paralyzed,  and  undergo  atrophy.  The  tendon  reflexes 
are  abolished.     Cardiac  symptoms  and  oedema  are  slight  or  absent. 

(3)  Dropsical  Form. — Beginning  as  in  (1)  preceding,  the  cedema 
becomes  universal  (general  anasarca),  and  effusions  into  the  serous 
sacs  may  take  place.  Dyspnoea  and  palpitation  are  common,  while 
anaesthesia  and  muscular  atrophy  are  not  marked. 

(4)  Acute  or  Cardiac  Form. — This  begins  as  does  the  rudimentary 
form,  but  the  symptoms  of  cardiac  weakness  are  predominant.  Death 
may  occur  in  24  hours  in  the  very  acute  cases,  but  the  disease  is  usu- 
ally prolonged  for  several  weeks. 

Diagnosis. — In  patients  living  in,  or  Just  from,  the  tropics,  the 
occurrence  of  general  cedema  with  the  evidences  of  multiple  periph- 
eral neuritis  {q.  v.)  will  suffice  for  the  diagnosis. 

Prognosis. — The  mortality  varies  from  2  to  50  per  cent. 


BERI-BERI— MOUNTAIN  AND  EPHEMERAL  FEVERS         749 

XXXV.    MOUNTAIN    FEVER    AND    MOUNTAIN 
SICKNESS 

The  cases  described  as  mountain  fever  are  for  the  most  part 
typhoid  fever ;  perhaps  more  rarely  lobar  pneumonia  (Cubtin). 

The  symptoms  of  mountain  sickness — due  to  the  effect  of  rarefied 
air — are  severe  headache,  vertigo,  dry  throat,  excessive  thirst,  intense 
dyspnoea,  anorexia,  nausea  and  vomiting  (occasional),  and  a  sense  of 
profound  weakness. 

XXXVI.     EPHEMERAL    FEVER— FEBRICULA 

(Simple  Continued  Fever) 

These  terms  are  applied  to  a  brief  fever,  without  discoverable 
local  lesions,  and  depending  upon  various  and  oftentimes  undeter- 
mined causes.  If  the  elevated  temperature  lasts  for  not  more  than 
24:  hours  it  is  an  ephemeral  fever ;  if  for  from  3  to  6  days  it  is  spoken 
of  as  febricula  or  simple  continued  fever. 

Symptoms. — The  onset  is  usually  abrupt,  but  is  sometimes  pre- 
ceded by  malaise.  The  temperature  runs  from  101°  to  103°,  in 
children  perhaps  to  104°  or  105°.  There  are  headache,  flushed  face, 
anorexia,  furring  of  the  tongue,  constipation,  and  in  children  rest- 
lessness, and  occasionally  drowsiness  and  nocturnal  delirium.  In 
infants  and  young  children  there  may  be  a  convulsion.  The  urine 
is  scanty  and  high-coloured.  Herpes  labialis  is  common.  The  fever 
terminates  by  an  abrupt  crisis  in  from  1  to  6  days,  often  with  free 
sweating  and  an  increased  flow  of  urine. 

Causes. — By  far  the  most  common  example  of  the  febrile  states 
grouped  under  this  heading  is  the  one-night  fever  of  infants  due  to 
an  acute  indigestion  or  gastro-intestinal  catarrh.  Other  examples 
are  the  unrecognised  or  abortive  forms  of  typhoid  fever,  scarlet 
fever,  measles,  rheumatism,  pneumonia,  or  tonsilitis ;  intestinal  auto- 
intoxication by  ptomaines ;  inhalation  of  noisome  vapours  from  de- 
composing material  (sewer  gas,  offensive  autopsies) ;  and  exposure  to 
the  sun,  or  excessive  muscular  fatigue. 

Diagnosis. — It  is  doubtless  a  fact  that  the  term  febricula  consti- 
tutes in  one  sense  a  confession  of  ignorance,  and  that  the  frequency 
with  which  the  diagnosis  of  this  fever  is  made  is  in  inverse  ratio  to 
the  diagnostic  thoroughness  and  acumen  of  the  observer.  "Wlien  a 
careful  search  fails  to  reveal  the  rashes  of  the  exanthemata,  or  evi- 
dence of  tonsilitis,  pneumonia,  or  other  local  cause  of  fever,  and  the 
elevation  of  temperature  disappears  in  from  1  to  6  days  without  the 
development  of  the  symptoms  which  characterize  any  other  recog- 
nised disease,  the  diagnosis  of  febricula  is  justified. 


*J50      '  DIAGNOSIS,   DIRECT  AXD  DIFFERENTIAL 

SECTION  II 
DISEASES   OF  THE  DIGESTIVE  SYSTEM 

I.    DISEASES    OF    THE    MOUTH 

(.S'ee  also  pages  221,  222) 

I.  Catarrhal  Stomatitis. — (a)  Causes. — Dentition  or  gastro- 
intestinal disturbances  in  children,  irritating  or  too  hot  food,  and  the 
acute  infectious  diseases. 

{J})  Symptoms. — The  mucous  membrane  of  the  mouth  is  more  or 
less  extensively  reddened,  dry,  and  hot,  with  associated  salivation  and 
swelling  of  the  tongue.  Feverishness  and  discomfort,  or  sharp  smart- 
ing when  food  is  taken,  may  be  present.  The  duration  of  this  con- 
dition is  about  one  week,  sometimes  longer. 

II.  Aphthous  or  Follicular  Stomatitis. — {a)  Causes. — 
*'  Canker  "  sore  mouth  is  most  common  in  infants  and  young  chil- 
dren, either  as  an  idiopathic  affection  or  as  a  result  of  indigestion 
or  a  febrile  attack ;  and  occurs  in  adults  when  the  general  health  is 
impaired. 

(J)  Symptoms. — Small  vesicles  appear  on  the  inner  surface  of  the 
lips  or  cheeks  or  edges  of  the  tongue  and  soon  rupture,  leaving 
small  and  very  sensitive  superficial  grayish  ulcers  with  red  areolae. 
There  is  feverishness,  a  heavy  breath,  salivation,  and  a  disinclination 
for  taking  food.  If  complicating  some  other  disease,  the  symptoms 
of  that  disease  will  coexist.  There  may  be  successive  crops  of  vesi- 
cles which  will  protract  the  disease  beyond  its  ordinary  period,  which 
is  from  4  to  7  days. 

It  is  to  be  discriminated  from  thrush.     See  (IV)  following. 

III.  Ulcerative  or  Foetid  Stomatitis.— («)  Causes. — Putrid 
sore  mouth  occurs  most  commonly  in  children  during  the  first  den- 
tition, and  may  be  epidemic,  even  in  adults,  in  asylums,  jails,  and 
camps,  where  the  hygienic  conditions  are  poor. 

{b)  Symptoms. — The  gums  become  swollen,  red,  spongy,  and 
bleed  readily,  and  upon  them  form  linear  ulcers  with  gray,  soft,  and 
sloughing  bases.  The  mucous  membrane  of  the  lips,  cheeks,  and 
tongue  is  swollen  (rarely  ulcerated),  there  are  salivation  and  a  pecul- 
iarly foul  breath.  The  submaxillary  glands  are  enlarged,  and  the 
teeth  may  become  loosened,  perhaps  with  necrosis  of  the  alveolar 
process.  Xausea,  vomiting,  and  an  ill-smelling  diarrhcea  may  be 
present,  and  the  general  symptoms  may  be  of  a  severe  grade.  Except 
in  marasmic  or  greatly  debilitated  children  with  extensive  ulceration 
and  alveolar  necrosis,  recovery  generally  occurs  in  about  one  week. 


STOMATITIS  751 

IV.  Parasitic  or  Mycotic  Stomatitis. — («)  Causes. — This 
affection  (thrush,  soor,  muguet)  is  dependent  upon  the  Saccharomyces 
(or  O'idium)  albicans.  It  occurs  mainly  in  bottle-fed  infants.  Pre- 
disposing conditions  are  uncleanliness  of  the  mouth  and  of  feeding 
utensils,  and  cachectic  or  diseased  states  in  general,  in  adults  as 
well  as  children. 

{h)  Symptoms. — Small,  slightly  elevated,  pearly  white  or  curdlike 
spots  are  seen,  first  upon  the  tongue,  which  increase  in  size  and  may 
coalesce.  Subsequently  the  patches  spread  to  the  lips,  cheeks,  and 
hard  palate,  perhaps  invading  the  tonsils,  pharynx,  and  esophagus, 
and  in  extreme  cases  lining  the  entire  cavity  of  the  mouth  and 
throat.  The  patches  can  readily  be  removed,  in  the  majority  of 
cases,  without  excoriating  the  mucous  membrane  or  causing  it  to 
bleed. 

(c)  Diagnosis. — Microscopical  examination  of  a  bit  of  the  mem- 
brane shows  the  branching  filaments,  with  their  spore-bearing  ends, 
of  the  causative  organism.  This  disease  may  be  confounded  with 
aphthous  stomatitis ;  but  aside  from  the  microscopical  examination, 
the  latter  may  be  recognised  by  its  distinct  red-bordered  ulcers, 
usually  few  in  number  and  very  painful ;  nor  can  the  grayish  base 
of  the  ulcer  be  removed  except  with  difl&culty  and  not  without 
bleeding. 

V.  Gangrenous  Stomatitis. — {a)  Causes. — Cancrum  oris  or 
noma  is  a  rare  disease,  affecting  children  of  from  2  to  5  years  of  age, 
and  occurring  usually  during  convalescence  from  the  acute  fevers. 
More  than  fifty  per  cent  of  the  cases  follow  measles,  less  frequently 
it  occurs  after  typhoid  fever,  scarlet  fever,  variola,  and  whooping 
cough.  Debilitated  and  cachectic  states  also  predispose.  The  excit- 
ing cause  is  probably  a  yet  unknown  micro-organism. 

(b)  Symptoins. — The  disease  begins  as  an  irregular,  dark,  slough- 
ing ulcer,  usually  on  the  inside  of  one  cheek,  more  rarely  on  the 
gum.  The  process  spreads  rapidly,  the  cheek  becomes  swollen  and 
brawny,  and  externally  red  and  glazed  ;  and  later  by  extension  of  the 
sloughing  shows  a  dark,  gangrenous  spot.  The  cheek  may  be  per- 
forated, and  the  disease  may  involve  the  jaw  bones,  tongue,  chin,  and 
even  the  eyelids  and  ears.  The  breath  is  intolerably  offensive.  The 
disease  always  remains  unilateral.  The  constitutional  symptoms  are 
necessarily  severe.  There  is  great  prostration,  fever  (103°  to  104°), 
rapid  pulse,  delirium,  and  diarrhoea.  Septic  pneumonia  (by  inhala- 
tion) is  common,  and  gangrene  of  the  external  genitalia  (in  female 
children)  and  colitis  may  occur. 

The  duration  of  the  disease  varies  from  7  to  14  days,  rarely  longer, 
and  it  almost  invariably  has  a  fatal  termination. 


752  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

YI.  Mercurial  Stomatitis. — Owing  to  personal  idiosyncrasies 
this  may  follow  the  use  of  repeated  minute  doses  of  a  mercurial ;  or 
it  may  be  an  occupation  poisoning. 

Symptoms. — The  early  symptoms  are  tenderness  of  the  teeth  on 
snapping  the  jaws  sharply  together,  a  metallic  taste  in  the  mouth, 
and  a  foetid  breath.  The  gums  become  swollen,  red,  spongy,  and 
sore.  There  is  profuse  salivation,  the  tongue  is  swollen,  ulcers  may 
form,  the  teeth  become  loose  and,  rarely,  necrosis  of  the  jaw  ensues. 
There  is  a  disinclination  to  take  food,  and  diarrhoea  may  be  present. 

The  duration  of  the  disease  varies  from  2  to  4  weeks  and  re- 
covery is  the  rule. 

YII.  Subvarieties  of  Stomatitis. — In  the  newborn  there 
may  be  small  ulcers  of  the  hard  palate,  symmetrically  placed  on 
either  side  of  the  median  line,  which  may  involve  the  bone  (Parrot). 
Similar  ulcers  on  the  hard  palate  may  be  caused  in  marasmic  chil- 
dren by  the  irritation  of  a  rubber  nipple  (Bedxar).  Jacobi  has  de- 
scribed a  chronic  recurring  herpetic  eruption  of  the  buccal  cavity  in 
neurotic  persons,  sometimes  coexisting  with  erythema  multiforme. 

II.    DISEASES    OF    THE    TONGUE 

{See  also  pages  225  to  233.) 

I.  Glossitis. — Causes. — Acute  parenchymatous  ijiflammation  of 
the  substance  of  the  tongue  (rare)  is  due  to  injuries  (biting,  burns, 
stings) ;  sometimes  to  local  infection  or  mercurial  stomatitis. 

Symptoms. — The  tongue  is  painful  and  greatly  swollen,  so  much 
so  that  it  may  protrude  beyond  the  teeth.  Chewing,  swallowing,  and 
talking  are  difficult  or  impossible  ;  there  is  salivation,  the  tongue 
may  be  dry  and  cracked,  and  obstructive  dyspnoea,  sometimes  to  a 
dangerous  degree,  may  develop.  The  inflammation  may  proceed  to 
suppuration,  generally  unilateral.  The  cervical  glands  are  swollen, 
and  there  is  fever,  usually  in  proportion  to  the  severity  of  the  local 
manifestations.  The  duration  of  the  disease  is  about  1  week,  and 
recovery  is  the  rule. 

There  is  a  chronic  superficial  glossitis,  due  to  the  persistent  and 
excessive  use  of  tobacco,  spirits,  and  highly  spiced  foods.  The  dor- 
sum of  the  tongue  is  reddened  and  fissured,  and  there  may  be  smooth 
glazed  patches  bounded  by  deep  furrows.  A  glossitis  desiccans  is 
also  described,  which  is  characterized  by  the  slow  formation  of  a 
number  of  deep  fissures  and  indentations,  in  the  depths  of  which 
there  are  ulcers  and  excoriations.  The  tongue  has  a  ragged  and 
uneven  appearance. 

II.  Eczem.a  or  Psoriasis  of  the  Tongue. — Rounded  patches 
resulting  from  thickening  and  desquamation  of  the  superficial  epi- 


DISEASES  OP  TONGUE,   SALIVARY  GLANDS,   PHARYNX     753 

thelium,  healing  in  the  centre  while  spreading  at  the  periphery,  and 
coalescing  with  each  other  to  give  a  maplike  appearance — the  geo- 
graphical tongue.  The  patches  may  burn  and  itch.  The  condition 
may  be  transient,  but  is  usually  chronic  or  recurrent. 

III.  Leucoplakia  Buccalis. — Smooth,  white  or  pearly  patches 
of  thickened  epidermis  appear  on  the  sides  of  the  tongue,  and  simi- 
lar spots  may  be  found  on  the  mucous  membrane  of  the  cheeks. 
They  do  not  ulcerate,  but  may  furnish  the  starting  point  of  an  epi- 
thelioma.    The  disease  is  chronic  and  intractable. 

m.    DISEASES    OF   THE    SALIVARY   GLANDS 

I.  Ptyalism  or  Salivation. — See  page  221. 

II.  Xerostomia. — The  salivary  and  buccal  secretions  cease,  the 
mucous  membrane  of  the  buccal  cavity,  palate,  and  tongue  becomes 
dry,  red,  and  glazed,  and  cracks  may  be  visible  on  the  surface  of  the 
tongue.  Chewing,  swallowing,  and  speaking  are  difficult.  "  Dry 
mouth  "  occurs  usually  in  neurotic  or  hysterical  women,  or  follows  a 
shock  or  fright,  or  in  some  instances  may  be  due  to  a  central  lesion. 
Usually  recovered  from,  but  may  prove  intractable. 

III.  Symptomatic  {Svpjnirative)  Parotitis. — Acute  swelling 
and  inflammation  tending  to  suppuration,  and  occurring  in  the  course 
of  certain  acute  specific  infections,  especially  typhoid  fever,  less  fre- 
quently scarlet  fever,  typhus  fever,  pneumonia,  pyaemia,  erysipelas, 
and  secondary  syphilis.  More  rarely  it  arises  in  connection  with 
various  diseases  or  injuries  of  the  abdomen  and  pelvis.  When  occur- 
ring in  febrile  diseases  it  constitutes  a  bad  prognostic  omen. 

IV.  Chronic  Parotitis. — A  persistent,  perhaps  tender,  enlarge- 
ment of  the  parotid  gland  may  follow  mumps,  or  succeed  mercurial 
or  lead  poisoning,  or  occur  in  the  course  of  chronic  nephritis  and 
syphilis. 

V.  Epidemic  Parotitis. — See  page  G78. 

VI.  Gaseous  Tumours  of  the  parotid  gland  or  its  duct. — A 
tumour  in  the  course  of  Steno's  duct,  which  may  contain  air,  saliva, 
and  pus,  and  reach  the  size  of  a  walnut  or  an  egg ;  or,  very  rarely, 
multiple  small,  crepitating  tumours  of  the  parotid  gland  may  be 
encountered  in  players  on  wind  instruments  and  in  glass-blowers. 

IV.    DISEASES    OF    THE    PHARYNX 

{See  also  pages  235  to  237.) 

I.  Disturbances  of  the  Circulation.— Hyperaemia,  evidenced 
by  a  dusky  reddened  tint  of  the  mucosa,  with  unusual  visibility  of  the 
veins,  is  frequent  in  smokers,  and  is  a  part  of  naso-pharyngeal  ca- 
tarrh.   Distended  veins  may  be  due  also  to  cardiac  valvular  disease, 


754  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

and  to  pressure  upon  the  superior  vena  cava  (tumour,  aneurism). 
Eupture  may  occur,  simulating  haemoptysis.  (Edema  of  the  uvula 
and  soft  palate  may  occur  in  nephritis,  or  grave  anaemia.  The  capil- 
lary pulse  and  carotid  throbbing  of  aortic  insufficiency  may  be  vis- 
ible in  the  pharynx,  the  strong  pulsation  of  the  artery  simulating  an 
aneurism. 

II.  Acute  Pharyngitis. — The  most  common  causes  are  expo- 
sure to  cold,  digestive  disorders,  rheumatism,  or  gout.  The  symp- 
toms are  dryness  and  soreness  of  the  throat,  with  dysphagia,  slight 
chilliness,  and  fever.  There  is  a  constant  desire  to  clear  the  throat, 
the  neck  is  stiff,  the  cervical  glands  may  be  slightly  enlarged  and 
painful,  and  the  inflammation  may  extend  to  the  larynx  (hoarseness) 
or  to  the  Eustachian  tubes  (slight  deafness). 

On  inspection,  there  is  a  general  dry,  red,  and  congested  condi- 
tion of  the  mucous  membrane,  perhaps  with  cedema  of  the  uvula. 
It  is  often  a  part  of  an  acute  catarrh  of  the  nasopharynx  and  larynx. 
Recovery  occurs  Avithin  a  week. 

III.  Membranous  Pharyngitis. — False  membrane  may  form 
in  the  pharynx  (diphtheroid  sore  throat)  due  to  the  streptococcus. 
It  can  be  distinguished  from  diphtheria  only  by  culture. 

IV.  Chronic  Pharyngitis. — "  Clergyman's  sore  throat "  may 
result  from  repeated  acute  attacks,  and  often  occurs  in  smokers  and 
persons  who  make  much  and  vigorous  use  of  the  voice,  or  it  may  be 
a  part  of  a  chronic  naso-pharyngeal  catarrh. 

The  symptoms  are  a  constant  hawking,  with  a  dropping  of  mucus 
from  the  upper  pharynx.  The  mucous  membrane,  especially  of  the 
posterior  pharyngeal  wall,  is  duskily  hyperaemic  and  studded  with  a 
variable  number  of  projecting  rounded  bodies  (enlarged  mucous  fol- 
licles). Occasionally  the  mucous  membrane  is  dry  and  glistening 
{pharyngitis  sicca). 

V.  Ulcers  in  the  Pharynx. — See  page  236. 

VI.  Acute  Infectious  Phlegmon  of  the  Pharynx.— The 
symptoms  are  soreness  of  the  throat,  dysphagia,  hoarseness,  swelling 
and  oedema  of  the  pharyngeal  mucosa,  with  rapid  suppuration,  swell- 
ing of  the  neck,  interference  with  respiration,  high  fever,  and  pros- 
tration. 

VII.  Retropharyngeal  Abscess. — As  a  rule  occurs  in  healthy 
children  under  2  years  of  age,  but  may  be  a  sequel  of  infectious 
fevers,  especially  diphtheria  and  scarlet  fever,  or  a  result  of  caries 
of  the  bodies  of  the  cervical  vertebrae.  The  symptoms  are  pain,  dys- 
phagia, difficult  and  impeded  breathing,  sometimes  cough,  hoarse- 
ness, and  stiffness  of  the  neck.  The  diagnosis  is  made  by  inspection 
and  palpation  of  the  pharynx,  by  which  is  discovered  a  fluctuating 


DISEASES  OF   PHARYNX  AND  TONSILS  755 

tumour  projecting  from  the  posterior  pharyngeal  wall.  The  progno- 
sis is  good  if  operated  early. 

VIII.  Angina  Ijudovici. — This  is  a  rare  disease,  not  so  much 
of  the  pharynx  as  of  the  floor  of  the  mouth  and  the  cellular  tissues 
of  the  neck.  It  is  a  streptococcus  inflammation,  occurring  either 
idiopathically  or  as  a  result  of  the  specific  infections,  especially  diph- 
theria and  scarlet  fever. 

The  symptoms  are :  Swelling  beginning  in  the  submaxillary  re- 
gion of  the  side,  and  spreading  to  the  floor  of  the  mouth  and  the 
front  of  the  neck.  There  is  much  pain,  with  dysphagia  and  difl&cult 
mastication  and  articulation.  Grave  dyspnoea  may  supervene  from 
compression  of  the  larynx  or  oedema  of  the  glottis. 

V.     DISEASES    OF    THE    TONSILS 

{See  also  page  235.) 

I.  Follicular  {Lacunar)  Tonsilitis. — (a)  Causes. — Xot  sel- 
dom precedes  an  attack  of  rheumatic  fever,  and  is  often  caused  by 
exposure  to  cold,  fatigue,  and  sewer-gas  poisoning.  The  streptococcus 
is  commonly  present.  It  occurs  mainly  between  the  ages  of  10  and 
25  years.  It  is  often  contagious,  and  repeated  attacks  in  the  same 
individual  are  very  common. 

{b)  Symptoms. — The  onset  is  usually  abrupt,  with  chilliness  or  a 
chill,  fever  (102°  to  105°),  headache,  backache,  and  general  aching, 
which  may  be  very  severe,  and  occasionally  initial  vomiting.  The 
tonsils  are  reddened,  more  or  less  swollen,  and  studded  with  punc- 
tate whitish  spots  corresponding  to  the  distended  lacunae.  The 
spots  may  coalesce  and  form  patches  nearly  or  quite  covering  the 
tonsils.  Both  tonsils  are  usually  affected,  although  one  often  starts 
a  day  or  two  previous  to  the  other.  The  cervical  glands  are  enlarged 
and  tender.  There  is  dysphagia,  furred  tongue,  foul  breath,  nasal 
voice,  and  scanty  and  high-coloured  urine,  sometimes  with  a  trace  of 
albumin.  The  pulse  is  rapid,  and  in  children  the  respiration  is 
accelerated.  The  constitutional  symptoms  are  often  out  of  all  pro- 
portion to  the  local  signs.  The  fever  not  infrequently  subsides  by 
crisis  on  the  3d  or  4th  day,  but  may  be  protracted  for  8  or  9  .days. 
Among  the  occasional  sequelw  which  occur  are  pneumonia,  rheumatic 
fever,  acute  nephritis,  endocarditis,  pericarditis,  and  otitis  media. 

(c)  Diagnosis. — There  is  often  so  little  initial  soreness  of  the 
throat  that  the  patient  considers  the  routine  examination  of  the 
buccal  cavity,  which  should  always  be  made  in  acute  febrile  cases,  to 
be  quite  unnecessary.  It  may  be  confounded  with  diphtheria  (p. 
692),  but  a  history  of  repeated  attacks  is  in  favour  of  tonsilitis. 


756  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

II.  Phlegmonous  or  Suppurative  Tonsilitis. — Quinsy 
occurs  mainly  between  15  and  35  years  of  age,  and  there  is  a  strong 
tendency  to  repetition  of  the  attacks  in  certain  individuals.  The 
causes  are  similar  to  those  of  follicular  tonsilitis. 

Symptoms. — The  throat  becomes  sore  and  dry,  and  is  excessively 
painful.  One  or  both  tonsils  are  seen  to  be  swollen,  sometimes 
meeting  in  the  median  line,  reddened,  and  at  first  hard.  The  uvula, 
soft  palate,  and  surrounding  parts  are  reddened  and  cedematous. 
There  is  salivation  and  the  secretion  of  a  tenacious  mucus,  which  is 
removed  with  difficulty  by  hawking.  Swallowing  is  excessively  pain- 
ful, and  perhaps  impossible.  The  lower  jaw  scarcely  can  be  moved, 
articulation  is  difficult,  and  the  voice  has  a  nasal  quality.  The  cer- 
vical glands  are  swollen.  In  from  2  to  6  days  suppuration  occurs 
and  fluctuation  can  be  felt  (if  the  finger  can  be  introduced)  usually 
in  the  tissues  of  the  soft  palate  above  and  anterior  to  the  tonsil, 
rather  than  in  the  gland  itself.  If  the  pus  is  not  evacuated  by 
incision  the  abscess  bursts  anteriorly,  or  more  rarely  toward  the 
pharynx,  with  immediate  relief  of  the  symptoms.  The  constitu- 
tional disturbance  may  be  severe ;  fever  (104°  to  105°),  with  a  rapid 
pulse,  occasional  nocturnal  delirium,  and  exhaustion. 

The  inflammation  sometimes  undergoes  resolution,  and  may  at 
times  be  apparently  aborted  by  treatment  (guaiacum,  salicylates). 
In  children  under  15  years  of  age  resolution  is  common  Avithiu  3  to 
5  days ;  in  adults  suppuration  is  frequent,  usually  unilateral,  and  the 
disease  runs  its  course  in  from  8  to  10  days.  The  prognosis  is  fa- 
vourable except  in  rare  instances  in  which  ulceration  of  the  internal 
carotid  or  internal  maxillary  arteries  with  fatal  haemorrhage  takes 
place,  or  a  large  abscess  ruptures  and  the  pus  enters  the  larynx, 
causing  fatal  suffocation.  (Edema  of  the  larynx  is  seldom  seen. 
Chronic  enlargement  of  the  tonsils  may  result  from  repeated  acute 
attacks. 

III.  Chronic  Tonsilitis,  and  Adenoids  of  the  Pharynx. 
— Enlarged  tonsils  and  adenoid  hypertrophy  are  usually  associated, 
but  the  latter  may  be  present  alone.  Occurs  mainly  between  the 
5th  and  15th  years  of  age,  and  is  most  frequently  the  result  of  re- 
peated naso-pharyngeal  inflammations,  or  a  sequel  of  the  exanthemata 
and  diphtheria. 

(a)  Symptoms. — The  cardinal  symptom  is  mouth -breathing,  espe- 
cially during  sleep.  The  child  is  restless,  wakes  frequently,  some- 
times with  dyspnoea  or  night  terrors,  the  respiration  is  irregular, 
noisy,  stertorous  or  snoring,  and  the  breath  is  often  fcetid.  Cough, 
frequent  hawking,  occasional  croupiness  or  asthmatic  attacks,  some 
dysphagia,  more  or  less  deafness  and  ringing  in  the  ears  from  in- 


DISEASES  OF  TONSILS  AND  ESOPHAGUS  757 

volvement  of  the  Eustachian  orifice,  and  impairment  of  taste  and 
smell,  may  occur. 

If  the  obstruction  is  allowed  to  continue  the  face  assumes  a  dull 
and  stupid  expression,  the  mouth  remains  permanently  open,  the 
nose  becomes  small  and  its  orifices  contracted,  the  lips  thicken,  the 
jaws  project,  the  hard  palate  is  arched  and  narrowed,  and  the  voice 
has  a  nasal  quality.  The  chest  may  become  barrel-shaped  in  conse- 
quence of  repeated  asthmatic  attacks,  or  more  commonly  presents 
the  deformity  known  as  pigeon  breast  or  funnel  chest.  Headache  is 
frequent,  wetting  the  bed  is  a  not  uncommon  occurrence,  and  habit- 
spasm  may  coexist.  The  child  becomes  listless,  stupid,  and  inatten- 
tive (aprosexia),  forgets  readily,  and  is  a  poor  student.  The  digestion 
is  impaired,  there  is  a  tendency  to  follicular  tonsilitis  and  a  marked 
liability  to  diphtheria. 

(Z»)  Diagnosis. — In  a  well-marked  case  the  facies  is  characteristic. 
The  enlarged  faucial  tonsils  can  be  readily  seen,  but  the  adenoid 
growths  in  the  upper  pharynx  usually  require  to  be  palpated,  when 
one  can  feel,  according  to  the  manner  of  their  growth,  the  flat  or 
grapelike  vegetations. 

VI.    DISEASES    OF   THE    ESOPHAGUS 

{For  methods  of  examination,  see  pages  44^i  44G-) 

I.  Acute  Esophagitis. — {a)  Causes. — Corrosive  poisons,  hot 
fluids,  foreign  bodies;  occurs  rarely  in  typhoid  fever,  pneumonia, 
smallpox,  diphtheria,  pyaemia,  and  thrush,  and  in  connection  with 
cancer  of,  or  near,  the  esophagus. 

(b)  Symptoms. — The  main  indication  is  substernal  pain,  often 
intense,  on  swallowing.  The  pain  may  be  dull  and  continuous.  If 
an  obstructing  foreign  body  is  present  there  may  be  spasm,  with 
regurgitation  of  food,  blood,  and  pus.  The  passage  of  a  sound  is 
painful. 

II.  Ulceration  of  the  Esophagus. — This  may  occur  in  ca- 
chectic states,  typhoid  fever,  and  cancerous  disease.  Perforation 
of  an  ulcer  in  the  upper  portion  of  the  esophagus  causes  a  brawny 
swelling  of  the  tissues  at  the  root  of  the  neck  and  in  the  supraclavic- 
ular space. 

III.  Spasm  of  the  Esophagus. — Occurs  in  hysteria,  hypo- 
chondriasis, epilepsy,  chorea,  and  above  all  hydrophobia. 

It  is  indicated  by  an  inability  to  swallow  solid  food,  although 
with  rare  exceptions  fluids  can  be  taken.  That  the  obstruction  is 
spasmodic,  and  not  organic,  may  be  inferred  from  its  occurrence  in 
neurotic  young  persons  or  elderly  hypochondriacs,  and  confirmed  by 

50 


758  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

the  passage  of  the  tube,  which  may  be  temporarily  arrested  at  the 
site  of  spasm,  but  after  a  moment  of  waiting  will  slip  past  the 
apparent  obstruction.  In  middle-aged  or  old  people  great  caution 
should  be  exercised  in  excluding  cancer  as  a  cause  of  the  dysphagia. 

IV.  Cancer  of  the  Esophagus. — May  occur  at  any  point  in. 
the  tube,  causing  stenosis  (unless  the  ulceration  and  destruction  of 
tissue  is  extensive),  with  dilatation  and  hypertrophy  above  the  seat 
of  the  disease. 

(a)  Symptoms. — Increasing  dysphagia,  progressive  emaciation, 
pain,  either  constant  or  upon  swallowing,  and  enlargement  of  the 
cervical  lymph  glands.  Kegurgitation  of  food  or  fluid,  perhaps  con- 
taining blood  and  tumour  particles,  occurs  at  once  or  from  10  to  15 
minutes  or  longer  after  taking  food,  depending  largely  upon  the  site 
of  the  growth.  Perforation  may  occur  into  the  trachea,  or  a  bron- 
chus, or  the  lung,  causing  pulmonary  gangrene  or  an  inhalation 
pneumonia  ;  or  into  the  mediastinum  ;  or  into  the  aorta  (fatal  haem- 
orrhage) ;  or  pericardium  (fatal  pericarditis).  Erosion  of  the  verte- 
bras with  compression  of  the  cord  has  been  noted ;  also  laryngeal 
paralysis  from  pressure  upon  the  recurrent  laryngeal  nerve.  The 
duration  of  the  disease  varies  from  a  few  months  to  a  year  and  a 
half,  death  usually  occurring  from  inanition  or  perforation. 

(b)  Diagnosis. — The  cardinal  symptoms  are  progressive  dysphagia 
and  rapid  emaciation  occurring  in  patients  over  50  years  of  age.  It 
is  necessary  to  eliminate  other  causes  of  stenosis :  foreign  bodies 
and  cicatricial  contraction  by  the  history ;  aneurism  (g.  v.)  or  me- 
diastinal tumour  (q.  v.)  by  the  absence  of  pressure  and  other  symp- 
toms which  characterize  them.  The  stomach  tube  is  to  be  passed 
without  violence,  and  tumour  particles  may  be  brought  up  by  it,  an 
examination  of  which  will  confirm  the  diagnosis, 

V.  Stricture  of  the  Esophagus. — (a)  Causes. — This  maybe 
congenital,  but  is  more  commonly  a  cicatricial  stricture  caused  by 
contraction  of  the  scar  tissue  resulting  from  ulceration  due  to  corro- 
sive poisons.  More  rarely  it  is  due  to  typhoid  ulcers,  gumma,  or 
tuberculosis.  Pressure  stricture,  the  next  most  frequent,  is  due  to 
aneurism,  enlarged  thyroid,  mediastinal  tumour  or  enlarged  medias- 
tinal glands,  vertebral  abscess,  and  sometimes  pericardial  effusion. 
Finally,  cancer  or  polypoid  tumour  of  the  esophagus  may  be  respon- 
sible for  the  stricture. 

(5)  Symptoms. — Dysphagia  with  emaciation  and  debility,  varying 
with  the  completeness  of  the  obstruction.  Eegurgitation  of  food,  or 
fluid  of  alkaline  reaction,  occurs,  at  once  if  the  obstruction  is  high 
up,  in  3  or  4  hours  if  it  is  low  down,  and  the  esophagus  above  the 
stricture  is  dilated.      Auscultation  of  the  esophagus  may  possibly 


DISEASES  OP  THE  ESOPHAGUS  759 

be  of  some  service  in  determining  the  presence  and  locality  of  the 
stricture,  but  the  use  of  the  sound  or  tube  will  prove  of  much  more 
value. 

(c)  Differential  Diagnosis. — It  is  evident  that,  having  determined 
the  presence  of  esophageal  stenosis  as  distinguished  from  spasm 
(III  preceding),  it  is  next  requisite  to  ascertain  the  cause  of  the 
narrowing  in  the  individual  case.  The  characteristics  of  cancerous 
stenosis  have  been  stated  in  IV,  preceding.  Pressure  stricture  is  to 
be  eliminated  by  a  careful  examination  for  thoracic  aneurism  (q.  v.), 
mediastinal  tumour  or  abscess  {q.  v.),  thyroid  enlargement  (q.  ?'.), 
disease  of  the  cervical  vertebrae,  and  pericardial  effusion  (q.v.). 
Cicatricial  stricture  usually  causes  more  pain  in  "swallowing,  and  a 
history  of  injury  by  a  foreign  body  or  of  ingestion  of  a  corrosive 
poison  is  usually  obtainable.  If  past  syphilitic  or  tuberculous  dis- 
ease is  responsible  for  the  cicatricial  tissue,  a  corroborative  history 
or  characteristic  lesions  elsewhere  may  be  found. 

VI.  Dilatation  of  the  Esophagus. — This  occurs  in  all  cases 
of  esophageal  stenosis,  the  walls  of  that  part  of  the  tube  above  the 
obstruction  becoming  hypertrophied,  and  the  tube  expanding.  Very 
rarely  it  is  a  congenital  condition.  The  symptoms  are  chronic  dys- 
phagia and  habitual  regurgitation.  If  the  sound  passes  readily  into 
the  stomach  stenosis  may  be  eliminated. 

VII.  Diverticula  of  the  Esophagus. — A  lateral  sac  or  cir- 
cumscribed dilatation  of  the  esophagus  may  be  due  to  pressure  from 
within  or  traction  from  without. 

(«)  Pressure  Diverticula. — These  may  occur  in  rapid  eaters,  usu- 
ally men,  who  gorge  large  masses  of  food.  The  sac  is  most  com- 
monly situated  on  the  posterior  wall  at  the  junction  of  the  pharynx 
and  esophagus.  The  muscular  coat  is  weakest  at  this  point,  and 
giving  way  allows  the  mucous  membrane  to  bulge  outward,  hernia- 
like, opposite  to  and  on  a  level  with  the  cricoid  cartilage.  Once 
started  it  continually  enlarges.  The  patient  is  conscious  that  at 
least  a  part  of  the  food  lodges  too  high  up,  and  at  intervals,  when 
endeavouring  to  swallow,  he  retches  and  regurgitates  the  contents 
(which  may  be  offensive)  of  the  sac.  The  diverticulum  may  be  so 
large  that  it  forms  a  visible  tumour  or  swelling  in  the  neck,  which 
when  compressed  causes  the  passage  of  its  contents  into  the  mouth. 
If  the  existence  of  a  small  and  not  palpable  sac  is  suspected,  a  sound 
slightly  bent  at  the  end  may  be  employed,  the  point  being  turned 
posteriorly  during  introduction,  when  it  will  enter  the  cavity. 

[b)  Traction  Diverticula. — These  are  small  conical  depressions 
occurring  usually  in  children,  situated  on  the  anterior  wall  of  the 
esophagus  on  a  level  with  the  bifurcation  of  the  trachea,  and  result 


Y60  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

from  the  adhesion  of  inflamed  bronchial  glands  to  the  wall  with  sub- 
sequent shrinking  and  outward  traction.  They  do  not  give  rise  to 
clinical  symptoms. 

VIII.  Rupture  of  the  Esophagus. — May  occur  as  an  effect 
of  prolonged  vomiting,  generally  when  intoxicated,  after  a  large  meal. 
The  clinical  evidence  of  the  accident  is  severe  pain,  emphysema  of 
the  neck  and  chest,  collapse,  and  death. 

VII.    DISEASES    OF   THE    STOMACH 

{For  the  physical  examination  of  the  stomach,  see  jmges  44S  to  456.      For  the 
examination  of  the  stomach  contents,  see  pages  6O4  to  618.) 

I.  Acute  Catarrhal  Gastritis. — («)  Causes. — Usually  due 
to  dietetic  imprudence  (unsuitable,  irritating,  or  decomposing  food, 
or  too  much  good  food),  or  to  the  abuse  of  alcohol ;  also  to  gout, 
fevers,  and  anaemia.  There  is  a  recognised  liability  to  "  dyspepsia  " 
in  certain  persons  or  families,  and  it  occurs  at  all  ages. 

{h)  Symptoms. — In  mild  cases,  especially  after  taking  food,  there 
is  headache  and  depression  of  spirits,  followed  by  epigastric  fulness, 
weight,  and  distress,  and  perhaps  dull  pain.  Eructations,  nausea, 
and  vomiting  ensue,  and  in  children  diarrhoea  and  spasmodic  abdom- 
inal pain  as  well.  The  vomitus  contains  undigested  food,  mucus, 
and  finally  bile.  The  tongue  is  furred,  the  breath  unpleasant,  and 
the  saliva  increased.  The  attack  lasts  about  24  hours,  usually  being 
relieved  by  the  vomiting. 

In  severe  cases  there  may  be  a  chill,  fever  (102°  to  103°),  severe 
headache,  delirium  (occasional  in  children),  vomiting,  diarrhoea  (fre- 
quent), or  constipation  (seldom),  with  slight  abdominal  distention 
and  epigastric  tenderness.  There  is  a  bitter  taste  in  the  mouth, 
herpes  on  the  lips  (frequent),  a  heavily  furred  tongue,  and  bad 
breath.  The  urine  is  scanty,  high  coloured,  and  loaded  with  urates. 
An  examination  of  the  vomitus  shows  diminished  or  absent  HCl,  and 
the  presence  of  lactic  and  fatty  acids  and  a  quantity  of  mucus.  If 
the  duodenum  and  bile  ducts  share  in  the  catarrhal  inflammation 
jaundice  ensues.  An  erythematous  rash  may  be  present  in  children. 
The  attack  lasts  from  2  to  4  days,  perhaps  longer. 

(c)  Differential  Diagnosis. — The  diagnosis  of  the  mild  form  is 
usually  easy,  but  the  severer  cases,  with  sudden  onset,  chill,  and 
fever,  may  require  observation  for  a  day  or  two  in  order  to  discrimi- 
nate them  from  the  acute  infectious  diseases — viz.,  from  abortive 
typhoid  fever  by  the  absence  of  prodromata,  of  bronchitis,  of  splenic 
enlargement,  rose  spots,  and  the  characteristic  temperature  curve  ; 
from  meningitis.)  which  the  cases  with  severe  headache  and  delirium 


DISEASES  OP  THE  STOMACH  761 

may  suggest,  by  the  history  and  subsequent  course  ;  from  the  crises 
of  locomotor  ataxia  by  the  presence  of  the  patellar  reflexes  and  the 
absence  of  the  Argyll-Robertson  pupil ;  from  scarlet  fever ^  which  the 
occasional  erythema  may  simulate,  by  the  absence  of  the  sore  throat, 
swollen  cervical  glands,  extraordinarily  rapid  pulse,  and  typical 
strawberry  tongue  of  the  specific  infection. 

II.  Phlegmonous  {Suppurative)  Gastritis. — («)  Causes. — 
Diffuse  or  circumscribed  suppuration  of  the  submucous  coat  of  the 
stomach  is  extremely  rare,  and  occurs  in  connection  with  pyaemia, 
puerperal  fever,  cancer  of  the  stomach,  peritonitis,  or  injury, 

{b)  Symptoms. — Fever,  dry  tongue,  delirium,  vomiting,  diarrhoea, 
weak  and  rapid  pulse,  with  epigastric  soreness,  abdominal  pain,  and 
meteorism,  followed  by  coma,  collapse,  and  death.  In  more  chronic 
cases  there  are  fever,  recurring  chills,  and  abdominal  pain. 

(c)  Diagnosis. — Earely  if  ever  made  ante-mortem.  The  circum- 
scribed abscess  has  been  felt  externally.  Even  if  a  quantity  of  pus 
is  vomited,  owing  to  rupture  of  a  large  submucous  abscess,  it  can  not 
be  separated  from  the  perforation  of  an  outside  pus  collection  into 
the  stomach, 

III.  Toxic  Gastritis. — (a)  Causes. — Ingestion  of  corrosive 
poisons. 

{h)  Symptoms. — Intense  burning  pain  in  mouth,  throat,  and  stom- 
ach, severe  epigastric  pain,  salivation,  unremitting  vomiting,  intense 
thirst,  and  dysphagia.  The  vomitus  contains  blood,  and  perhaps 
fragments  of  mucous  membrane.  Later  there  are  abdominal  pain, 
tenderness,  and  distention,  with  diarrhoea.  There  may  be  petechias, 
haematuria,  and  albuminuria.  In  severe  cases  the  symptoms  of  col- 
lapse (cold,  wet  skin,  lowered  temperature,  small  rapid  pulse)  may 
supervene, 

{c)  Sequelm. — Cicatricial  stricture  of  the  esophagus,  or  an  ulti- 
mately fatal  chronic  atrophy  of  the  gastric  mucosa. 

{d)  Diagnosis. — The  history,  the  inspection  of  the  mouth  and 
tongue  (page  226),  and  an  examination  of  the  vomitus  will  usually 
enable  a  diagnosis. 

IV.  Diphtheritic  Gastritis. — The  membranous  form  of  gas- 
tritis may  be  due  to  the  infection  of  diphtheria,  but  is  usually  sec- 
ondary to  pneumonia,  pyaemia,  variola,  typhus  and  typhoid  fever. 
It  can  not  be  recognised  ante-mortem. 

V.  Chronic  Catarrhal  Gastritis. — («)  Causes. — Dietetic  er- 
rors (very  frequent)  and  the  excessive  use  of  alcohol  (common).  It 
may  be  secondary  to  diabetes,  gout,  nephritis,  tuberculosis,  anaemia, 
or  chlorosis ;  or  to  ulcer,  cancer,  and  dilatation  of  the  stomach ;  or 
to  chronic  pulmonary  disease,  chronic  heart  disease,  and  cirrhosis  of 


762  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

the  liver,  all  of  which  cause  a  persistent  passive  congestion  of  the 
gastric  mucosa.  Pathologically  two  forms  of  the  disease  are  recog- 
nised, a  simple  catarrhal,  and  a  sclerotic,  gastritis.  The  latter  results 
in  atrophy  of  the  secretory  mucous  membrane,  either  with  thinning 
of  the  walls  of  -the  stomach,  or  with  thickening,  contraction,  and  a 
diminution  in  size  of  the  whole  organ. 

{h)  Symptoms. — These  are  varied.  Headache  is  common,  vertigo 
not  infrequent,  disturbed  or  dreaming  sleep,  depression  of  spirits, 
drowsiness,  and  a  feeling  of  languor  are  almost  always  present.  The 
appetite  is  fickle,  sometimes  abnormally  great.  After  eating  there  is 
epigastric  oppression,  fulness,  distress,  or  burning  pain  {hearthiirn, 
when  substernal),  with  tenderness.  There  may  be  frequent  eructa- 
tions of  bitter  fluid,  belching  of  gas,  and  well-marked  tympanitic  dis- 
tention of  the  abdomen.  Vomiting  after  meals  is  not  very  common, 
but  in  chronic  alcoholism  "  dry  retching,"  or  vomiting  of  watery  mu- 
cus, or  nausea  alone,  occurs  in  the  morning  with  great  frequency. 
Constipation  is  usual,  but  may  alternate  with  diarrhoea.  The  tongue 
is  often  swollen  and  indented,  its  tip  and  margin  red,  there  is  a  bad 
taste  in  the  mouth,  and  salivation  often  occurs.  The  urine  is  fre- 
quently high-coloured,  and  throws  down  a  heavy  uratic  deposit. 
Palpitation  is  not  uncommon,  and  "  stomach  "  cough  due  to  a  chronic 
catarrhal  pharyngitis  may  be  present. 

The  symptoms  of  atrophy  of  the  mucous  membrane,  the  final  re- 
sult of  prolonged  and  severe  simple  gastritis,  resemble,  in  the  major- 
ity of  cases,  those  of  gastric  cancer — i.  e.,  pain,  vomiting,  and  pro- 
gressive loss  of  flesh  and  strength  ;  less  frequently  the  symptoms  of 
pernicious  anaemia,  resulting  from  the  destruction  of  the  gastric  mu- 
cosa, announce  the  causative  condition. 

According  to  the  results  of  an  examination  of  the  stomach  con- 
tents three  forms  of  chronic  gastritis  are  recognised,  viz. : 

Simple  Gastritis. — After  Ewald's  meal,  HCl  diminished  or  ab- 
sent, lactic  and  acetic  acids  present  (the  latter  two  absent  after 
Boas's  meal),  pepsin  and  rennin  always  present ;  fasting  stomach 
contains  a  little  slimy  fluid. 

Mucous  Gastritis. — As  in  simple  gastritis,  except  that  a  large 
amount  of  mucus  is  found. 

Atrojihic  Gastritis. — HCl,  pepsin,  and  rennin  absent;  fasting 
stomach  empty. 

(c)  Diagnosis. — The  presence  of  chronic  gastritis  as  an  indirect 
symptom  of  chronic  disease  of  the  heart  or  lung,  or  of  a  cirrhotic 
liver  should  be  borne  in  mind.  The  severe  forms  of  chronic  gas- 
tritis require  to  be  differentiated  from  cancer  {q.  v.),  and  the  distinc- 
tion, in  the  absence  of  tumour,  may  be  extremely  difficult,  unless 


DISEASES  OF  THE  STOMACH  763 

the  history  or  prolonged  observation  shows  that  the  symptoms  cover 
a  longer  period  than  the  utmost  duration  of  cancer.  In  the  cirrhotic 
form  of  gastritis  tlie  contracted  stomach  may  in  rare  cases  form  a 
palpable  tumour. 

VI.  Gastric  {Peptic)  Ulcer. — {a)  Causes.— Occurs  at  all  ages, 
but  is  most  common  in  women,  especially  between  20  and  30  years  of 
age.  Less  frequently  it  is  found  in  men,  usually  between  30  and  40 
years  of  age.  Is  often  associated  with  overwork,  poor  food,  anaemia, 
chlorosis,  and  amenorrhoea,  and  is  especially  common  in  servant 
maids,  and  in  those  whose  work  involves  pressure  on  the  epigastrium 
(tailors,  cobblers,  weavers).  Hepatic  and  cardiac  disease  and  arterio- 
sclerosis predispose. 

{b)  Symptoms. — The  disease  may  be  entirely  latent  and  discov- 
ered only  at  autopsy.  More  commonly  the  initial  symptoms  are 
those  of  dyspepsia  or  chronic  gastritis — viz.,  anorexia,  epigastric  ful- 
ness or  oppression,  eructations,  and  pyrosis.  Eventually  in  well- 
marked  cases  symptoms  more  or  less  characteristic  of  ulcer  super- 
vene.    These  are : 

Pam^  which  may  be  dull  and  oppressive.  More  significant  is  an 
attack  of  sharp,  boring,  or  burning  pain,  excited  by  taking  food,  and 
occurring  either  immediately  or  from  1  to  2  hours  after  eating.  In 
many  cases  there  are  two  points  at  which  the  pain  is  most  intense : 
anteriorly  in  the  epigastrium,  posteriorly  at  the  level  of  the  10th 
dorsal  vertebra.  It  is  relieved  if  vomiting  takes  place.  Such  par- 
oxysms of  pain  (gastralgia)  may,  however,  be  independent  of  the 
ingestion  of  food,  and  are  often  of  indescribable  severity.  Pressure 
may  either  aggravate  or  relieve  the  pain  of  gastric  ulcer.  It  is  doubt- 
ful whether,  as  often  alleged,  the  sooner  the  pain  comes  after  eating 
the  nearer  is  the  ulcer  to  the  cardia ;  so  also  with  reference  to  the 
relief  afforded  by  posture,  an  amelioration  of  the  pain  by  lying  on 
the  face  indicating  that  the  ulcer  is  situated  on  the  posterior  wall  of 
the  stomach,  and  per  contra. 

Tenderness,  which  is  a  common  symptom,  but  only  of  diagnostic 
value  when  strictly  circumscribed  in  the  epigastrium  so  that  a  fin- 
ger tip  almost  covers  it,  or  when  a  tender  spot  is  found  to  the  left  of 
the  11th  or  12th  dorsal  vertebrae. 

II(ematemesis,  a  most  significant  event  when  a  considerable  quan- 
tity of  unaltered  blood  is  vomited,  but  occurring  in  only  50  per  cent 
of  the  cases.  It  may  be  slight  (coffee-ground),  but  ordinarily  is 
large,  and  sometimes  so  excessive  as  to  be  immediately  fatal.  Re- 
current attacks  at  intervals  of  hours  or  days  are  not  uncommon. 
After  a  gastric  hemorrhage  tarry  blood  is  found  in  the  stools,  and 
may  be  the  only  evidence  of  the  slighter  bleedings.     Syncope  or  con- 


764  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

vulsions  may  attend,  or  hemiplegia  and  severe  ansemia  follow,  large 
hemorrhages. 

Hyperclilorhydria^  often  with  hypersecretion,  is  usually  present. 
On  palpation  in  old  ulcers  a  distinct  induration,  resulting  from  in- 
flammatory changes,  may  at  times  be  felt  near  the  pylorus.  Anaemia 
is  usually  present  and  may  be  severe  (1,000,000,  or  less,  reds  to  the 
cu.  mm.).     Loss  of  flesh  is  customary. 

The  course  of  the  disease  is  usually  chronic,  rarely  acute,  and 
recurrences  (new  ulcers  or  renewal  of  old  ulceration)  are  not  un- 
common. 

(c)  Complications  and  Sequelae. — Of  these  the  most  important  is 
perforation,  occurring  in  about  6  per  cent  of  all  cases.  It  may  be 
the  first  evidence  of  hitherto  latent  ulcer.  Perforation  of  the  ante- 
rior wall  may  take  place  into  the  general  peritoneal  cavity,  in  which 
case  the  symptoms  are  those  of  an  acute  perforation  peritonitis ; 
ulcers  of  the  upper  and  posterior  walls  may  perforate  and  cause  a 
subphrenic  abscess,  or,  if  the  lesser  peritoneal  cavity,  and  subsequent- 
ly the  pleura,  is  entered,  subphrenic  pyopneumothorax.  Rarely,  by 
adhesion  and  ulceration,  fistulous  communications  may  be  established 
with  the  duodenum,  colon  (most  common),  or  the  external  surface 
in  the  epigastric  region.  Cicatricial  stenosis  of  the  pylorus,  with 
resulting  dilatation  or  hour-glass  contraction  of  the  stomach,  may 
follow  the  healing  of  a  large  ulcer.  Cancer  may  develop  on  the  site 
of  an  old  ulcer. 

(fZ)  Differential  Diagnosis. — The  cardinal  symptoms  are  gastral- 
gia  and  haematemesis,  usually  with  dyspeptic  symptoms,  and  in 
cases  presenting  this  triad  the  diagnosis  is  readily  made.  If  hsema- 
temesis  does  not  occur  it  may  be  very  difl&cult  to  arrive  at  a  positive 
conclusion.     The  following  conditions  require  discrimination : 

(1)  Gastralgia. — Gastralgia  is  not  only  associated  with  ulcer,  but 
also  constitutes  an  independent  form  or  symptom  of  nervous  dys- 
pepsia, and  with  the  exception  of  hemorrhage  may  exactly  simulate 
gastric  ulcer.  The  discrimination  can  not  always  be  made.  In 
gastralgia  of  the  neurotic  form,  as  contrasted  with  ulcer,  the  at- 
tacks occur  more  frequently  when  the  stomach  is  empty,  pressure 
and  the  taking  of  food  afford  relief,  vomiting  of  blood  is  absent, 
hyperchlorhydria  is  not  constant,  circumscribed  tenderness  is  absent,, 
gastric  dilatation  and  pyloric  hardening  (from  healed  ulcer)  are  never 
present,  ordinarily  there  are  no  dyspeptic  symptoms  between  the 
paroxysms,  there  is  less  emaciation  and  loss  of  strength,  and,  as  a 
rule,  symptoms  of  hysteria  or  neurasthenia  are  found,  or  there  are 
neuralgias  in  other  parts  of  the  body. 

(2)  Gastric   Crises. — The  attacks  of  pain  and  vomiting   which 


DISEASES  OF  THE  STOMACH  765 

occur  in  certain  spinal-cord  diseases,  especially  tabes,  may  simulate 
gastric  ulcer,  but  the  absent  knee-jerks,  lightning  pains  in  the  legs, 
and  Argyll-Eobertson  pupil  will  announce  the  true  character  of  the 
attacks. 

(3)  Hepatic  Colic. — In  this  affection,  swelling  and  tenderness  of 
the  liver,  a  palpable  gall  bladder,  the  abrupt  onset,  longer  continu- 
ance and  sudden  cessation  of  the  painful  paroxysm,  and  perhaps  the 
subsequent  occurrence  of  jaundice,  will  prevent  its  confusion  with 
gastric  ulcer. 

(4)  Cirrhosis  of  the  Liver. — The  vomiting  of  blood  which  occurs 
in  some  cases  of  this  malady  may  suggest  ulcer,  but  the  usual  al- 
coholic history,  the  ascites,  the  hardened  and  palpable  liver,  will 
declare  the  true  cause  of  the  haematemesis. 

(5)  Chronic  Gastritis. — Very  rarely  is  there  hsematemesis,  the 
pain  is  not  severe,  the  tenderness  is  diffuse,  vomiting  is  not  so  fre- 
quent and  when  it  occurs  is  not  so  painful,  and  HCl  is  diminished 
or  absent. 

(6)  Cancer  of  the  Stomach. — As  a  rule  this  is  not  mistaken  for 
ulcer.  Comparing  the  two,  in  cancer  there  is  often  a  tumour,  lactic 
acid  is  usually  present,  and  HCl  is  deficient  or  absent ;  blood  when 
vomited  is  "  coffee-ground  "  or  mixed  in  small  quantity  with  mucus ; 
there  is  usually  great  emaciation  with  cachexia,  and  the  subject  is 
more  frequently  middle-aged,  almost  invariably  past  30.  If,  how- 
ever, there  is  cicatricial  contraction  about  the  pylorus,  forming  a 
palpable  tumour,  a  differential  diagnosis  may  be  impossible,  espe- 
cially when  it  is  borne  in  mind  that  cancer  may  develop  upon  the 
site  of  an  old  ulcer,  and  that  in  such  cases  there  may  be  hyper- 
chlorhydria  as  in  ulcer,  instead  of  the  absence  of  HCl  as  is  usual  in 
cancer. 

VII.  Duodenal  Ulcer. — In  the  vast  majority  of  cases  the  symp- 
toms of  duodenal  ulcer  are  identical  with  those  of  gastric  ulcer.  In 
favour  of  duodenal  ulcer  are  pain  in  the  right  hypochondriac  region 
2  or  3  hours  after  meals,  sudden  and  recurring  intestinal  hemor- 
rhages (tarry  or  bright-red  stools)  sufficient  to  produce  anaemia  in  an 
otherwise  well  person,  occasional  jaundice,  and  violent  gastralgic 
attacks,  often  followed  by  melaena. 

VIII.  Cancer  of  the  Stomach. — Xext  to  the  uterus  the  stom- 
ach is  the  most  frequent  seat  of  primary  carcinoma.  Barely  it  is  sec- 
ondary to  mammary  cancer.  Gastric  cancer  is  rather  more  common 
(5  to  4)  in  men,  and  three  fourths  of  the  cases  occur  between  40  and 
70  years  of  age.  It  is  seated  in  the  pylorus  in  8  out  of  every  13 
cases.  Alcoholism,  previous  ulcer,  worry,  and  a  family  history  of 
cancer  or  tuberculosis  predispose. 


Y66  DIAGNOSIS,   DIRECT   AND  DIFFERENTIAL 

Symptoms. — ^'ot  seldom  the  disease  is  latent,  or  perhaps  there  is 
simply  gradual  loss  of  strength  without  local  signs  of  disease,  or 
there  is  evidence  of  malignant  disease  elsewhere,  without  symptoms 
of  involvement  of  the  stomach.  Ordinarily  the  initial  symptoms  are 
gastric  oppression  and  eructations  after  eating,  anorexia  (a  valuable 
symptom),  nausea,  occasional  vomiting,  constipation,  and  pain  ;  and 
some  cases  present  the  features  of  pernicious  anaemia.  As  a  rule 
these  are  of  gradual,  less  commonly  of  rather  sudden,  onset.  The 
symptoms  persist  and  often  become  more  severe.  The  pain  may  be 
gnawing,  burning,  or  gastralgic,  and  felt  in  the  epigastrium,  or  re- 
ferred to  the  dorsal  region  of  the  back,  or  posterior  lumbar  regions. 
The  vomiting  becomes  more  frequent  and  contains  blood,  almost 
always  in  small  amount,  constituting  the  rather  characteristic  coffee- 
ground  vomitus.  If  the  growth  causes  pyloric  stenosis  and  sequent 
gastric  dilatation,  there  may  be,  at  intervals  of  several  days,  vomit- 
ing of  enormous  quantities  of  partly  digested  food.  There  is  epi- 
gastric tenderness,  and  pressure  over  the  back  between  the  5th  and 
12th  dorsal  vertebrae  may  also  be  painful.  Usually  (in  at  least  two 
thirds  of  the  cases)  a  tumour  is  palpable,  which,  especially  if  pyloric, 
may,  on  account  of  its  mobility,  vary  widely  in  position  in  different 
cases  and  at  different  times,  having  been  found  not  only  in  the  epi- 
gastric but  also  in  the  umbilical,  the  right  and  left  hypochondriac, 
and  even  in  the  pubic,  regions.  It  may  move  (ordinarily  not)  with 
respiration  or  with  the  peristaltic  waves  of  the  stomach,  or  be  dis- 
placed by  the  examiner,  or  when  lying  over  the  aorta  may  exhibit 
pulsating  movements. 

Progressive  loss  of  weight  (and  usually  of  strength)  is  almost 
invariable ;  cachexia  develops,  the  count  of  the  reds,  however,  rarely 
going  below  2,000,000  to  the  cu.  mm.,  and  the  whites  seldom  above 
12,000  to  15,000 ;  slight  fever  (101°  or  less)  is  not  uncommon,  rarely 
with  chills ;  constipation,  sometimes  with  slightly  tarry  stools,  is  cus- 
tomary ;  indicanuria  is  common,  and  glycosuria,  acetonuria,  and  albu- 
mosuria have  been  noted  ;  oedema  of  the  lower  extremities  toward  the 
end  is  common,  and  occasionally  a  general  anasarca  occurs ;  infre- 
quently there  is  a  terminal  coma. 

Examination  of  the  stomach  contents  shows  in  a  large  proportion 
of  cases  a  great  diminution  or  absence  of  HCl,  and  the  presence  of 
lactic  acid  after  Boas's  test  meal.  The  persistent  presence  of  blood 
is  characteristic.  Occasionally  tumour  particles  may  be  found.  If 
cancer  develops  on  the  site  of  an  old  ulcer  HCl  may  be  normal  or 
even  increased,  but  this  is  of  rare  occurrence. 

Complications. — Metastatic  growths  are  not  infrequent,  occurring 
in  the  following  order  of  frequency :  Lymph  glands,  liver,  perito- 


DISEASES  OF  THE  STOMACH  Y67 

neum,  pancreas,  intestine,  lung,  pleura,  kidneys,  and  spleen.  Per- 
foration may  occur,  usually  but  not  always  causing  diffuse  peritonitis ; 
or  a  fistulous  communication  with  the  colon,  or  more  rarely  the  small 
intestine,  may  be  established. 

Duration. — The  average  duration  of  gastric  cancer  is  from  1  year 
to  18  months ;  more  rarely  life  is  prolonged  for  from  2^  to  3  years. 
It  is  always  fatal. 

Differential  Diagnosis. — The  cardinal  symptoms  are  progressive 
emaciation,  pain,  tumour,  coffee-ground  vomiting,  dilated  stomach, 
constant  absence  of  HCl,  and  presence  of  lactic  acid  after  a  Boas 
meal,  in  a  person  between  40  and  70  years  of  age. 

In  the  absence  of  tumour  such  a  set  of  symptoms  will  warrant  a 
quite  positive  diagnosis  of  cancer.  The  disease  should  be  suspected 
if,  in  elderly  persons,  the  ordinary  symptoms  of  chronic  gastric  ca- 
tarrh obstinately  persist  and  a  cachexia  out  of  proportion  to  the 
apparent  cause  develops.  The  cases  of  cancer  which  present  severe 
anaemia  or  gastric  s3"mptoms,  without  tumour,  may  simulate  very 
closely  and  be  mistaken  for  pernicious  anaemia  or  chronic  gastritis. 
Ulcer  of  the  stomach,  with  cicatricial  thickening  at  the  pylorus,  may 
exactly  resemble  cancer.  Enlargement  of  the  supraclavicular  or  in- 
guinal glands,  or  a  nodule  at  or  in  the  neighbourhood  of  the  navel, 
may  be  of  great  value  as  a  clew  to  the  existence  of  gastric  cancer. 

The  following  diseases  may  require  to  be  differentiated.  As 
Osier  well  says,  "  there  are  cases  of  cancer  of  the  stomach  in  which 
a  positive  diagnosis  can  not  be  reached  for  weeks  or  months." 

(1)  Clironic  Gastritis. — This,  as  contrasted  with  cancer,  occurs  at 
any  age,  pain  and  tenderness  are  less  marked,  vomiting  is  not  com- 
mon, haemorrhage  is  rare,  or  when  present  consists  simply  of  blood 
streaks  (not  coffee-grounds),  there  is  no  fever,  loss  of  flesh  is  not 
marked,  and  there  is  no  cachexia,  no  tumour,  and  no  oedema.  More- 
over, its  duration  may  be  much  longer  than  that  of  cancer,  and,  on 
the  other  hand,  it  is  susceptible  of  cure.  Xo  lactic  acid  is  found 
after  a  Boas  meal. 

(2)  Gastric  Ulcer. — As  compared  with  cancer,  ulcer  of  the  stom- 
ach occurs  most  frequently  in  early  adult  age  and  in  women ;  the 
pain  is  more  apt  to  be  gastralgic  and  to  be  excited  by  the  taking  of 
food,  and  may  be  entirely  lacking  for  days  or  even  weeks ;  tender- 
ness is  strictly  circumscribed  in  the  epigastrium,  or  posteriorly  at 
the  level  of  the  5th  dorsal  vertebra ;  the  ordinary  symptoms  of  indi- 
gestion may  be  slight ;  vomiting  is  by  no  means  a  frequent  symp- 
tom ;  tumour  (cicatricial)  is  very  rare  ;  there  is  no  oedema ;  bleeding 
from  the  stomach  is  common,  and  as  a  rule  characteristically  profuse ; 
there  is  no  fever.     Gastric  ulcer  may  recover  or  continue  for  several 


768  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

years ;  no  lactic  acid  is  found  after  a  Boas  meal,  and  there  is  usu- 
ally an  excess  of  HCl. 

(3)  Gastric  Ulcer  with  Cicatricial  Pyloric  Thickening  and  Steno- 
sis.— This  condition,  which,  because  of  the  presence  of  tumour  and 
dilatation  of  the  stomach,  exactly  resembles  cancer  of  the  pylorus, 
may  perhaps  be  differentiated  from  the  latter  by  the  comparative 
youth  of  the  patient,  the  history,  the  abundant  heematemesis,  the 
hyperchlorhydria,  and  the  longer  duration. 

(4)  Pernicious  Ancemia. — In  this  disease,  as  compared  with  gas- 
tric cancer,  the  number  of  reds  is  very  frequently  below  2,000,000  to 
the  cu.  mm. ;  indeed,  if  1,000,000  or  below,  it  points  strongly  to  anae- 
mia rather  than  cancer  (Osler)  ;  megaloblasts  are  present,  leucocy- 
tosis  is  less  frequent,  the  colour  index  is  higher,  and  there  is  rarely 
the  loss  of  flesh  that  occurs  in  malignant  tumour  of  the  stomach. 

(5)  Cancer  of  the  Pancreas. — In  this  disease  when  a  tumour  ia 
palpable  it  is  immovable,  jaundice  often  exists,  dilatation  of  the 
stomach  and  coffee-ground  vomiting  are  absent,  HCl  is  present,  fat 
may  be  found  in  the  stools,  and  lipuria  and  glycosuria  may  exist. 

(6)  Occasional  Causes  of  Error. — Cancer  of  the  transverse  colon 
lacks  coffee-ground  vomiting  and  anachlorhydria,  and  later  often 
presents  symptoms  of  intestinal  obstruction.  In  duodenal  cancer 
HCl  is  usually  absent,  but  jaundice  may  be  present.  Impacted 
faeces  in  the  colon  disappear  by  treatment.  Movable  kidney  is  rec- 
ognised by  its  shape  and  the  practicability  of  reduction.  Cancer  of 
the  liver  or  gall  bladder  lacks  the  gastric  pain  and  frequent  coffee- 
ground  vomiting  of  gastric  cancer.  Tumour  of  the  abdominal  wall 
is  unattended  by  gastric  disorders.  Tumours  of  the  omentum  are 
nodular  and  irregular,  and  subsequently  lead  to  peritoneal  effusion. 
The  rare  and  remarkable  tumour-like  mass  of  swallowed  hair  in  hys- 
terical women  is  a  clinical  curiosity,  and  is  usually  recognised  by 
operation,  but  the  history  may  give  rise  to  a  suspicion. 

IX.  Hypertrophic  Stenosis  of  the  Pylorus. — Xon-malig- 
nant  thickening  of  the  pylorus,  due  to  hypertrophy  of  the  muscu- 
lar and  submucous  tissues,  may  occur  in  adults,  and,  as  a  congenital 
condition,  in  infants  of  the  average  age  of  5  months. 

The  symptoms  are  those  of  a  dilated  stomach. 

X.  Dilatation  of  the  Stomach. — Causes. — In  rare  instances 
gastrectasia  is  acute  and  due  to  overstretching,  as  in  the  taking  of 
huge  quantities  of  food  and  drink,  or  sudden  weakness  of  the  mus- 
cular coats  as  in  shock,  or  rapid  degenerative  processes  as  in  the 
specific  fevers.  Chronic  gastrectasia,  according  to  its  origin,  may  be 
divided  into  two  classes,  the  stenotic  and  the  atonic. 

The  first  class  is  due  to  pyloric  or  duodenal  stenosis,  either  an. 


DISEASES  OF  THE  STOMACH  Y69 

actual  narrowing  caused  by  cancer,  cicatricial  contraction  from  ulcer 
or  corrosive  poison,  or  simple  hypertrophic  stenosis ;  or  narrowing 
by  outside  pressure  from  cancer  of  the  liver,  gall  bladder,  pancreas, 
and  omentum,  or  by  large  gallstones ;  or  a  floating  right  kidney,  or 
kinking  of  the  pylorus  from  adhesions  to  the  gall  bladder  and  liver. 

The  second  class  is  due  to  atony  of  the  muscular  coats  incident 
to  chronic  gastritis,  the  degenerative  changes  of  anaemia,  tuberculo- 
sis and  like  diseases,  habitual  overdistention  of  the  organ  as  in  beer- 
drinkers  and  diabetics,  congenital  weakness,  and  deficient  innerva- 
tion. 

Symptoms. — Epigastric  fulness  or  distress,  flatulence,  eructations, 
and  vomiting.  There  may  be  anorexia,  but  not  uncommonly  the 
appetite  is  particularly  good  and  there  is  great  thirst.  The  skin  is 
dry,  constipation  is  present,  and  the  urine  is  scanty.  Great  loss  of 
flesh,  anaemia,  and  debility  commonly  ensue.  There  may  be  cramps 
of  the  calf  muscles,  or  occasionally  tetany. 

The  characteristic  symptoms  are  the  manner  of  vomiting  and  the 
composition  of  the  vomitus.  The  stomach  empties  itself  at  inter- 
vals of  several  days,  ejecting  large  quantities  (1  to  3  gallons)  of 
stagnant  fluid  and  remnants  of  partially  digested  or  undigested 
food.  The  vomitus  is  acid  from  the  presence  of  lactic,  butyric,  and 
acetic  acids.  Hydrochloric  acid  may  be  normal,  diminished,  absent, 
or  increased.  Offensive  odours  may  be  due  to  the  presence  of  sul- 
phuretted or  phosphuretted  hydrogen.  The  fluid  contains  the  Sarcina 
ve?itricuU,  yeast  fungus,  and  many  bacteria.  On  standing,  it  sepa- 
rates into  a  sediment  of  undigested  food,  and  a  supernatant  grayish 
turl)id  fluid  capped  by  a  brownish  froth. 

The  physical  signs  are,  in  brief,  as  follows  :  The  outline  of  the  dis- 
tended organ  (Fig.  1-45,  page  455),  together  with  its  pet-istaltic  waves, 
may  often  be  seen ;  if  not,  it  is  to  be  inflated.  Pyloric  tumour  may 
be  felt,  and  the  peculiar  resiliency  of  the  dilated  stomach  and  its  peri- 
stalsis may  be  perceived  by  palpation.  Splashing  or  succussion 
sounds  may  be  elicited,  either  by  the  hand  of  the  examiner  or  upon 
deep  and  rapid  breathing  by  the  patient.  Percussion  after  drinking 
water  may  enable  the  lower  border  of  the  organ  to  be  recognised. 
Auscultatory  percussion  is  of  much  service  in  determining  the  out- 
lines of  the  stomach. 

Diflferential  Diagnosis. — The  cardinal  symptoms  are  the  charac- 
teristic vomiting  and  the  results  of  a  physical  examination  of  the 
stomach,  especially  inspection  of  the  inflated  organ  or  auscultatory 
percussion.  The  finding  of  a  pyloric  tumour  will  decide  against  the 
atonic  nature  of  the  dilatation,  and  in  the  majority  of  cases  the 
tumour  is  due  to  cancer  of  the  stomach  (page  765). 


YYO  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Gastrectasia  is  to  be  distinguished  from  gastroptosis  or  prolapse 
of  the  stomach  (page  456).  An  unusually  large  stomach  (megalo- 
gastria)  may  be  found,  but  unless  evidence  of  stagnation  of  the  gas- 
tric contents — i.  e.,  the  finding  of  a  quantity  of  food  or  fluid  in  the 
stomach  7  hours  after  a  full  meal,  or  periodic  vomiting  of  large 
amounts — is  present,  the  condition  can  not  be  considered  abnormal. 

Experience  teaches  proper  humility,  but  it  is  difficult  to  con- 
ceive of  confounding  ascites  or  ovarian  tumour  with  a  dilated  stom- 
ach, yet  both  the'se  errors  have  occurred. 

Prognosis. — This  depends  upon  the  cause.  Atonic  cases  often 
recover  ;  cancerous  stenosis  is,  of  course,  fatal ;  simple  stenosis  may 
be  greatly  benefited.  Modern  surgery  (by  gastro-enterostomy,  gas- 
troplication,  or  stretching  of  the  pylorus)  may  afford  material  help. 

XL  Hsematemesis. — See  page  122. 

XII.  Neuroses  of  the  Stomach.— These  consist  of  various 
more  or  less  serious  functional  disturbances  of  the  stomach — i.  e., 
without  discoverable  local  lesions.  Karely  these  disturbances  arise 
reflexly  from  organic  disease  in  other  parts  or  organs  of  the  body. 
Almost  invariably  they  form  a  part  of  the  protean  manifestations  of 
a  congenital  neurotic  diathesis,  or  of  an  acquired  neurasthenia  or 
hysteria.  In  a  certain  proportion  of  cases  the  neuropathic  basis  of 
the  dyspeptic  symptoms  may  elude  recognition  without  careful  in- 
quiry and  prolonged  observation. 

The  term  nervous  dyspepsia  is  in  reality  a  generic  term  covering 
the  various  gastric  neuroses — sensory,  motor,  or  secretory — about  to 
be  described.  The  individual  patient  rarely  suffers  from  a  single 
one  of  these  separate  disturbances.  Usually  two  or  more,  in  vary- 
ing or  complex  combinations,  are  found  to  be  associated.  Leube, 
however,  limits  the  meaning  of  the  term  to  cases  in  which  sev- 
eral neuroses,  mainly  sensory  and  of  a  mild  grade,  coexist,  and  are 
manifested  only  during  the  act  of  digestion  ;  while  any  one  of  the 
neuroses,  if  severe  and  extreme  and  perhaps  occurring  alone,  is 
considered  as  a  separate  and  distinct  disease — e.  g.,  nervous  vomit- 
ing ;  or  hyperchlorhydria,  either  periodic  or  continuous.  It  is  best, 
therefore,  to  describe  first  the  ordinary  form  of  nervous  dyspepsia, 
and  subsequently  the  special  gastric  neuroses  which  may  be  a  part 
of  the  ordinary  nervous  dyspepsia,  but  may  also  be  so  intense  and 
overshadowing  as  to  be  justly  regarded  as  well-nigh  independent 
affections. 

A.  Xeryous  Dyspepsia. — (a)  Symptoms. — There  is  anorexia, 
less  frequently  bulimia.  After  eating  there  is  a  sense  of  epigastric 
distress  and  oppression,  eructations,  belching,  pyrosis,  acidity  of  the 
mouth,  rumbling  of  gas,  and  sometimes  nausea  or  vomiting.     There 


DISEASES  OF   THE  STOMACH  Y71 

may  be  headache,  vertigo,  cephalic  pressure-sensations,  numbness, 
cold  hands  and  feet,  bad  taste  in  the  mouth,  and  palpitation.  Con- 
'stipation  may  be  present.  As  a  rule  there  are  marked  depression  of 
spirits,  anxious  forebodings,  and  perhaps  a  well-defined  hypochon- 
driacal condition.  In  spite  of  these  symptoms  the  stomach  is  found 
to  be  empty  6  or  7  hours  after  a  full  meal,  showing  that  the  food  is 
digested  and  that  there  is  no  stagnation.  The  gastric  juice  is  usu- 
ally of  normal  composition,  although  the  HCl  may  be  either  increased 
or  diminished. 

{b)  Diagnosis. — As  the  symptoms  of  nervous  dyspepsia  closely 
resemble  those  of  chronic  gastric  catarrh  it  is  necessary  to  distin- 
guish between  them.  Contrasting  the  two,  in  nervous  dyspepsia 
relief  may  follow  the  taking  of  food,  there  is  less  epigastric  tender- 
ness, and  the  symptoms  may  disappear  at  irregular  intervals.  The 
stomach  contents  usually  contain  little  or  no  mucus  or  undigested 
food,  and  as  a  rule  (with  a  number  of  exceptions)  the  HCl  is  in 
normal  amount.  The  tongue  is  not  so  apt  to  be  flabby,  indented,  and 
furred  as  in  gastric  catarrh.  In  certain  cases  the  prominence  of 
gastralgia  or  the  presence  of  emaciation  may  suggest  ulcer  or  cancer. 
After  all,  it  is  upon  the  existence  of  a  neuropathic  diathesis  or 
temperament,  to  be  discovered  by  careful  and  often  necessarily  pro- 
longed observation  of  the  patient  and  his  neurotic  peculiarities,  that 
the  diagnosis  of  the  nervous  character  of  the  dyspepsia  depends. 
Moreover,  there  are  no  obvious  organic  changes. 

B.  Secretory  Xeuroses. — (I)  Hyperchlorhydria. — The  se- 
cretion of  gastric  juice  containing  an  excessive  amount  of  gastric 
juice  (over  70  degrees)  07ili/  during  digestion  is  encountered  mainly  in 
adults,  but  is  common  in  young  chlorotic  women.  Worry,  grief,  and 
mental  overwork  are  important  antecedent  causes.  The  liberal  use 
of  condiments  and  alcoholic  beverages  will  predispose. 

Symptoms. — Ordinarily  the  onset  is  gradual.  There  is  at  first 
simply  a  feeling  of  discomfort  about  2  or  3  hours  after  a  meal,  but 
in  course  of  time  it  develops  into  a  burning  pain,  with  weight  and 
pressure,  in  the  epigastrium,  often  with  acid  eructations,  regurgita- 
tion, and  pyrosis,  sometimes  followed  by  nausea  and  vomiting.  Se- 
vere headache  and  attacks  of  vertigo  are  common,  the  urine  may  be 
scanty,  and  constipation  exist.  Loss  of  weight  does  not  usually 
occur.  The  pain  lasts  for  from  1  to  3  hours,  and  is  relieved  by  vom- 
iting, or  more  characteristically  by  taking  albuminous  food  (milk, 
meat,  white  of  egg)  or  alkalies  (soda,  magnesia).  The  physical  ex- 
amination may  reveal  a  moderate  diffuse  epigastric  tenderness,  and 
occasionally  evidence  of  slight  gastrectasia.  The  examination  of 
the  stomach  contents  1  hour  after  eating  Ewald's  meal  shows  an 


772  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

excess  of  HCl ;  so  also  3  or  4  hours  after  a  Leube-Rigel  meal,  while 
in  the  latter  the  meat  is  quite  digested  and  the  starches  practically 
unchanged. 

Hyperchlorhydria  may  be,  and  at  first  usually  is,  remittent,  occur- 
ring daily  for  several  days  or  many  weeks,  and  then,  having  ceased 
for  a  variable  period,  returning  with  or  without  obvious  causes,  such 
as  grief  or  mental  worry  or  overwork.  Finally,  it  may  become  a  con- 
tinuous condition.     Ordinarily  the  prognosis  is  favourable. 

Differential  Diagnosis. — The  cardinal  symptoms  are  burning  pain, 
occurring  2  to  3  hours  after  eating,  and  immediately  relieved  by  alka- 
lies or  nitrogenous  food,  no  marked  emaciation  or  anaemia,  and  (the 
only  positive  evidence)  a  constant  excess  of  HCl  1  hour  after 
Ewald's  meal.     It  is  necessary  to  exclude  the  following  diseases : 

(1)  Gallstone  Colic. — In  this  the  pain  is  felt  in  the  right  hypo- 
chondriac and  the  corresponding  half  of  the  epigastric  regions, 
rather  than  in  the  middle  of  the  latter  ;  it  occurs  4  or  5  hours  after 
a  meal,  and  is  not  promptly  relieved  by  alkalies  or  food.  Confusion 
can  arise  only  in  the  absence  of  jaundice  or  a  swollen  gall  bladder. 

(2)  Gastric  Ulcer. — This  condition  is  accompanied  by  hyper- 
chlorhydria, but  in  addition  to  the  other  symptoms  of  gastric  ulcer 
(page  763)  the  pain  is  not  completely  abolished  by  alkalies,  and  is 
aggravated  by  albuminous  food. 

(3)  Chronic  Hypersecretion. — In  this,  vomiting  is  more  common, 
the  paroxysms  of  pain  usually  occur  during  the  night,  and  from  the 
fasting  stomach  large  amounts  of  gastric  juice  may  be  obtained. 

(II)  Hypersecretion  {Gastrosuccorrhma). — An  excessive  secre- 
tion of  hyperchlorhydric  gastric  juice  in  the  fasting  stomach.  Two 
forms  are  recognised,  the  periodic  or  intermittent  (gastroxynsis, 
Rossbach),  and  the  continuous  or  chronic  (Reichmanx). 

(a)  Periodic  Hypersecretioti. — Into  a  state  of  health  a  sensation 
of  epigastric  uneasiness  intrudes,  deepening  into  pain,  and  shortly 
followed  by  nausea  and  the  vomiting  of  a  large  quantity  of  very  acid 
gastric  juice,  which  ultimately  may  be  greenish  with  bile.  The  nau- 
sea and  retching  are  persistent,  and  at  intervals  of  a  few  hours  other 
large  quantities  of  gastric  juice  are  ejected.  The  throat  may  be- 
come raw  and  sore.  The  paroxysms  often  occur  in  the  night  or  in 
the  early  morning  hours.  The  attack  as  a  whole  lasts  from  1  to  3 
days,  terminating  with  characteristic  abruptness,  but  tending  to 
recur  at  intervals  varying  from  a  few  weeks  to  a  year  or  longer. 
When  recurrences  tread  one  upon  the  heels  of  the  other  the  condi- 
tion merges  into  the  continuous  or  chronic  form.  The  pain  may  be 
severe,  intense  headache  may  be  present,  and  pallor,  coldness  of  the 
extremities,  and  constipation  are  common.     Before  this  disease  can 


DISEASES  OP  THE  STOMACH  773 

be  considered  a  pure  neurosis  it  is  necessary  to  exclude  gastric  ulcer 
(page  763)  and  the  gastric  crises  of  locomotor  ataxia  {q.  v.). 

{b)  Continuous  Hypersecretion. — The  early  symptoms  are  those  of 
hyperchlorhydria  (page  771)  or  periodic  hypersecretion.  Epigastric 
pain  becomes  habitual  after  meals,  and  vomiting  of  an  acid  fluid,  at 
first  occasional,  occurs  once  or  more  daily,  most  commonly  after 
breakfast,  rarely  at  night.  From  the  fasting  stomach  an  abnormally 
large  amount  of  acid  gastric  juice  free  from  fragments  of  food  may 
be  obtained.     The  prognosis  is  not  bad. 

As  a  pure  neurosis  this  is  a  rare  disease,  and  it  is  necessary  to 
rule  out  pyloric  stenosis  and  dilatation  of  the  stomach  (page  768) 
and  gastric  ulcer  (page  763),  before  making  a  definite  diagnosis. 

(Ill)  Hypochlorhydria. — Diminution  or  absence  of  HCl  is 
common  in  gastric  cancer  and  in  gastritis,  especially  of  the  atrophic 
form.  As  a  not  infrequent  neurosis  it  may  occur  in  hysteria,  neu- 
rasthenia, and  locomotor  ataxia.  Very  rarely  as  a  neurosis  there  is 
a  total  absence  not  only  of  HCl,  but  also  of  the  ferments  (achylia  gas- 
trica,  EixHORx) ;  but  this  is  more  commonly  due  to  organic  changes, 
particularly  in  atrophic  gastritis.  The  symptoms  of  achylia  of  ner- 
vous origin  may  be  negative ;  ordinarily  they  resemble  those  of  chronic 
gastritis.  The  diagnosis  is  to  be  made  by  the  result  of  the  examina- 
tion of  the  contents  of  the  stomach.  The  total  acidity  is  4,  HCl  and 
ferments  absent,  mucus  absent,  and  lactic  acid  absent  except  in 
traces.  This  condition  is  to  be  discriminated  from  the  atrophic  form 
of  gastritis  (page  762)  and  cancer  of  the  stomach  (page  765). 

C.  Sexsory  Neuroses. — (I)  Disturbances  of  the  Hunger-sense. — 
Elsewhere  (page  112)  have  been  considered,  in  general,  bulimia, 
polyphagia,  akoria,  anorexia,  and  pica.  Two  special  forms  are  the 
following : 

(1)  Paroxysmal  Bulimia. — Sudden  attacks  of  burning  epigastric 
pain,  faintness,  headache,  and  excessive  hunger,  often  occurring  in 
the  night,  although  the  paroxysm  may  come  on  directly  after  a 
hearty  meal.  It  is  relieved  by  taking  food.  Frequent  attacks  may 
produce  gastritis  and  dilatation.  This  condition  is  seen  in  hysteria, 
neurasthenia,  exophthalmic  goitre,  migraine,  epilepsy,  and  cerebral 
tumours. 

(2)  Anore.ria  Xervosa. — An  absolute  absence  of  appetite,  which 
may  be  so  extreme  that  the  sight  of  food  excites  spasm.  This  con- 
dition is  a  manifestation  of  hysteria,  and  is  commonly  seen  in  girls 
between  15  and  20  years  of  age,  more  rarely  as  early  as  the  12th 
year.  The  patient  is  restless,  but  ultimately  takes  to  bed  ;  the  ema- 
ciation may  reach  the  last  degree ;  the  skin  becomes  dry  and  brawny, 
and  contractures  of  the  lower  extremities  may  develop.     Death  has 

51 


774  DIAGNOSIS,    DIRECT  AND   DIFFERENTIAL 

been  known  to  follow,  but  under  proper  treatment  the  prognosis  is 
not  unfavourable. 

(II)  Gastric  HypersBsthesia. — The  symptoms  are  a  sense  of  pres- 
sure, burning,  fulness  or  weight,  or  gnawing  pain,  with  tenderness 
in  the  epigastrium  during  the  act  of  digestion.  As  these  sensations 
may  occur  in  organic  disease  of  the  stomach  it  is  necessary  to  ex- 
clude gastritis  (page  761)  and  gastric  ulcer  (page  703)  by  the  absence 
of  certain  more  or  less  distinctive  symptoms,  and  by  finding  the  gas- 
tric juice  to  be  of  normal  composition  and  that  the  food  is  digested 
within  the  proper  period. 

(III)  Gastralgia. — Paroxysmal  gastric  pain,  which  may  be  purely 
a  neurosis,  but  occurs  also,  as  a  symptom,  in  cancer  or  ulcer  of  the 
stomach,  or  in  locomotor  ataxia  (gastric  crises). 

(a)  Symptoms. — The  pain  generally  bears  no  relation  to  the  tak- 
ing of  food.  The  attack  is  frequently  preceded  by  slight  nausea 
or  epigastric  pressure,  salivation,  faintness,  vertigo,  or  headache. 
Shortly  a  severe  and  agonizing  pain  begins  in  the  epigastrium,  radi- 
ating through  to  the  back  and  along  the  costal  margins,  especially 
toward  the  left,  extending  in  some  cases  to  the  scapulae  and  entire 
abdomen.  The  face  is  pale  and  anxious,  the  hands  and  feet  are  cold, 
and  the  skin  cool  and  wet.  The  body  is  curved  forward  and  the 
abdomen  hollowed.  There  is  slight  epigastric  tenderness,  but  pres- 
sure with  the  flat  hand  is  often  grateful.  The  attack  may  last  from 
a  few  minutes  to  several  hours.  Eecurrences  may  take  place  at 
intervals  varying  from  a  day  to  a  year  or  more. 

{b)  Differential  Diagnosis. — Before  gastralgia  is  definitely  de- 
cided to  be  of  purely  neurotic  character  it  is  necessary  to  exclude  it 
as  a  symptom  of  organic  nervous  or  gastric  disease,  and  to  separate 
it  from  other  somewhat  similar  painful  conditions. 

As  a  neurosis  it  occurs  mainly  in  women  with  menstrual  irregu- 
larities, especially  at  the  menopause  ;  is  most  common  in  brunettes,, 
and  is  favoured  by  worry,  anaemia,  and  constipation.  Healthy  men 
are  not  exempt.  It  may  be  almost  the  only  symptom  of  a  neuras- 
thenia (q.  V.)  or  hysteria  {q.  v.),  but  more  commonly  is  simply  one 
manifestation  of  either  of  these  conditions.  The  direct  diagnosis  of 
neurotic  gastralgia  is  based  principally  upon  the  presence  of  neuras- 
thenic or  hysterical  symptoms,  together  with  the  absence  of  signs 
of  any  causative  organic  lesion  of  the  stomach  or  nervous  system. 

Without  here  going  into  the  details  of  the  different  conditions 
which  may  be  attended  by  or  simulate  gastralgic  attacks,  the  fol- 
lowing list  will  serve  to  point  out  the  affections  from  which  neurotic 
gastralgia  must  be  discriminated  by  a  careful  consideration  of  the 
associated  signs  and  symptoms,  viz.,  cancer  of  the  stomach,  ulcer  of 


DISEASES  OP  THE  STOMACH  Y75 

the  stomach,  pyloric  stenosis,  the  gastric  crises  of  locomotor  ataxia, 
hyperchlorhydria  or  hypersecretion,  achylia  gastrica,  gallstone  colic, 
renal  colic,  and  flatulent  colic. 

D.  Motor  Xeuroses.— (I)  Peristaltic  Unrest.— This  is  seen 
especially  after  eating.  The  peristaltic  movements  are  hyperactive, 
causing  loud  borborygnii,  gurgling,  and  splashing,  which  may  be 
audible  at  a  distance.  Emotion  intensifies  their  activity.  The  hyper- 
activity may  extend  to  the  intestines.  Peristaltic  unrest  is  a  fre- 
quent symptom  of  hysteria  or  neurasthenia.  This  mortifying  condi- 
tion has  led  to  prolonged  periods  of  seclusion. 

(II)  Nervous  Vomiting. — This  may  occur  either  in  children  or 
adults,  usually  in  hysterical  women.  Without  preliminary  nausea  and 
Avithout  straining,  the  contents  of  the  stomach  are  partly  vomited, 
partly  regurgitated.  It  usually,  but  not  always,  takes  place  shortly 
after  eating.  The  attacks  come  on  at  irregular  intervals.  As  a  rule 
the  general  health  is  unimpaired,  a  point  in  favour  of  its  hysterical 
origin  in  the  absence  of  other  neurotic  manifestations.  Primary 
periodical  vomiting  (Levden)  may  occur  as  a  neurosis  in  otherwise 
perfectly  healthy  persons,  especially  in  women  while  menstruating. 

(III)  Nervous  Eructations. — Loud  belchings  of  air  which  has 
been  swallowed  or  aspirated  into  the  esophagus  or  stomach,  either 
continuing  from  hours  to  days,  or  occurring  in  paroxysms  which  are 
excited  by  emotion.  They  may  occur  in  hysterical  women  and  chil- 
dren or  in  neurasthenic  persons.  In  the  young  the  attacks  may 
be  contagious  by  imitation.  Anxiety,  palpitation,  epigastric  fulness 
and  distress  may  attend  the  paroxysms. 

(IV)  Rumination  or  Merycism. — In  this  infrequent  condition  the 
swallowed  food  is  returned  to  the  mouth  and  again  chewed  and 
swallowed.  It  occurs  in  hysterical,  neurasthenic,  or  epileptic  per- 
sons, and  in  idiots.     It  is  sometimes  hereditary. 

(V)  Spasm  of  the  Stomach. — The  spasmodic  contraction  may 
affect  either  the  cardiac  or  the  pyloric  extremity  of  the  stomach. 
If  both  are  simultaneously  present  and  the  stomach  is  full  of  gas 
(pneumatosis),  the  upper  abdomen  may  be  enormously  distended, 
the  patient  being  unable  to  belch  up  the  confined  gas.  It  occurs  in 
neurotic  young  persons. 

(1)  Spasm  of  the  Cardia. — This  may  be  painful,  and  is  associated 
with  a  sensation  as  of  a  low-down  obstruction  opposite  the  lower  end 
of  the  sternum.  It  is  not  a  common  condition,  but  may  occur  in 
hysteria,  neurasthenia,  tetanus,  or  with  the  rapid  taking  of  very  hot 
or  cold  food. 

(2)  Spasm  of  the  Pylorus. — The  symptoms  are  pain,  perhaps  a 
sense  of  resistance  over  the  site  of  the  pylorus,  and  increased  gastric 


Y76  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

peristalsis.  It  may  be  due  to  the  irritation  of  highly  spiced  food,  or 
of  a  hyperchlorhydria.  If  the  latter  is  associated  with  long-contin- 
ued hypersecretion,  dilatation  of  the  stomach  may  ensue. 

(VI)  Relaxation  of  the  Stomach. — (1)  Atony  of  the  Stomach  or 
Atonic  Dyspepsia. — This  is  most  commonly  a  symptom  of  chronic 
gastritis  or  general  debility,  but  may  infrequently  occur  as  a  neu- 
rosis. Organic  disease  must  be  excluded.  The  symptoms  are  epi- 
gastric discomfort,  pressure,  weight  or  distention,  often  with  eructa- 
tions. The  physical  signs  are  those  of  a  moderate  dilatation.  The 
motility  is  impaired,  as  evidenced  by  the  presence  of  food  3  hours 
after  Ewald's,  7  hours  after  Leube-Rigel's,  meal. 

(2)  Pyloric  Incompetency. — Insufficiency  of  the  pylorus,  whereby 
the  contents  of  the  stomach  are  allowed  to  pass  prematurely  into  the 
duodenum,  or  the  contents  of  the  latter  to  regurgitate  into  the  stom- 
ach. It  is  recognised  upon  inflation  of  the  stomach,  when,  if  this 
condition  exists,  there  is  an  immediate  and  visible  passage  of  gas 
into  the  intestine. 

E.  General  Diagkosis  of  Gastric  Xeuroses. — In  general 
the  diagnosis  of  the  purely  neurotic  character  of  the  gastric  disturb- 
ances just  described  is  dependent  upon  two  points :  first,  the  exclu- 
sion of  organic  disease  ;  second,  and  most  important,  the  recognition 
of  an  abnormal  weakness  or  excitability  of  the  nervous  system,  as 
evidenced  by  the  coexistence  of  one  or  more  of  the  manifold  symp- 
toms of  hysteria  or  neurasthenia  (congenital  or  acquired)  the  charac- 
teristic exaggeration  in  the  manner  of  describing  the  condition,  and 
the  precipitation  of  an  attack  or  an  exacerbation  by  worry,  anxiety, 
and  mental  overwork  or  strong  emotions. 

VIII.    DISEASES    OF    THE    INTESTINES 

{See  also  j>ages  113  to  139,  4^7  to  444,  «"^  4^*^  ^o  461) 

I.  Splanchnoptosis. — "  Glenard's  disease,"  a  general  term  ap- 
plied to  falling  or  dropping  of  certain  abdominal  viscera,  embracing 
prolapse  of  the  stomach  (gastroptosis),  of  the  kidney  (nephroptosis), 
of  the  intestines  (enteroptosis),  and  more  rarely  of  the  spleen  (splen- 
optosis) and  of  the  liver  (hepatoptosis). 

(a)  Causes. — This  condition  is  due  to  looseness  of  the  attach- 
ments of  the  organs  involved,  to  overstretching  and  consequent 
relaxation  of  the  abdominal  wall  by  repeated  pregnancies  or  ascites, 
to  tight  lacing,  and  to  a  rapid  loss  of  flesh. 

(h)  Symptoms. — In  many  instances  one  or  more  pronounced  ptoses 
may  be  found,  especially  in  multiparae,  without  any  symptoms  what- 
ever.   With  other  cases  varying  symptoms  are  associated.    There  may 


DISEASES  OF  THE  INTESTINES  777 

be  excessive  flatulence,  constipation  alternating  with  diarrhoea, 
mucous  "  colic "  or  neurosis  (the  so-called  membranous  enteritis), 
gastric  disturbances  or  neuroses,  throbbing  of  the  abdominal  aorta ; 
dragging,  aching,  or  weakness  in  the  back  ;  vasomotor  instability  or 
ataxia ;  chronic  tire,  and  other  of  the  diverse  symptoms  of  neuras- 
thenia or  hysteria.  The  cases  of  abdominal  ptosis  with  symptoms 
occur  more  frequently  in  thin  young  women,  especially  those  who 
have  rapidly  lost  flesh  from  any  cause  or  undergone  a  long  and 
exhausting  nervous  strain. 

(e)  Diagnosis. — The  existence  of  the  symptoms  just  rehearsed 
plus  the  finding  of  the  prolapsed  abdominal  viscera  makes  the  diag- 
nosis. Elsewhere  will  be  found  descriptions  of  the  physical  exam- 
ination required  to  determine  the  presence  of  displacement  of  the 
stomach  (page  456),  kidney  (page  478),  spleen  (page  475),  and  liver 
(page  468).  Of  the  intestines  the  transverse  colon  is  usually  involved 
{coloptosis).  It  sinks  so  as  to  form  a  V  with  acute  bending  or  ob- 
structive kinking  at  the  hepatic  and  splenic  flexures  (Fig.  148,  page 
459).  Glenard  says  that  it  may  be  palpated  as  a  cordlike  body  at 
or  below  the  level  of  the  umbilicus,  although  others  claim  that  the 
body  felt  is  the  pancreas  uncovered  by  the  prolapse  of  the  stomach. 

II.  Acute  Catarrhal  Enteritis. — Causes. — Intestinal  catarrh 
may  be  primary,  and  excited  by  hot  weather,  sudden  falls  of  tem- 
perature, improper  or  decomposing  food  or  spoiled  milk,  and  irritant 
poisons ;  or  secondary  to  infectious  diseases,  cachectic  states,  portal 
engorgement  (disease  of  heart,  lungs,  liver),  or  by  extension  from 
inflammatory  processes  in  the  abdomen. 

Symptoms. — The  cardinal  symptom  is  diarrhoea.  In  addition 
there  may  be  colicky  abdominal  pain,  moderate  gaseous  distention  of 
the  abdomen  with  rumbling  and  gurgling  noises,  and  occasionally 
vomiting.  Fever,  if  present  at  all,  is  slight  (99.5°  to  100.5°)  ;  there  is 
a  furred  tongue,  with  thirst,  anorexia,  and  scanty  urine.  These  symp- 
toms indicate  the  condition  most  commonly  encountered,  namely, 
an  inflammation  of  both  small  and  large  intestine,  or  ileo-colitis. 

In  some  cases  the  clinical  symptoms  are  sufficiently  distinctive  to 
allow  an  inference  that  the  chief  seat  of  the  inflammation  is  in  cer- 
tain definite  portions  of  the  intestine,  viz.,  the  duodenum,  the  small 
intestine,  the  colon,  or  the  rectum. 

(1)  Duodenum. — If  the  duodenum  alone  is  affected  (duodenitis) 
there  is  constipation  instead  of  diarrhoea,  with  some  localized  dis- 
comfort or  slight  pain  and  tenderness,  but  these  symptoms  are  not 
at  all  definite.  Usually  gastritis  coexists,  with  nausea,  vomiting, 
and  gastric  pain  (gastro-duodenitis),  but  the  vague  duodenal  symp- 
toms are  obscured  by  those  relating  to  the  stomach.     In  a  certain 


Y78  DIAGNOSIS,    DIRECT  AND   DIFFERENTIAL 

proportion  of  cases,  however,  jaundice,  due  to  involvement  of  tlie 
bile  duct,  appears,  constituting  the  only  positive  proof  of  duodenitis. 
Otherwise  the  duodenal  inflammation  is  clinically  unrecognisable. 

(3)  Small  Intestine. — That  the  small  intestine  (jejunum,  ileum) 
is  bearing  the  brunt  of  the  inflammation  and  that  the  colon  has 
escaped  may  be  inferred  by  the  absence  of  a  marked  diarrhoea  and 
the  presence  of  colicky  pain  and  rumbling,  with  slight  distention 
and  tenderness  over  the  area  in  which  lies  the  bulk  of  the  small 
intestines.  The  stools  are  flocculent,  contain  undigested  food,  un- 
changed bile,  and  small,  scarcely  visible  masses  of  mucus — findings 
which  are  quite  characteristic  of  a  small-intestine  catarrh. 

(3)  Colon. — Considerable  pain,  a  marked  diarrhoea,  with  tender- 
ness along  the  course  of  the  colon,  and  souplike  stools  containing 
mucus,  perhaps  in  large  and  easily  seen  masses,  indicate  that  the 
affection  is  in  the  main  a  colitis. 

(4)  Rectum. — Considerable  quantities  of  mucus  and  pus,  passed 
with  painful  tenesmus,  indicate  proctitis. 

The  duration  of  acute  catarrhal  enteritis  varies  from  3  days  in 
mild  cases  to  7  or  10  days  in  severe  cases.     Prognosis  usually  good. 

Diagnosis. — The  symptoms  and  short  duration  of  the  disease  gen- 
erally enable  a  ready  recognition  of  its  character.  Diarrhoea  is  the 
important  symptom. 

There  is  rarely  any  difficulty  in  distinguishing  it  from  typhoid 
fever  by  its  brief  duration,  slight  and  atypical  fever,  and  absence  of 
splenic  swelling  and  rose  spots.  Occasionally  one  meets  severe 
cases,  which,  because  of  unusually  severe  pain  and  marked  tender- 
ness, strongly  suggest  peritonitis,  but  the  presence  of  diarrhoea  in 
particular,  and  the  absence  of  a  high  degree  of  meteorism  and  ab- 
dominal rigidity,  will  usually  suffice  to  rule  out  peritoneal  inflamma- 
tion. Xevertheless  in  some  cases  it  is  impossible  to  resist  the  con- 
viction that  the  peritoneum  is  sufficiently  irritated  and  congested  to 
cause  "  peritoneal "  symptoms.  During  an  epidemic  of  cholera 
Asiatica  all  diarrhceal  cases  are  to  be  regarded  and  treated  as  chol- 
erine (page  704)  or  possible  beginning  cases  of  the  full-fledged  dis- 
ease.    For  the  separation  of  diarrhoea  from  dysentery,  see  page  703. 

III.  Chronic  Catarrhal  Enteritis.— (r^  Cavses.—lt  may  be 
a  sequel  of  repeated  acute  attacks  of  enteritis  or  dysentery,  or  de- 
velop as  a  consequence  of  obstruction  to  the  portal  circulation  by 
hepatic  cirrhosis  or  chronic  disease  of  the  heart  or  lungs,  or  arise 
independently. 

{h)  Symptoms. — Mainly  a  chronic  diarrhoea,  which  may  alternate 
with  constipation,  particularly  if  the  colon  alone  is  affected.  Colicky 
pain  and  abdominal  tenderness  are  infrequent.     The  stools  may  be 


DISEASES  OF  THE  INTESTINES  779 

lienteric,  containing  undigested  food,  when  the  small  intestine  is 
chiefly  involved,  or  fluid  and  mucous  if  the  main  seat  of  the  disease 
is  in  the  colon.  In  course  of  time  anaemia  and  emaciation  become 
manifest,  and  mental  depression  or  hypochondriasis  may  develop. 
Prognosis  is  usually  good  as  to  life,  but  recovery  is  not  common. 

IV.  Enteritis  in  Infancy  and  Childhood. — The  greatest 
number  of  cases  are  found  during  the  hot  months,  from  May  to  Sep- 
tember inclusive,  in  infants  from  6  to  18  months  of  age,  and  with 
few  exceptions  in  those  who  are  fed  artificially.  Many  varieties  of  bac- 
teria are  found  in  the  diarrhoeas  of  children,  but  no  one  form  can  be 
held  responsible  for  the  toxic  products  which  develop  in  the  intes- 
tine as  the  result  of  bacterial  growth.  Adopting  Osier's  classifica- 
tion, the  following  varieties  may  be  recognised  : 

(I)  Acute  Dyspeptic  Diarrhoea. — {a)  Symptoms. — After  drinking 
spoiled  milk  or  eating  unripe  fruit  or  improper  food  the  child  be- 
comes ill.  The  symptoms  may  develop  slowly,  with  restlessness  and 
perhaps  slight  fever,  followed  by  diarrhcea  with  offensive,  sometimes 
greenish,  stools,  varying  from  4  to  20  in  24  hours,  which  contain  milk 
curds,  undigested  food,  and  occasionally  mucus.  In  the  severer 
forms  the  onset  is  sudden,  sometimes  attended  by  an  initial  convul- 
sion, with  vomiting,  thirst,  scanty  urine,  colicky  pain,  abdominal 
tenderness,  and  a  rapid  rise  of  temperature  to  104°  or  105°. 

{b)  Diagnosis. — The  small  quantity  of  mucus  in  the  stools  will 
rule  out  entero-colitis.  The  serous  stools  and  severe  symptoms  of 
cholera  infantum  are  absent. 

(c)  Duration  and  Prognosis. — In  well-nourished  children  under 
good  hygienic  surroundings  and  with  proper  care  recovery  occurs  in 
a  few  days.  Otherwise  it  may  merge  into  an  entero-colitis,  or,  in 
very  weakly  children,  prove  fatal. 

(II)  Cholera  Infantum. — This  occurs  in  but  2  or  3  per  cent  of  the 
hot-weather  diarrhoeas  (Holt).  It  is  generally  preceded  by  some 
intestinal  disturbance. 

{a)  Symptoms.— The  disease  usually  begins  with  vomiting,  which 
becomes  excessive  and  persistent,  at  first  containing  bile,  later  be- 
coming serous.  At  the  same  time  purging  sets  in,  with  copious  and 
frequent  stools  varying  from  10  to  30  in  24  hours.  Primarily  the 
stools  are  offensive,  fluid,  and  faecal,  but  ultimately  become  serous, 
watery,  odourless,  and  alkaline,  and  are  voided  with  force.  The  tem- 
perature by  rectum  is  105°  to  108°,  by  axilla  3  or  more  degrees 
lower.  The  tongue  becomes  red  and  dry,  there  is  intense  thirst, 
great  restlessness,  rapid,  weak  pulse,  and  scanty  or  absent  urine. 
The  prostration,  which  is  present  from  the  beginning,  becomes  ex- 
treme, the  face  is  ashy,  pallid,  and  pinched,  the  eyes  are  sunken  and 


780  DIAGNOSIS,   DIRECT  AND  DIFFEEENTIAL 

the  eyelids  but  partly  closed,  the  mouth  is  open,  the  fontanel  de- 
pressed, and  the  extremities  cold.  The  skin  loses  its  elasticity,  and 
if  pinched  remains  in  folds.  Death  may  ensue  within  24  hours  with 
hyperpyrexia  or  collapse  symptoms ;  or  after  a  few  days  gradual  im- 
provement may  take  place,  or  the  disease  pass  into  an  entero-colitis  ; 
or  the  symptoms  of  spurious  hydrocephalus,  the  hydrencephaloid 
state,  may  supervene.  In  the  latter  there  is  an  apathetic  or  semi- 
comatose condition,  with  irregular  or  Cheyne-Stokes  respiration,  cer- 
vical retraction,  clinching  of  the  hands,  sunken  abdomen,  and  per- 
haps convulsions.  Autopsies  usually  fail  to  reveal  any  organic 
changes  in  the  brain. 

(b)  Diagnosis. — The  cardinal  symptoms  are  the  incessant  vomit- 
ing, the  uncontrollable  diarrhoea,  the  serous  stools,  and  the  collapse 
symptoms.  This  clinical  picture  renders  a  mistake  in  diagnosis 
almost  impossible. 

(c)  Duration  and  Prognosis. — Death,  convalescence,  or  a  change 
to  a  less  acute  form  of  intestinal  inflammation  usually  occurs  in  from 
1  to  4  days.     The  prognosis  in  the  majority  of  cases  is  unfavourable. 

(Ill)  Acute  Entero-colitis. — Follicular  or  catarrhal  ulceration, 
especially  of  the  ileum  and  colon.  It  occurs  during  hot  weather,  or 
may  follow  dyspeptic  diarrhoea,  cholera  infantum,  or  the  specific 
fevers. 

{a)  Symptoms. — Usually  with  preliminary  diarrhoeal  symptoms 
the  temperature  rises,  perhaps  to  104°,  and  the  stools,  which  are 
passed  without  pain  and  are  rarely  offensive,  become  blood-streaked, 
contain  much  mucus,  and  vary  from  15  to  30  in  24  hours.  There  is 
abdominal  pain  and  distention,  with  tenderness  along  the  course  of 
the  colon.     Vomiting  is  not  a  prominent  symptom. 

{h)  Dtiration  and  Course. — The  severity  and  course  of  the  disease 
are  variable.  After  lasting  for  2  or  3  weeks  convalescence  may  begin  ; 
or  the  symptoms  may  moderate  and  the  fever  cease,  but  the  diarrhoea 
continues  and  the  child  wastes  away,  until  at  the  end  of  5  or  6  weeks 
recovery  begins  or  death  occurs.  In  certain  instances  the  disease 
may  have  a  sudden  onset  with  high  fever,  intense  abdominal  pain, 
vomiting,  diarrhoea  with  frequent  stools  containing  much  blood  and 
mucus,  prostration,  collapse,  and  death,  within  from  2  to  7  days. 

(c)  Diagnosis. — This  disease  presents  higher  fever,  a  more  severe 
type  of  symptoms,  and  much  larger  quantities  of  mucus  in  the  stools 
than  the  simple  dyspeptic  diarrhoea,  as  well  as  a  more  protracted 
course. 

V.  The  Coeliac  Affection.— This  disease  of  children  from  1  to 
5  years  old— of  unknown  origin  and  pathology  except  that  in  some 
cases  the  Filaria  sanguinis  has  been  found  in  the  dejections — resem- 


DISEASES  OF  THE  INTESTINES  Y81 

bles  the  "  hill  diarrhoea  "  of  the  tropics  affecting  adults.  The  stools 
are  large,  gruel-like,  frothy,  fermenting,  and  offensive.  Anasmia, 
debility,  and  wasting  of  the  body  gradually  occur.  The  disease  is 
protracted,  with  many  relapses,  and  usually  terminates  fatally. 

VI.  Phlegmonous  Enteritis. — A  rare  diffuse  or  circumscribed 
suppurative  inflammation  of  the  submucosa,  occurring  in  connection 
with  chronic  intestinal  obstruction,  strangulated  hernia,  and  intus- 
susception ;  or,  usually  affecting  the  duodenum,  as  a  complication 
of  the  severer  types  of  the  specific  infections  or  pyaemia.  The  symp- 
toms resemble  those  of  peritonitis,  with  severe,  sometimes  faecal, 
vomiting,  high  temperature  perhaps  with  chills,  intense  pain,  and 
tenesmus,  the  latter  especially  in  cases  of  obstruction.  A  diagnosis 
is  impossible,  but  the  condition  may  be  suspected  when  such  symp- 
toms occur  in  connection  with  intussusception  or  strangulated 
hernia. 

VII.  Diphtheritic  (Croupous)  Enteritis. — A  membranous 
inflammation  of  the  mucosa  of  the  small  intestine  and  colon  may 
occur,  most  commonly  as  a  result  of  pneumonia,  scarlet  fever,  typhoid 
fever,  and  pyaemia ;  or  from  poisoning  by  arsenic,  mercury,  and  lead ; 
or  as  a  terminal  event  in  various  cachexiae,  especially  chronic  ne- 
phritis, malignant  disease,  and  hepatic  cirrhosis.  The  disease  is  often 
latent  and  clinically  unrecognisable.  There  may  be  in  some,  espe- 
cially the  toxic,  cases,  pain,  diarrhoea,  blood-stained  mucous  stools, 
and,  more  rarely,  tenesmus,  but  these  symptoms  are  not  very  dis- 
tinctive. 

VIII.  Ulceration  of  the  Intestine. — Ulcers  in  the  intestine 
occur  in  dysentery,  typhoid  fever,  chronic  enteritis,  tuberculosis, 
sjrphilis,  and  cancer ;  other  ulcers  are  the  duodenal,  stercoral  (due 
to  the  pressure  of  hardened  faecal  masses),  the  solitary  ulcer  of 
caecum  or  colon,  the  embolic  ulcer  (due  to  embolism  of  an  intestinal 
artery  in  the  course  of  valvular  disease  or  pyaeraic  processes),  and 
simple  ulcerative  colitis.  Furthermore,  ulceration  and  perforation 
of  the  bowel  from  without  inward  may  result  from  the  pressure  and 
erosion  of  outside  neoplasms,  or  more  commonly  from  the  localized 
abscesses  of  appendicitis  or  suppurative  or  gangrenous  pancreatitis. 

The  symptoms  of  intestinal  ulceration,  apart  from  those  of  the 
causative  condition,  are  not  very  distinctive.  In  general,  intestinal 
hemorrhage,  especially  if  profuse,  manifested  by  bloody  or  tarry 
stools;  the  presence  of  pus  in  moderate  quantity,  large  amounts 
indicating  rather  the  perforation  of  a  neighbouring  abscess  cavity 
(usually  pericaecal  or  from  the  broad  ligament) ;  and  the  finding  of 
tissue  shreds  or  particles,  constitute  the  most  significant  symptoms. 
Diarrhoea,  colicky  pain,  and  finally  perforation  followed  by  peri  to- 


782  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

nitis  may  occur.  All  of  these  symptoms  are  most  marked  when  the 
colon  is  involved,  as  ulcers  of  the  small  intestine  tend  to  latency. 
The  following  forms  require  special  but  brief  mention  : 

(1)  Simple  Ulcerative  Colitis. — The  ulceration  of  the  colon  may 
be  very  extensive.  The  disease  is  not  infrequent,  and  usually  occurs 
in  men  past  middle  life.  The  symptoms  are  a  lienteric  diarrhoea, 
often  alternating  with  constipation,  a  protracted  course  with  weak- 
ness and  loss  of  flesh,  and  possibly  perforation.  The  disease  usually 
becomes  chronic.  The  differential  diagnosis  is  to  be  made  from 
dysentery,  to  which  it  bears  a  close  resemblance,  by  the  presence  of 
undigested  food  in  the  stools  and  the  absence  of  blood  and  pus. 

(3)  Stercoral  Ulcers. — In  very  chronic  cases  of  constipation,  small, 
hard,  rounded  scybalae,  perhaps  covered  by  a  deposit  of  lime  salts 
(enteroliths),  may  be  retained  for  so  long  a  time  as  to  cause  distinct 
ulcers  in  the  saccules  of  the  colon  in  which  they  lie.  There  is  often 
tenesmus,  colicky  pain  which  may  occur  in  severe  paroxysms,  diar- 
rhoea from  the  irritation  of  the  hardened  masses  which  nevertheless 
fail  to  be  dislodged,  and  the  stools  may  contain  mucus,  pus,  and 
perhaps  blood.  The  diagnosis  is  not  easy,  but  the  condition  should 
be  borne  in  mind  as  a  possible  explanation  of  the  symptoms.  The 
rectum  should  be  digitally  examined  for  the  presence  of  hard  scyb- 
alae, and  the  abdomen  palpated  to  discover,  if  possible,  a  cylindrical 
fsBcal  mass,  or  the  circumscribed  tenderness  of  an  ulcer  in  the  colon, 
both  of  which  are  rare  findings. 

IX.  Appendicitis. — Pathologically  there  are  three  forms  of  ap- 
pendicitis :  ohliterative,  in  which  the  appendix  may  become  occluded 
at  its  proximal  end  and  dilate  into  a  cyst,  or  its  lumen  becomes  en- 
tirely obliterated,  or  ulceration  and  perforation  occur,  or  the  process 
may  terminate  in  resolution  ;  ulcerative^  in  which  the  ulceration  may 
heal  with  or  without  the  formation  of  a  stricture,  or  may  perforate ; 
and  interstitial.,  in  which  gangrene,  usually  limited,  occurs,  followed 
by  perforation  and  peritonitis.  Faecal  concretions  often,  and  foreign 
bodies  more  rarely,  play  an  important  part  in  initiating  ulcerative 
or  necrotic  changes.  The  micro-organisms  which  are  associated 
with  the  infective  inflammatory,  ulcerative,  or  necrotic  processes 
are  the  Bacterium  coli  communis  (most  common).  Streptococcus 
pyogenes  (most  virulent).  Staphylococcus  pyogenes  aureus.  Bacillus 
pyocyaneus,  proteus,  Bacillus  typhosus,  Bacillus  ttiberculosis,  and 
Actinomyces. 

The  majority  of  cases  occur  between  the  15th  and  30th  year  of 
life,  although  no  age  is  exempt,  and  about  four  fifths  of  the  cases 
are  in  males.  Important  predisposing  causes  are  blows,  falls,  excess- 
ive physical  exertion,  fatigue,  improper  food  and  digestive  disturb- 


DISEASES  OF  THE  INTESTINES  Y83 

ances,  faecal  concretions  or  foreign  bodies,  exposure  to  cold,  rheuma- 
tism, influenza,  and  typhoid  fever. 

According  to  the  intensity,  frequency  of  occurrence,  and  dura- 
tion of  the  disease  three  clinical  varieties  of  the  disease  are  recog- 
nised :  acute.,  chronic^  or  recurrent. 

(I)  Acute  Appendicitis. — {a)  Symptoms. — In  a  large  majority  of 
cases  the  onset  is  sudden  with  abdominal  pain,  at  first  diffuse,  later 
localized  over  the  appendix ;  nausea,  vomiting,  and  frequently  con- 
stipation ;  circumscribed  tenderness  in  the  appendical  region,  and 
fever.  Pain  may  be  colicky  and  sharp,  or  dull  and  aching.  It  is 
often  diffuse  at  the  outset,  or  felt  in  any  part  of  the  abdomen,  but  in 
-24  or  48  hours  settles  in  the  site  of  the  appendix,  whence  it  may 
radiate  into  the  testicle  or  down  the  right  leg.  It  is  usually  in- 
creased by  movement  or  coughing.  G astro-intestinal  symptoms  are 
usually  present.  Xausea  and  vomiting,  which  in  mild  cases  are 
neither  severe  j\ov  prolonged,  are  common  at  the  outset.  Constipa- 
tion is  usual  and  may  be  so  obstinate  as  to  simulate  obstruction,  but 
it  must  not  be  forgotten  that  there  may  be  an  initial  diarrhoea,  espe- 
cially in  children  or  in  early  adult  life. 

Palpation  reveals  localized  tender7iess,  generaWj  situated  at  McBur- 
ney's  point  (Fig.  146,  page  457),  although  in  exceptional  instances  of 
an  unusual  location  of  the  appendix  the  "  tender  point "  may  be  found 
in  the  right  groin  or  deep  in  the  pelvis,  or  in  the  left  iliac,  umbilical, 
right  hypochondriac  and  right  lumbar  regions.  Rigidity  of  tlie 
right  rectus,  another  important  early  symptom,  and  which,  because 
of  its  one-sided  character,  is  determined  with  ease,  usually  coexists 
■with  the  tenderness.  Tumour  may  or  may  not  be  palpable  after  the 
first  24  or  48  hours.  It  may  be  quite  absent  in  the  severest  cases. 
When  present  it  may  be  either  an  indefinite  induration  or  a  circum- 
scribed mass,  and  its  extent  and  character  are  often  obscured  by  the 
coincident  tenderness  and  rigidity.  Percussion  gives  uncertain  re- 
sults. The  note  may  be  dull,  dull  tympanitic,  or  tympanitic  accord- 
ing to  the  relative  amounts  of  gas,  faecal  matter,  and  exudate.  The 
induration  is  found  about  1^  to  2  inches  above  Poupart's  ligament,  un- 
less the  appendix  is  in  some  one  of  the  unusual  situations  previously 
mentioned. 

Fever.,  an  important  diagnostic  symptom,  is  commonly  present, 
varying  from  100°  to  102°,  or  at  the  outset  in  children  rising  to  103° 
or  over.  When  an  intense  diffuse  peritonitis  or  a  gangrenous  appen- 
dix is  present,  or  a  circumscribed  abscess  has  formed,  the  temperature 
may  be  normal  or  subnormal,  but  the  associated  symptoms  are  of  too 
grave  a  character  to  be  in  keeping.  A  chill  at  the  onset  is  very  in- 
frequent. 


784  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

The  urme  is  scanty,  and  usually  contains  an  excess  of  indican, 
often  also  a  trace  of  albumin.  The  bladder  is  often  irritable  at  the 
onset,  and  the  frequent  micturition  may  suggest  a  cystitis.  Later 
in  the  disease  retention  may  occur.     Leucocytosis  is  usually  present. 

When  the  peritoneum  is  involved  the  facies  is  often  indicative  of 
anxiety.  The  dorsal  posture,  with  the  right  leg  persistently  drawn 
up,  is  common  and  often  suggestive.  The  tongue  is  moist  and  furred^ 
becoming  later,  in  severe  cases,  dry  and  brown.  The  pulse  corre- 
sponds at  first  with  the  temperature ;  subsequently,  but  not  always^ 
with  the  gravity  of  the  local  condition. 

{h)  Possibilities  and  Terminations. — In  general  there  are  three 
eventualities  in  every  case  of  acute  appendicitis  :  resolutio7i,  abscess- 
formation,  or  diffuse  peritonitis. 

(1)  Eesolution. — In  the  majority  of  the  milder  cases  the  pain 
rapidly  settles  into  the  appendical  region ;  the  tenderness  is  moder- 
ate and  steadily  diminishes,  requiring  deep  pressure  to  elicit  it ;  the 
abdominal  distention  and  rectus  rigidity  are  not  marked  and  steadily 
lessen ;  the  initial  nausea  and  vomiting,  if  present,  soon  subside ; 
the  fever  continues  for  from  3  to  5  days  and  then  departs.  In  a 
week  or  10  days  the  patient  is  thoroughly  convalescent.  In  some 
instances  a  slight  elevation  of  temperature  may  continue  for  2  or  3 
weeks,  and  while  apparent  recovery  takes  place  there  remains  some 
hardness  or  a  small  swelling  in  the  appendical  region,  a  condition 
ominous  of  recurrence.  ' 

(3)  Circumscribed  Suppuration. — Earlier  in  the  severe  cases,  later 
in  the  mild,  in  both  usually  as  the  result  of  ulceration  and  perfora- 
tion, less  commonly  from  extension  of  the  inflammation  through  the 
non-perforated  appendical  walls,  a  circumscribed  abscess,  generally 
intraperitoneal,  may  form. 

As  evidences  of  suppuration  the  fever  persists,  the  pain  increases,. 
the  tenderness  covers  a  wider  area  from  hour  to  hour,  especially^ 
downward  toward  the  pelvis,  the  constipation  becomes  more  obsti- 
nate, and  frequent  urination  or  retention  is  common.  A  tumour, 
deep-seated  or  superficial,  becomes  manifest,  or,  if  present,  increases 
in  size,  and  in  either  case  is  apt  to  be  excessively  tender.  It  is  to  be 
remembered  that  an  amelioration  of  the  general  symptoms  may  occur 
after  the  abscess  has  become  thoroughly  walled  off. 

The  abscess  cavity  may  be  small  or  large,  symmetrical  or  irregu- 
lar, and  is  limited  by  adherent  coils  of  intestine  or,  partly,  by  vari- 
ous portions  of  the  abdominal  or  pelvic  walls.  If  the  abscess  is  not 
surgically  evacuated  it  may  empty  itself  into  the  bladder,  vagina, 
rectum,  or  caecum,  or  enter  the  hip  joint,  or  pass  out  through  the 
obturator  foramen.     If  it  is  retroperitoneal  it  may  discharge   ex- 


DISEASES  OP  THE  INTESTINES  785 

ternally  in  the  groin,  or  form  a  large  perinephric  abscess,  or,  lying 
under  the  diaphragm,  give  rise  to  the  symptoms  of  subphrenic  ab- 
scess or  (if  it  contains  air)  of  pneumothorax,  perhaps  followed  by 
perforation  of  the  pleura  and  a  resulting  pleuro-faecal  fistula.  Finally, 
a  localized  periappendicular  abscess  may  rupture  slowly  or  suddenly 
into  the  general  peritoneal  cavity  with  resulting  diffuse  peritonitis. 

(3)  Acute  Diffuse  Peritonitis. — Following  perforation  of  the  ap- 
pendix, or  rupture  of  an  abscess  either  in  mild  or  severe  cases,  a 
general  peritonitis  may  ensue.  The  symptoms  indicating  the  super- 
vention of  general  peritonitis  are  extreme  and  diffuse  pain,  a  rigid 
and  distended  abdomen,  nausea  and  vomiting,  rapid  pulse,  dry  tongue, 
anxious  countenance,  dorsal  posture  with  the  knees  drawn  up,  and 
often  a  normal  or  subnormal  temperature. 

This  condition  may  develop  rapidly  from  the  outset  in  cases  of 
€arly  perforation  in  which  an  immediate  general  infection  occurs 
without  a  limiting  inflammation ;  or  more  gradually  when  the  per- 
foration has  occurred  later  in  the  disease  after  a  certain  amount  of 
protective  adhesion  has  taken  place,  or  when  a  periappendicular  ab- 
scess has  ruptured  and  its  contents  slowly  infect  the  peritoneum. 
The  symptoms  of  gangrene  of  the  appendix  may  be  latent  and  excess- 
ively deceptive. 

(c)  Complications. — Some  of  the  events  previously  mentioned 
may  be  considered  as  complications.  Under  this  head  may  be  in- 
cluded suppurative  pylephlebitis,  causing  multiple  hepatic  abscesses  ; 
thrombosis  or  compression  of  the  right  iliac  vein ;  hemorrhage 
from  perforation  of  the  intestine  or  necrosis  of  the  iliac  arteries ; 
subphrenic  abscess,  perhaps  followed  by  perforation  of  the  diaphragm, 
and  pleurisy  (serous  or  suppurative)  or  pericarditis ;  and  appendi- 
citis in  a  hernial  protrusion.  The  majority  of  these  are  of  rare 
occurrence. 

(d)  Diagnosis. — The  cardinal  symptoms  are  acute  pain  in  the 
right  lower  abdomen,  localized  tenderness  with  or  without  tumour, 
and  fever,  even  if  slight.  As  Fowler  well  says,  "  pronounced  tender- 
ness in  the  right  iliac  fossa  is  almost  as  pathognomonic  of  appendi- 
citis as  rusty  sputum  is  of  pneumonia."  If  to  the  symptoms  just 
mentioned  are  added  nausea,  vomiting,  right  rectus  rigidity,  and 
tumour,  the  diagnosis  is  absolute. 

Although  a  typical  case  of  appendicitis  is  unmistakable,  there 
are  variations  in  the  severity  and  manner  of  onset,  and  an  occasional 
lack  of  correspondence  between  the  symptoms  and  the  actual  local 
condition  which  may  cause  the  most  expert  diagnostician  to  trip. 
For  example,  the  disease  may  begin  with  diarrhoea,  and  be  mistaken 
for  catarrhal  enteritis ;  mild  cases,  with  slight  symptoms  and  lasting 


786  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

only  for  a  few  hours,  are  often  self-diagnosed  as  "  biliousness  "  or 
"cold,"  and  in  others  the  symptoms  may  be  insignificant  and  the 
patient  may  be  up  and  around  carrying  an  abscess ;  the  tenderness 
may  be  in  an  unusual  location  ;  the  severest  cases  may  have  a  sub- 
normal temperature;  rectus  rigidity  may  be  lacking  if  the  perito- 
neum is  not  involved ;  the  symptoms  may  lessen  and  yet  the  patient 
get  up  with  an  abscess ;  a  gangrenous  appendix  may  be  present  with 
a  most  misleading  mildness  of  symptoms ;  and,  finally,  a  diffuse  peri- 
tonitis may  be  present  from  the  very  outset  of  the  disease. 

Careful,  complete,  and  repeated  abdominal  palpation  in  all  cases, 
and  examination  by  the  rectum  (emphasized  by  Delatour)  and  vagina 
in  obscure  or  suspicious  cases  should  never  be  omitted. 

Suppuration  is  announced  especially  by  an  exacerbation  of  pre- 
vious symptoms  and  a  slow  increase  in  the  size  of  the  tumour. 

Perforation  of  the  appendix^  present  or  imminent,  is  usually  indi- 
cated by  severe  pain,  excessive  tenderness,  and  marked  right  rectus 
rigidity.  Imminent  perforation  of  the  bladder  may  be  signified  by 
painful,  scanty,  and  frequent  urination.  Imminent  perforation  of 
the  rectum  may  be  heralded  by  tenesmus  and  the  passage  of  thick 
blood-stained  mucus.  Multiple  suppurations  of  the  liver  are  an- 
nounced by  chills,  irregular  fever,  and  swelling  with  tenderness  of 
the  organ. 

With  reference  to  the  leucocyte  count  in  appendicitis  Greenough 
concludes  that  a  leucocytosis  is  a  fairly  constant  symptom  ;  that  a 
count  of  20,000  on  the  first  or  second  day  suggests  general  peritoni- 
tis ;  that  a  count  of  10,000  or  less  after  the  first  week  indicates,  if 
the  symptoms  are  grave  a  general  peritonitis,  if  the  symptoms  are 
severe  a  mild  catarrhal  inflammation  or  a  subacute  well-walled-ofE 
abscess ;  and  that  a  count  of  20,000  or  over  after  the  first  week  or 
ten  days  is  significant  of  a  local  abscess. 

(e)  Differential  Diagnosis. — The  following  conditions  may  require 
differentiation : 

(1)  Renal  Colic. — There  is  no  tumour,  no  fever,  no  "  spot  "  of 
tenderness,  haematuria  is  present,  and  the  pain  radiates  into  the 
groin  and  testicle. 

(2)  Acute  Cholecystitis. — An  inflamed  and  distended  gall  bladder 
presents  pain,  tenderness,  tumour,  and  fever,  but  the  tumour  is 
rather  above  than  below  the  level  of  the  navel ;  it  is  pear-shaped, 
movable,  and  usually  lies  superficially,  and  jaundice  is  often  present. 
Nevertheless  mistakes  will  occur. 

(3)  Indigestion  and  Entero-colitis. — In  these,  nausea,  vomiting, 
and  epigastric  or  colicky  abdominal  pain  may  closely  simulate  ap- 
pendicitis, but  there  is  no  circumscribed  tenderness,  no  rigidity. 


DISEASES  OP  THE  INTESTINES  Y87 

no  tumour,  and   while  diarrhoea  may  initiate  an  appendicitis  it  is 
exceptional. 

(4)  Acute  Intestinal  Obstruction. — There  may  be  a  more  or  less 
distinct  tumour  with  localized  tenderness,  but  this  is  not  necessarily 
in  the  appendical  region.  If  due  to  intussusception,  there  will  be, 
especially  in  children,  rectal  tenesmus  with  the  frequent  passage  of 
bloody  mucus  ;  if  to  internal  strangulation,  faecal  vomiting  may  be 
present,  neither  of  which  occur  in  appendicitis.  Moreover,  the  onset 
is  more  gradual,  fever,  if  present  at  all,  is  usually  of  late  occurrence, 
and  constipation  is  more  apt  to  be  complete.  Nevertheless  mistakes 
will  be  made. 

(5)  Typhoid  Fever.— See  page  667. 

(6)  Salpingitis,  Ovaritis,  or  Ectopic  Gestation. — An  abscess  of  the 
right  ovary  or  a  right-side  salpingitis  may  in  some  instances  simulate 
very  closely  a  low-down  appendical  abscess.  Both  cause  fever  and 
right-side  pain  and  tenderness,  but  a  history  of  previous  or  present 
menstrual  irregularities,  together  with  a  pelvic  examination  which 
reveals  a  fixed  uterus,  an  indurated  pelvic  exudate,  or  an  abscess 
cavity  joined  to  the  uterus  by  the  ridge  of  the  broad  ligament,  will, 
as  a  rule,  suflBce  for  the  discrimination.  But  in  one  case  a  distinct 
ovoid  mass  easily  palpated  in  the  right  iliac  region  proved  at  opera- 
tion to  be  an  unusually  high  ovarian  abscess.  Extra-uterine  preg- 
nancy affords  a  rather  characteristic  previous  history  of  morning 
nausea,  breast  signs,  menstrual  irregularities,  and  attacks  of  colicky 
pain  with  faintness,  and  the  physical  examination  shows  a  movable 
mass  lateral  to  the  uterus.  Fever  is  absent.  If  rupture  has  occurred 
collapse  symptoms  are  superadded.  A  diseased  right  ovary  is  often 
associated  with  appendicitis,  especially  the  chronic  form  of  the  latter. 

(7)  Dietle's  Crises.— If  the  ureter  of  a  right  floating  kidney 
becomes  twisted,  the  resulting  nausea,  vomiting,  pain,  and  tumour 
may  simulate  appendicitis,  but  the  outline  and  mobility  of  the 
tumour,  the  occasional  haematuria,  the  absence  of  fever,  and  the  sud- 
den relief  of  the  symptoms  (by  spontaneous  untwisting),  point  to  the 
kidney  as  the  offending  organ. 

(8)  Perinephric  Abscess.— As  this  in  rare  instances  may  arise 
from  appendicitis,  an  absolutely  positive  differentiation  can  not  be 
made  previous  to  operation. 

(9)  Tuberculous  Peritonitis.- In  this  the  invasion  is  gradual, 
right  iliac  tumour  is  absent,  and  the  course  is  more  protracted.  If 
a  local  peritonitis  in  the  right  iliac  fossa  occurs  from  tuberculous 
mesenteric  glands,  time  or  operation  may  be  required  to  separate  it 
from  appendicitis.  In  both  cases  the  existence  of  tuberculous  dis- 
ease elsewhere  may  offer  a  valuable  clew. 


^88  DIAGNOSIS,  DIRECT  AND  DIFFERENTIAL 

(10)  Hysteria  and  Mucous  Colic. — In  nervous  or  hypochondriacal 
women  (or  men)  presenting  mucous  colic  {q.  v.),  formerly  termed 
membranous  enteritis,  as  one  of  the  evidences  of  the  neuropathic 
constitution,  a  mistaken  diagnosis  is  not  uncommon.  It  is  to  be 
discriminated  from  appendicitis  by  the  absence  of  fever  or  of  strictly 
limited  tenderness  or  tumour,  and  especially  by  the  presence  of  some 
of  the  multiform  neurotic  symptoms  of  the  condition  in  question. 

(11)  Appendicular  Colic. — Kecurring  pain  in  the  appendical 
region,  sometimes  of  great  severity,  and  explained  theoretically  as 
an  effort  on  the  part  of  the  appendix  to  expel  mucus  or  faecal  matter 
through  a  somewhat  narrowed  orifice,  may  be  mistaken  for  appendi- 
citis, but  the  total  absence  of  fever  will  rule  out  the  latter. 

(12)  Pericaecal  Abscess  from  perforation  of  the  intestine  in  the 
appendical  region  by  a  simple,  typhoid,  or  carcinomatous  ulcer  can 
not  be  separated  from  appendicitis  except  by  operation. 

(13)  Disease  of  Hip  Joint. — In  young  children  appendicitis  may 
"be  mistaken  for  disease  of  the  right  hip  joint  (Gibxey). 

(14)  Typhlitis. — Inflammation  of  the  cgecum  and  its  peritoneal 
covering  (typhlitis  and  perityphlitis),  especially  the  form  supposed 
of  old  to  be  due  to  filling  of  the  caecum  with  hardened  fgeces  (ster- 
coral typhlitis),  is  in  reality  appendicitis.  It  is  desirable,  in  the  light 
of  the  knowledge  of  to-day,  that  these  terms  should  be  dismissed 
from  use. 

(/)  Prognosis. — The  mild  types  usually  recover,  those  with  local- 
ized abscesses  generally  get  well  if  operated,  the  majority  of  the 
severe  cases  with  diffuse  peritonitis  will  die,  operation  or  no  opera- 
tion. The  prognosis  in  the  individual  case  is  uncertain.  My  own 
rule  is  to  have  a  competent  surgeon  watch  the  case  with  me  from 
the  onset.  The  tendency  of  the  practitioner  of  internal  medicine  to 
temporize  is  thus  counterbalanced  by  the  frequently  opposite  trend 
of  the  surgical  mind,  and  the  middle  way  of  wisdom  is  more  apt  to 
be  trodden. 

(II)  Chronic  and  Recurrent  Appendicitis. — If  relapses  occur  at 
comparatively  short  intervals,  of  weeks  or  months,  the  condition  is 
termed  chronic  or  relapsing  appendicitis ;  if  at  longer  intervals,  of 
months  or  years,  it  is  termed  recurrent  appendicitis.  The  frequency 
of  relapse  in  all  cases  has  been  variously  estimated  at  from  23  to  41 
per  cent.  The  symptoms  of  the  relapse  or  recurrence  are  similar  in 
all  respects  to  those  of  the  primary  attack. 

(1)  In  the  chronic  or  relapsing  form  there  may  be  no  symptoms 
in  the  intervals  between  the  attacks.  More  commonly  the  patient 
complains  of  a  slight  but  constant  sense  of  discomfort  or  moderate 
soreness  in  the  appendical  region.     From  time  to  time,  as  a  result  of 


DISEASES  OF  THE  INTESTIKES  789 

muscular  effort,  dietetic  imprudences,  digestive  disturbances,  or  the 
collection  of  faeces  in  the  caecum,  the  uneasy  sensation  may  develop 
into  moderate  pain  with  perhaps  slight  fever,  the  symptoms  not  being 
sufficiently  acute  to  be  entitled  a  relapse.  Xot  infrequently  the 
abiding  consciousness  of  the  nature  of  the  ailment  will,  by  causing 
persistent  anxiety,  lead  to  the  development  of  neurasthenic  or  hypo- 
chondriacal symptoms  with  impairment  of  the  general  health. 

The  diagnosis  of  chronic  appendicitis  is  not  often  doubtful. 
The  presence  of  localized  tenderness,  possibly  of  tumour,  perhaps 
with  occasional  slight  fever,  will  serve  to  distinguish  it  from  a  mere 
"  appendicular  hypochondriasis  "  or  phobia.  Moreover,  by  suitable 
diversion  of  the  patient's  mind  during  the  examination  an  apparent 
right  iliac  tenderness  may  be  made  to  disappear.  It  is  an  open 
question  whether  the  normal  or  thickened  appendix  itself  can  be  so 
distinctly  palpated  and  recognised  as  is  claimed  by  some  writers. 
Surgeons  of  my  acquaintance  of  as  wide  experience  and  with  quite 
as  good  a  tactus  eriiditus  deny  it  positively. 

Malignant  disease  of  the  ceecum,  by  causing  pain,  tenderness,  and 
tumour,  may  closely  simulate  chronic  appendicitis,  but  a  history 
of  gradually  increasing  constipation,  progressive  loss  of  flesh  and 
strength,  the  development  of  a  cachexia,  and  the  usual  absence  of 
febrile  movement  point  toward  carcinoma.  Nevertheless,  operation 
may  be  required  for  the  discrimination. 

(2)  In  recurring  appendicitis  the  separate  attacks  may  differ  in 
severity,  but  during  the  intervals  the  patient  is  practically  well. 

X.  Intestinal  Obstruction. — («)  Causes. — Strangulation,  in- 
tussusception, volvulus,  fgecal  impaction,  enteroliths,  gallstones,  tu- 
mours, strictures,  intestinal  paralysis,  and  foreign  bodies. 

{I)  Symptoms. — With  reference  to  its  suddenness  of  occurrence, 
two  clinical  forms  of  obstruction  are  recognised :  acute  and  chronic. 

(1)  Acute  Obstruction. — The  cardinal  symptoms  are  abdominal 
pain,  vomiting,  and  obstinate  constipation. 

Pain.,  which  may  be  in  any  part  of  the  abdomen,  is  the  earliest  of 
these,  and  generally  comes  on  during  movement  or  some  sudden  ex- 
ertion. It  is  at  first  colicky  and  intermittent  because  the  obstruc- 
tion is  partial,  but  when  the  stenosis  is  complete  it  becomes  intense 
and  continuous.  Abdominal  tenderness,  absent  at  first,  may  become 
excessive.  Constant  and  distressing  vomiting  soon  ensues,  at  first 
of  the  stomach  contents,  then  of  bile  containing  green  fluid,  finally 
of  a  dark  fluid  with  a  faecal  odour — a  most  important  symptom.  Con- 
stipation may  be  present  from  the  outset,  but  very  often  the  contents 
of  the  intestine  below  the  point  of  stenosis  are  evacuated,  after  which 
no  further  fgecal  stools  are  voided.  Tympanites  makes  its  appear- 
52 


790  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

ance  from  the  second  to  the  sixth  day.  It  is  most  marked  when  the 
obstruction  is  in  the  colon,  and  slight  when  the  stenosis  is  high  up 
in  the  small  intestine.  Tumour  is  rare,  except  in  intussusception. 
Tenesmus  is  frequent  if  the  obstruction  is  in  the  colon,  especially  if 
there  is  intussusception,  less  often  with  volvulus  and  stricture.  Ex- 
cessive peristalsis  may  be  seen,  accompanied  by  easily  audible  rum- 
bling, gurgling,  or  splashing  sounds. 

The  general  symptoms  are  well  marked  and  grave  from  the  begin- 
ning of  the  disease.  They  are  prostration,  pallor,  an  anxious  expres- 
sion, cold  sweating  skin,  and  a  normal  or  subnormal  temperature, 
more  rarely  moderate  fever  (100°  to  102°),  usually  late  in  the  disease. 
Thirst  is  extreme,  the  tongue  is  dry,  the  respiration  accelerated,  and 
the  pulse  feeble  and  rapid.  The  urine  is  scanty,  high  coloured,  and 
may  be  suppressed.  The  duration  of  acute  obstruction  is  usually 
from  3  to  G  days,  the  patient  becoming  comatose  or  dying  from  ex- 
haustion, or  in  very  acute  cases  from  rapid  collapse. 

(3)  Chronic  Obstruction. — The  obstruction  for  a  long  time  may 
be  only  partial,  but  with  a  gradually  increasing  degree  of  constipa- 
tion. Occasional  diarrhoea  may  occur,  especially  in  faecal  impaction, 
from  a  colitis  excited  by  the  irritation  of  hardened  scybalae ;  or 
regular  but  inadequate  stools  may  be  passed  by  a  way  channelled 
through  the  retained  mass.  In  stenosis  due  to  tumour  or  cicatricial 
stricture  the  degree  of  constipation  varies  from  time  to  time.  There 
may  be,  at  irregular  intervals,  passing  attacks  of  vomiting,  with 
colicky  abdominal  pain  and  distention.  In  chronic  obstruction  the 
stools  may  be  small,  hard,  and  scybalous,  or  ribbon-shaped,  perhaps 
containing  mucus  and  blood,  especially  if  the  colon  is  the  seat  of  the 
stenosis.  The  general  health  is  impaired,  particularly  in  malignant 
disease,  anaemia,  emaciation,  or  cachexia  occurring. 

In  any  case  of  chronic  stenosis  the  symptoms  may  become  those 
of  the  acute  form  from  the  sudden  completion  of  the  occlusion,  death 
occurring  in  from  10  to  12  days. 

(f)  Complications. — There  may  be  catarrhal,  diphtheritic,  or  sup- 
purative inflammation  of  the  mucous  membrane,  with  localized  peri- 
tonitis in  the  immediate  neighbourhood  of  the  obstruction ;  gangrene 
or  ulceration,  with  perforation  and  a  resulting  diffuse  peritonitis ;  or 
pyaemia. 

{d)  Diagnosis. — The  existence  of  obstruction  having  been  deter- 
mined by  the  cardinal  symptoms — acute  and  severe  abdominal  pain  ; 
vomiting,  at  first  gastric,  then  bilious,  later  faecal ;  early  prostration ; 
and  obstinate  constipation  followed  by  tympanitic  distention — it  be- 
comes desirable  to  ascertain,  if  possible,  the  site  and  the  cause  of  tho 
obstruction. 


DISEASES  OP  THE  INTESTINES  79I 

(1)  The  Site  of  the  Obstructiox. — Is  it  in  the  small  intes- 
tine or  in  the  colon  ? 

In  general,  if  in  the  small  intestine^  vomiting,  soon  becoming 
faecal,  is  an  early  symptom,  and  the  tympanitic  distention  is  not 
prominent  and  may  be  slight.  If  the  obstruction  is  high  up,  in  the 
duodenum  or  jejunum,  the  meteorism  is  slight,  faecal  vomiting  may 
not  be  marked,  indicanuria  is  common,  collapse  and  suppression  of 
urine  occur  early  and  rapidly.  If  in  the  ileum,  the  distention  is 
greater,  is  manifest  mainly  in  the  mid-abdomen,  and  faecal  vomiting 
is  early  present. 

In  general,  if  the  obstruction  is  in  the  coloti,  abdominal  distention 
is  marked,  faecal  vomiting  is  much  less  frequent,  and  indicanuria  is 
seldom  found.  If  the  obstruction  is  in  the  lower  end  of  the  ileum 
or  in  the  csecum,  inspection  may  show  the  ladder  pattern  of  tumidity 
in  the  lower  mid-abdomen ;  if  in  the  rectum  or  sigmoid  flexure  of 
the  colon,  the  latter  may  stand  out  prominently,  in  a  horseshoe 
shape,  around  the  upper  and  lateral  portions  of  the  abdomen,  and 
tenesmus  with  the  passage  of  blood  and  mucus  may  be  present. 

Abdominal  examination  may  reveal  a  tumour  or  swelling,  but  this 
is  rare  except  in  intussusception  or  faecal  accumulation.  Digital  ex- 
amination of  the  rectum  may  enable  the  recognition  of  a  tumour  or 
stricture,  or  the  emptiness  or  fulness  of  the  cavity.  Information  may 
be  gained  by  noting  the  amount  of  water  which  may  be  injected, 
under  anaesthesia,  by  the  fountain  syringe,  the  patient  lying  upon 
the  back  with  the  hips  elevated.  Normally,  in  an  adult,  6  quarts,  in 
an  infant,  1^  pints,  under  a  pressure  of  3  feet,  will  enter.  Unless 
more  than  3  pints  will  enter  in  an  adult,  obstruction  at  the  sigmoid 
flexure  can  not  be  eliminated.  Auscultation  over  the  caecum  may  be 
employed  during  the  inflow,  to  recognise  the  arrival  of  fluid  at  this 
point  (Treves). 

(2)  The  Cause  of  the  Obstructiox. — If  it  is  diflBcult  to  de- 
termine its  site,  it  is  still  more  diflBcult  to  decide  the  nature  of  the 
obstruction.  The  doctrine  of  probabilities  does  not  apply  to  the 
individual  case,  but  it  is  helpful  to  remember  that,  roughly,  accord- 
ing to  Fitz,  of  all  cases,  strangulation  will  be  present  in  about  35  per 
cent,  intussusception  also  in  35  per  cent,  volvulus  in  15  per  cent, 
gallstones  in  8  per  cent,  and  stricture  or  tumour  in  6  per  cent. 

Obstruction  in  the  small  intestine  is  usually  due  to  strangulation 
(72  per  cent)  or  gallstones  (U  per  cent),  less  frequently  to  intussus- 
ception (8  per  cent),  volvulus  (5  per  cent),  rarely  to  stricture  or 
tumour ;  in  the  colon  mainly  to  intussusception  (51  per  cent)  and 
volvulus  (30  per  cent),  less  commonly  to  stricture  or  tumour  (12  per 
cent). 


Y92  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Acute  obstruction  is  usually  due  either  to  strangulation  or  intus- 
susception, less  commonly  to  volvulus;  chronic  obstruction  mainly 
to  strictures,  tumours,  or  faecal  impaction. 

The  following  points  may  be  of  some  assistance  in  determining 
the  cause  of  the  obstruction  : 

Strangulation. — Most  commonly  due  to  adhesions  from  previous 
peritonitis  or  coeliotomy  ;  next  most  commonly  to  Meckel's  divertic- 
ulum (the  remains  of  the  omphalo-mesenteric  duct)  which  springs 
from  the  ileum,  about  1^  feet  from  the  ileo-csecal  valve,  as  a  finger- 
like projection  3  to  10  inches  in  length,  the  free  end  of  which  may 
become  adherent  to  the  abdominal  wall  near  the  umbilicus  or  to  the 
mesentery.  Strangulation  may  also  occur  as  a  result  of  the  tip  of 
the  appendix  or  the  Fallopian  tube  becomiug  adherent ;  or  of  the 
existence  of  omental  and  mesenteric  slits,  or  peritoneal  openings  and 
pockets  (foramen  of  AVinslow,  duodeno-Jejunal  fossa) ;  or  a  peduncu- 
lated tumour ;  or  rupture  of  the  diaphragm  with  hernia.  Through 
any  of  the  rings,  slits,  or  openings  a  loop  of  intestine  may  slip  and 
become  strangulated. 

The  evidence  pointing  toward  strangulation  is,  the  age  of  the 
patient,  between  15  and  30  years  ;  the  sex,  predominating  in  males  ;  a 
previous  history  of  peritonitis  or  coeliotomy ;  early  faecal  vomiting ; 
and  usually  acuteness  of  obstruction.     A  palpable  tumour  is  rare. 

Intussusception. — A  portion  of  the  intestine,  because  of  irregular 
peristalsis,  becomes  invaginated  into  a  lower  portion,  the  invagina- 
tion increasing  downward.  In  most  cases — 75  per  cent — the  ileum 
enters  the  cascum  {ileo-ccecal)  or  the  colon  (ileo-coh'c)  ;  less  fre- 
quently the  ileum  (ileal)  or  the  colon  or  cascum  (colic)  enters  itself, 
or  the  colon  enters  the  rectum  (colico-rectal). 

In  intussusception  there  are  no  previous  symptoms  ;  the  patient 
is  usually  an  infant  or  child  (56  per  cent  of  all  cases  occurring  from 
the  4th  month  to  the  10th  year)  or  a  young  adult ;  the  onset  is 
acute ;  tenesmus,  mucous  and  bloody  stools  are  present ;  and  a  pal- 
pable sausage-shaped  tumour  is  generally  to  be  felt  (63  out  of  93 
cases)  in  the  right  iliac  or  umbilical  regions,  less  frequently  to  be 
palpated  by  the  rectum. 

Volvulus. — A  twist,  usually  axial  and  of  the  large  intestine  (87 
per  cent).  In  50  per  cent  it  is  in  the  sigmoid  flexure,  next  most 
commonly  (33  per  cent)  about  the  caecum. 

The  symptoms  are  not  distinctive  and  the  condition  is  seldom 
diagnosed.  There  is,  in  volvulus,  often  previous  constipation  and 
flatulence,  the  patient  is  rarely  under  40  years  of  age,  the  onset  is 
usually  acute,  the  abdomen  is  greatly  distended,  tender,  and  often 
rigid.     Because  of  the  frequent  occurrence  of  volvulus  at  the  sig- 


DISEASES  OF  THE  INTESTINES  793 

moid  flexure  the  injection  of  fluid  may  be  of  diagnostic  value  by 
pro^^ng  that  the  usual  amount  will  not  enter. 

Fcecal  Ohstriiction. — The  obstruction  is  usually  chronic.  There 
is  a  history  of  habitual  constipation,  becoming  progressively  more 
difficult  to  overcome  ;  the  patient  is  apt  to  be  a  woman,  probably  in 
middle  or  advanced  life ;  abdominal  pain,  meteorism,  nausea,  and 
faecal  vomiting  are  not  constant  and  appear  late  ;  and  faecal  masses, 
dull  on  percussion,  sometimes  indentable,  occasionally  tender,  can  be 
felt  along  the  distended  colon,  especially  in  the  caecum  and  sigmoid 
flexure,  and  by  rectum.  The  diagnosis  can  usually  be  made,  but  the 
possible  tunnelling  of  tlie  mass,  with  the  passage  of  fluid  stools,  is  to 
be  remembered.  If  the  impaction  is  in  the  rectum,  especially  in  old 
persons,  there  may  be  constant  tenesmus. 

Obstruction  iy  Gallstones. — A  large  concretion  which  has  ulcer- 
ated through  into  the  intestine  may  cause  obstruction.  It  may  be 
suspected  if  in  a  person  over  50  years  of  age  there  is  a  previous  his- 
tory of  hepatic  colic  with  or  without  jaundice ;  occasionally  a  hard 
movable  nodule  can  be  found  by  abdominal  palpation.  Pain  and 
vomiting,  usually  fgecal,  are  early  symptoms.  I  have  watched  the 
travels  of  a  palpable  gallstone  through  the  intestine,  causing  inter- 
mittent obstruction  as  it  lodged  transiently  from  time  to  time. 

Stricture  or  Tumour. — In  strictures  resulting  from  dysenteric, 
tuberculous,  syphilitic,  or  malignant  ulceration,  or  due  to  tumour, 
the  obstruction  is  chronic.  Abdominal  examination  may  reveal  a 
tumour,  and  rectal  exploration  a  stricture  or  tumour. 

Paresis  of  the  Intestine. — As  a  result  of  sepsis,  peritonitis,  or  de- 
fective innervation,  or  following  a  coeliotomy,  the  intestinal  muscu- 
laris  may  lose  its  motor  activity — a  condition  practically  equivalent 
to  obstruction.  The  history  is  of  service  in  its  recognition ;  the 
abdomen  is  uniformly  rounded,  smooth,  and  very  tympanitic,  and, 
most  important,  patient  auscultation  reveals  an  absence  of  the  usual 
sounds. 

The  presence  of  miscellaneous  and  rare  causes  of  obstruction, 
such  as  knots,  foreign  bodies  (masses  of  roundworms,  peanuts,  glass, 
stones,  false  teeth,  nails)  or  enteroliths  (deposition  of  salts  about 
bits  of  bone,  clumps  of  hair,  fruit  stones,  thread)  can,  as  a  rule,  only 
be  conjectured. 

(e)  Differential  Diagnosis. — Acute  intestinal  obstruction,  without 
reference  to  its  site  or  cause,  is  to  be  distinguished  from  the  follow- 
ing conditions : 

(1)  E.rternal  Hernia. — A  strangulated  external  hernia  (inguinal, 
femoral,  umbilical,  etc.)  must  be  excluded  as  a  cause  of  obstruction 
by  a  careful  examination  of  the  usual  sites  of  protrusion. 


Y94  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

(2)  Acute  Enteritis. — Severe  cases  of  this  disease  with  pain,  tym- 
pany, intestinal  paresis,  and  vomiting,  may  simulate  acute  obstruc- 
tion so  closely  that  in  certain  instances  a  differential  diagnosis  is 
impossible.  Ordinarily  the  presence  of  fever,  and  of  diarrhoea  with 
mucus  and  blood ;  and  the  absence  of  intractable  constipation, 
faecal  vomiting,  tumour,  or  marked  meteorism,  will  declare  against 
obstruction. 

(3)  Acute  Diffuse  Peritonitis. — Contrasting  peritonitis  with  ob- 
struction, there  is  in  the  former  an  initial  and  decided  rise  of  tem- 
perature ;  constant  and  general  abdominal  distention,  sometimes 
with  effusion ;  and  absence  of  tumour,  of  intestinal  sounds  on  aus- 
cultation, of  excessive  visible  peristalsis,  and  of  faecal  vomiting. 
Inquiry  may  reveal  some  of  the  antecedent  causes  of  peritonitis 
{q.  v.).  Nevertheless  time  is  often  requisite  for  a  diagnosis,  and 
mistakes  will  occur. 

(4)  Acute  hemorrhagic  pancreatitis  {q.  v.)  may  be  readily  mis- 
taken for  obstruction ;  hepatic  colic  may  be  eliminated  by  the  site  of 
the  pain  and  perhaps  the  appearance  of  jaundice  ;  reyial  colic  by  the 
site  and  radiation  of  the  pain,  and  the  presence  of  blood  in  the  urine. 

(/)  Prognosis. — This  is  always  grave,  particularly  in  acute 
obstruction.     It  is  more  favourable  in  fgecal  obstruction. 

XI.  Carcinoma  of  the  Intestine. — As  a  result  of  carcinom- 
atous or  other  tumour  of  the  bowel  the  lumen  of  the  intestine  is 
usually,  but  not  necessarily,  obstructed.  Carcinoma  occurs  more 
frequently  in  men,  particularly  after  50  years  of  age. 

The  growth  is  almost  invariably  found  in  the  large  intestine  (95 
per  cent  of  all  cases) ;  in  the  rectum  in  80  per  cent,  in  the  caecum  or 
colon  in  15  per  cent.  In  the  colon  it  involves  the  flexures — hepatic, 
splenic,  and  sigmoid — in  particular.  The  order  of  frequency  in 
various  parts  of  the  intestine  is,  rectum,  sigmoid  flexure,  transverse 
colon,  opening  of  the  common  bile  duct  (papilla  duodenalis),  ascend- 
ing colon,  lower  portion  of  ileum. 

(fl)  Symptoms. — The  early  symptoms  are  not  at  all  distinctive, 
consisting  merely  of  an  irregularity  of  the  bowels,  which  may  con- 
tinue for  a  long  time  before  the  growth  ulcerates  or  becomes  of  such 
a  size  and  character  as  to  cause  narrowing  or  palpable  tumour, 
although  an  associated  and  apparently  disproportionate  loss  of  flesh 
and  strength  is  suggestive  of  malignancy.  In  time  the  symptoms 
usually  become  those  of  chronic  obstruction  (page  790).  Marked  con- 
stipation exists,  sometimes  alternating  with  diarrhoea.  At  irregular 
intervals  there  may  be  attacks  of  colicky  pain  with  vomiting,  obsti- 
nate constipation,  and  moderate  abdominal  distention ;  or  beginning 
as  a  constant  localized  discomfort,  the  pain  may  become  colicky  and 


DISEASES  OF  THE  INTESTINES  Y95 

of  daily  occurrence,  especially  a  few  hours  after  eating,  and  there  is 
moderate  local  tenderness.  The  faeces  may  be  voided  in  pellets  or 
larger  scybalse,  or,  if  the  narrowing  is  low  down,  as  ribbon-shaped 
pieces.  The  presence  of  blood  or  bloody  mucus,  pus,  or  shreds  of 
tissue  (which  sometimes  show  a  carcinomatous  structure)  may  be 
taken  as  evidence  of  ulceration ;  when  this  occurs  there  may  be  a 
diarrhoea.  At  any  time  complete  obstruction  may  take  place  with 
severe  pain,  meteorism,  and  faecal  vomiting.  Important  symptoms 
are  anorexia,  emaciation,  and  progressive  pallor  and  yellowness  of 
the  skin,  indicative  of  the  cancerous  cachexia. 

If,  as  it  may  be,  the  growth  is  so  situated  that  it  does  not  cause 
stenosis  of  the  bowel,  the  obstructive  s)'mptoms  may  be  absent,  the 
cachexia  and  perhaps  the  finding  of  a  tumour  constituting  the  most 
significant  evidence. 

(b)  Duration,  Prognosis,  and  Complications. — Death  usually  occurs 
from  asthenia,  perhaps  with  pulmonary  oedema,  in  from  6  months  to 
1  year  (in  rare  instances  2  to  3  years)  after  the  discovery  of  tumour, 
ulceration,  or  obstruction.  Surgical  treatment,  however,  may  pro- 
long life,  and  in  cancer  of  the  rectum  some  excellent  results  have 
followed  removal. 

The  complications  are  hydronephrosis  and  renal  changes  from 
involvement  of  the  ureters ;  cancerous  peritonitis ;  perforation  of  the 
intestine  and  sequent  diffuse  peritonitis;  recto-vaginal  and  recto- 
vesical fistula ;  embolism  of  pulmonary  artery  from  a  thrombus  in 
an  iliac  vein ;  cellulitis ;  pyaemia ;  and,  rarely,  rupture  of  the  intes- 
tine from  distention  due  to  accumulated  faeces.  Secondary  deposits 
may  occur  in  the  liver  and  lungs,  less  commonly  in  more  distant 
parts  or  organs. 

(c)  Diagnosis. — (1)  Of  Carcinoma. — The  cardinal  symptoms  are 
the  age  of  the  patient  (over  50),  cachexia,  the  detection  of  a  tumour, 
and,  usually,  the  signs  of  chronic  obstruction.  All  malignant 
tumours  are  included  under  this  head.  As  a  benign  tumour  may 
give  rise  to  many  of  the  symptoms  mentioned,  exploratory  operation, 
or  the  progressively  downward  course  of  the  case,  or  the  appearance 
of  secondary  deposits,  may  afford  the  only  positive  evidence  of  malig- 
nancy. 

(2)  Of  I'fs  Site.— It  an  abdominal  tumour  has  been  found  and  is 
judged  to  be  malignant,  it  remains,  if  practicable,  to  determine  its 
site.  If  the  tumour  is  nodular  and  hard,  and  lies  near  the  junction 
of  the  epigastric  and  umbilical  regions,  and  there  is  obstinate  jaun- 
dice of  the  obstructive  type,  it  may  be  inferred  that  the  disease  is  in 
the  duodenum  and  involves  the  opening  of  the  common  bile  duct 
(rare) ;  if  without  jaundice  the  transverse  colon.     If  the  tumour  is 


796  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

low  in  the  right  iliac  region,  it  may  implicate  the  caecum ;  if  on  a 
level  with  the  umbilicus  and  to  the  right,  the  ascending  colon  or 
hepatic  flexure  ;  if  in  the  left  iliac  region  or  higher,  the  sigmoid  flex- 
ure, ascending  colon,  or  splenic  flexure.  Inflation  of  the  colon  with 
air,  or  distention  with  water,  may  serve  to  determine  the  height  of 
the  stenosis,  or  make  the  relation  of  the  tumour  to  the  colon  more 
distinct.  Carcinoma  of  the  rectum  is  often  mistaken  for  chronic 
dysentery,  because  of  the  pain,  tenesmus,  and  voiding  of  foetid  mu- 
cous and  bloody  stools,  but  a  digital  examination  will  reveal  an 
ulcerated  mass  or  annular  hard  infiltration. 

{d)  Differential  Diagnosis. — Certain  conditions  may  be  mistaken 
for  carcinoma  intestinalis.  The  differentiation  must  be  made  by  the 
presence  of  the  signs  and  symptoms  Just  described,  a  consideration 
of  the  characteristics  of  the  possible  confusing  ailments,  and,  in  not 
a  few  cases,  by  exploratory  operation,  a  procedure  which  will  not  add 
to  the  gravity  of  carcinoma  and  in  other  cases  may  result  in  recov- 
ery. These  conditions  are :  Faecal  impaction,  which  may  also  co- 
exist with  cancerous  stenosis ;  the  tumour  of  intussusception  ;  pyloric 
tumour ;  cancer  of  the  head  of  the  pancreas,  which  is  immovable  and 
deep-seated ;  distended  or  carcinomatous  gall  bladder,  or  "  lacing  '* 
liver ;  movable  or  enlarged  kidney,  and  chronic  appendicitis. 

XII.  Dilatation  of  the  Colon. — This  may  occur  as  a  result 
of  obstruction  (tumour,  volvulus)  in  some  part  of  the  colon ;  as  an 
acute  condition  due  to  twisting  of  the  meso-colon,  or  acute  and  tem- 
porary from  gaseous  distention  ;  as  a  consequence  of  habitual  consti- 
pation and  coprostasis ;  or  it  may  be  idiopathic,  due  perhaps  to  a  low- 
down  congenital  narrowing  of  the  colon.  The.  symjjtoms  are  usually 
those  of  obstinate  or  habitual  constipation,  often  with  extreme  ab- 
dominal distention  and  meteorism,  which  may  be  sufiicient  to  cause 
upward  displacement  of  the  liver,  spleen,  diaphragm,  heart,  and  hmgs^ 

XIII.  Diseases  of  the  Mesentery. — The  diseases  of  clinical 
interest  are  cysts  and  infarctions. 

(a)  Mesenteric  Cysts. — These  may  be  chylous,  dermoid,  hydatid,, 
serous,  or  sanguineous ;  of  varying  size,  in  rare  instances  filling  the 
abdomen;  and  frequently  becoming  adherent  to  the  liver,  spleen, 
sigmoid  flexure,  and  uterus.  The  symptoms  are  those  of  a  steadily 
growing  abdominal  tumour,  usually  in  the  epigastric  region,  occa- 
sionally with  colicky  pain  and  constipation.  The  diagiiosis,  usually 
made  at  autopsy,  is  extremely  doubtful,  and  may  be  suggested  by  the 
chronic  course  (10  to  20  years),  the  tympanitic  note  due  to  the  pres- 
ence of  intestine  over  the  growth,  and  the  situation  of  the  tumour 
in  the  middle  line.  Commonly  it  is  supposed  to  be  an  ovarian 
tumour,  or  an  omental  or  hydronephrotic  cyst,  or  a  movable  kidney. 


DISEASES  OP  THE  INTESTINES  797 

(b)  Intestinal  Infarction. — The  superior  mesenteric  artery  may  be 
occluded  by  emboli  or  thrombi  derived  from  diseased  heart  valves  or 
aneurism  of  the  abdominal  aorta,  with  resulting  hemorrhagic  infarc- 
tion of  a  portion  of  the  jejunum  or  ileum.  The  symptoms  comprise 
violent  and  colicky  abdominal  pain;  diarrhoea,  perhaps  with  blood- 
stained stools ;  vomiting,  which  may  be  faecal ;  and  abdominal  dis- 
tention. As  the  clinical  picture  is  almost  exactly  that  of  acute 
obstruction,  a  diagnosis  is  rarely  possible  prior  to  operation,  unless 
the  presence  of  the  causative  conditions  may  suggest  the  true  nature 
of  the  case. 

XI Y.  Intestinal  Neuroses. — These  may  be  motor,  sensory,  or 
secretory. 

(1)  Motor  Xeuroses.— (1)  Nervous  Constipation. — In  neurasthe- 
nia, hysteria,  and  various  forms  of  nervous  disease,  constipation,  often 
associated  with  slow  or  sudden  gaseous  distention,  is  due  to  deficient 
innervation  and  muscular  atony  of  the  intestinal  muscularis.  Paral- 
ysis of  the  voluntary  control  of  the  sphincter  ani,  the  act  of  defeca- 
tion becoming  reflex  and  involuntary,  is  met  with  not  only  as  a 
result  of  organic  or  functional  central  nervous  disease,  but  also  of 
local  inflammatory  processes. 

(2)  Nervous  Diarrhoea.  —  This  occurs  mainly  in  neurasthenic, 
hysterical,  or  "  nervous  "  persons,  and  is  due  to  an  unusual  irrita- 
bility of  the  motor  nerves  of  the  intestine,  which  results  in  exces- 
sive peristalsis.  In  such  persons  anxiety,  worry,  fright,  or  any  strong 
emotion  will  produce  or  aggravate  a  diarrhoea.  It  may  also  occur 
as  a  symptom  of  organic  disease  of  the  nervous  system,  especially 
tabes. 

The  stools  are  soft  or  watery  and  do  not  contain  blood  or  mucus 
(except  in  mucous  colic),  and  vary  from  2  to  20  per  day.  Charac- 
teristically, the  diarrhcea  may  occur  only  in  the  morning  (morning 
diarrhoea,  Delafield),  may  come  suddenly  and  after  lasting  several 
days  suddenly  stop,  or  the  condition  may  persist  continuously  for 
months  or  years.  Aside  from  the  nervous  symptoms  the  general 
health  may  remain  good.  Inflammatory  or  other  organic  disease  of 
the  intestine  must  be  excluded  before  this  diagnosis  is  made. 

(3)  Enterospasm. — Excessive  contraction  of  the  muscular  fibres 
of  the  intestine  is  usually  associated  with  enteralgia  (page  798),  but 
may  exist  without  pain.  It  may  produce  transient  severe  constipa- 
tion or  even  obstruction,  but  this  diagnosis  can  seldom  be  made 
because  of  the  extreme  difficulty  in  positively  excluding  the  organic 
and  other  causes  of  constipation  or  stenosis.  Spasm  of  the  rectum 
and  sphincter  (proctospasm)  is  not  uncommon  as  a  neurasthenic  or 
hysterical  neurosis,  or  as  a  symptom  of  hemorrhoids  or  anal  fissure. 


798  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

It  is  usually  discovered  on  attempting  a  digital  examination  of  the 
rectum,  but  may  be  responsible  for  ribbon-shaped  stools. 

(II)  Sexsory  Xeueoses. — These  comprise  enteralgia,  neuralgia 
of  the  rectum,  and  diminished  intestinal  sensihiliiy. 

(1)  Enteralgia. — Neuralgia  of  the  intestines,  which,  when  asso- 
ciated with  spasm  of  the  muscularis,  is  termed  intestinal  colic,  may 
be  a  pure  or  a  reflex  neurosis,  or  may  be  symptomatic  of  organic  dis- 
ease. As  a  neurosis  it  occurs  particularly  in  anaemic,  neurasthenic, 
or  hypochondriacal  persons,  because  of  the  increased  sensibility  of  the 
sensory  nerves,  and  may  be  excited  by  sudden,  especially  unpleasant, 
emotions.  As  a  reflex  neurosis  it  arises  from  exposure  to  cold,  or 
from  gout ;  from  foreign  bodies  and  the  irritation  of  worms,  accumu- 
lated faeces,  enteroliths,  indigestible  food,  or  an  excessive  amount  of 
gas  (flatulent  colic)  in  the  intestine.  As  a  symptom  of  organic  dis- 
ease it  occurs  in  locomotor  ataxia  ( "  crisis  ") ;  in  lead-poisoning,  prob- 
ably by  direct  action  of  the  toxic  agent  upon  the  nerves ;  and  in 
various  abdominal  diseases,  such  as  intestinal  obstruction,  appendici- 
tis, peritonitis,  enteritis,  and  the  like. 

The  symptoms  comprise  pain,  usually  diffuse,  sometimes  localized, 
which  may  be  extremely  severe.  It  is  often,  but  not  always,  of  sud- 
den onset,  may  be  relieved  by  pressure  or  forward  doubling  of  the 
body,  and  commonly  lasts  for  a  few  hours,  rarely  days,  and  may  ter- 
minate gradually  or  suddenly.  There  is  often  a  free  discharge  of 
flatus,  after  which  the  attack  tends  to  subside.  Kecurrences  at  vary- 
ing intervals  are  common.  In  the  diagnosis  of  a  neurotic  or  reflex 
enteralgia  it  is  necessary  to  exclude  the  colicky  pain  which  is  symp- 
tomatic of  inflammatory  abdominal  disease  by  the  absence  of  fever 
and  the  relief  afforded  by  pressure  ;  lead  colic  and  tabes  by  the  asso- 
ciated symptoms.  It  is  usually  easy  to  separate  enteralgia  from 
renal  or  hepatic  colic  and  rheumatism  of  the  abdominal  walls.  As  a 
matter  of  fact,  a  purely  neurotic  enteralgia  is  not  common. 

(2)  Rectal  or  Pubic  Neuralgia. — This  occurs  in  neurasthenic,  hys- 
terical, or  tabic  individuals,  sometimes  in  connection  with  hemor- 
rhoids. There  is  an  undue  sensibility  of  the  hemorrhoidal  plexus  of 
nerves,  manifested  by  a  feeling  of  pain  or  discomfort  in  the  pubic 
region,  sacrum,  and  perinaeum,  often  extending  to  the  thighs,  with 
an  aching  tenesmic  desire  to  evacuate  the  rectum,  although  the  lat- 
ter may  be  empty. 

(3)  Dimlnislied  Intestinal  Sensibility. — There  may  be  anaesthesia 
of  the  intestine,  so  that  the  normal  indication  of  the  need  of  defeca- 
tion is  absent  and  constipation  ensues.  It  is  a  common  symptom  of 
the  spinal  paralyses.  Unless  motor  paralysis  is  present  purposive 
defecation  still  takes  place. 


DISEASES   OF  THE   INTESTINES  799 

(III)  Secretory  Xeuroses. — Mucous  Colic— The  only  clinically 
interesting  secretory  intestinal  neurosis  is  the  mucous  neurosis  (mem- 
branous enteritis,  mucous  colic)  affecting  the  follicles  of  the  colon. 
It  is  properly  considered  to  be  one  of  the  manifestations  of  hysteria, 
neurasthenia,  or  the  neuropathic  constitution.  The  great  majority 
of  cases  occur  in  women,  and  it  is  most  frequent  between  the  30th 
and  40th  years,  but  has  been  observed  in  children  of  from  3  to  12 
years  of  age. 

(a)  Si/mptoms. — The  disease  generally  begins  in  a  subacute  man- 
ner. Whether  its  onset  is  acute  or  subacute,  its  subsequent  course 
is  chronic.  There  are  more  or  less  persistent  symptoms  of  gastro- 
intestinal derangement,  which  differ  little  from  those  of  ordinary 
occurrence.  The  characteristic  events  are  the  painful  paroxysmal 
passage  of  membrane  and  a  peculiar  train  of  phenomena  referable  to 
the  nervous  system.  The  paroxysms  may  occur  daily,  or  at  intervals 
of  a  month,  or  at  any  intermediate  period.  The  pain  begins  lightly, 
is  referred  to  the  lower  abdomen,  increases  in  severity,  reaches  its 
acme,  and  in  many  cases  is  relieved  by  the  passage  of  membrane, 
after  which  it  gradually  declines.  The  paroxysms  may  last  for  a  day 
or  a  week.  The  pain  itself  is  colicky,  tenesmic,  and  of  a  peculiarly 
sickening  character,  producing  a  facies  like  that  which  accompanies 
jjressure  on  a  tender  ovary.  There  is  almost  invariable  abdominal 
tenderness,  sometimes  so  great  and  general  as  to  simulate  perito- 
nitis. It  is  usually  circumscribed  in  either  iliac  fossa,  especially  the 
left.  This  abdominal  tenderness  may  be  persistent  in  varying  degrees 
during  the  continuance  of  the  disease.  There  may  be  vesical  and 
uterine  tenesmus,  and  mucous  discharges  from  these  organs.  The 
membranes  may  be  shreddy,  ribbon-shaped,  cordlike,  or  may  consti- 
tute perfect  cylindrical  casts  of  the  intestine.  The  quantity  ranges 
from  a  very  small  amount  up  to  three  kilogrammes  in  one  parox- 
ysm. It  may  be  passed  with  faecal  matter  or  alone.  By  stirring  and 
decantation  with  water  separation  is  readily  effected.  Chemically 
the  membrane  is  composed  of  dense  transformed  mucus  (Osler). 
The  temperature  is  always  normal  or  subnormal.  The  general  nutri- 
tion usually,  but  not  invariably,  suffers.  Emaciation,  anaemia,  and 
loss  of  strength  may  occur  in  varying  degrees.  Diarrhoea  and  con- 
stipation, hemorrhoids,  rectal  prolapse,  jaundice,  polydipsia,  aphthous 
stomatitis,  and  furuncles  may  coexist  with  the  disease. 

The  nervous  phenomena  are  peculiar  and  striking  in  the  extreme. 
Some  of  these  are  practically  of  invariable  occurrence  in  this  disease. 
Among  them  are  hysteria  and  hysterical  stigmata  of  all  kinds :  hys- 
terical coma,  convulsions,  and  aphasia  ;  neurasthenia,  vertigo,  attacks 
of  blue  nails  and  lips,  tingling  and  numbness  of  hands  and  feet, 


800  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

acute  neuralgias  of  all  parts  of  the  body,  pain  in  the  external  ear^ 
tender  scalp,  tinnitus  aurium,  liyperaesthesia,  paraesthesia,  anaesthe- 
sia, temporary  defects  of  vision,  morbid  alterations  of  taste,  irregular 
muscular  tremors,  paresis,  paralyses,  chorea,  catalepsy,  amnesic  apha- 
sia, mental  depression,  poor  memory,  hypochondriasis,  and  melan- 
cholia. Many  if  not  all  of  these  are  transient  and,  in  the  absence  of 
definitely  ascertained  lesions,  largely  functional  in  character.  Finally, 
to  these  may  be  added  the  peculiar  paroxysmal  pain  and  tenderness. 
When  occurring  in  children  it  is  found,  after  eliminating  simple 
intestinal  catarrh,  that  the  subjects  are  from  parents  whose  nervous 
systems  are  diseased,  or  who  have  suffered  from  convulsions,  hys- 
teria, neuralgia,  rheumatism,  or  insanity.  The  children  themselves 
have  shown  convulsions,  passionateness,  morbid  timidity,  chorea,  or 
rheumatism  (Edwards), 

(b)  Diagnosis. — I  am  persuaded  that  the  existence  of  this  disease 
is  not  infrequently  overlooked.  Da  Costa's  rule  is  good  and  prac- 
tical— to  suspect  this  disease  "  in  every  case  of  anomalous  nervous 
symptoms,  particularly  hysterical,  in  which  there  is  abdominal  pain." 
.Membrane,  if  found,  must  be  discriminated  from  ascaris  lumbricoides 
and  the  varieties  of  tasuia,  fatty  discharges,  undigested  portions  of 
vegetable  food,  arteries,  ligaments,  fibrous  and  elastic  tissues  of  meat, 
sausage  skins,  necrosed  mucous  membrane,  fibrinous  and  diphtheritic 
shreds,  and  anal  fissure  with  hypersecretion. 

(c)  Prognosis. — The  outlook  for  permanent  recovery  is  not  good. 
Nevertheless,  the  prognosis,  with  appropriate  and  judicious  treat- 
ment, is  not  so  gloomy  as  it  is  usually  stated  to  be. 

IX.    DISEASES    OF    THE    LIVER,    GALL   BLADDER,  AND 

BILE   DUCTS 

{See  Jaundice,  pages  78  to  81;  and  Physical  Examination  of  the  Liver,  pages 

461  to  470) 

I.  Abnormal  Form. — Aside  from  the  alterations  in  shape 
which  are  caused  by  disease  of  the  organ  or  by  deformities  or  tumour 
of  the  ribs,  the  only  malformation  of  clinical  interest  is  the  "  lacing  " 
or  "  corset  "  liver.  In  this  the  anterior  portion  of  the  right  lobe  is 
divided  from  the  body  of  the  organ  by  a  transverse  groove  made  by 
the  ribs,  the  tongue  or  lappet  of  liver  extending  down  to  or  even 
below  the  horizontal  umbilical  line.  In  rare  cases  the  laced-off  por- 
tion may  be  connected  with  the  liver  simply  by  a  thin  membranous 
isthmus  or  band. 

Subjective  symptoms  are  usually  absent,  but  there  may  be  sensa- 
tions of  weight  and  pressure  ;  rarely  swelling  and  pain  in  the  lappet 


DISEASES  OF  LIVER  AND  BILE  PASSAGES  801 

as  a  consequence  of  interference  with  the  venous  outflow.  The  diag- 
nosis is  important  mainly  because  of  the  likelihood  of  mistaking  the 
separated  portion  for  amyloid  disease,  passive  congestion,  or  tumour 
of  the  liver,  abdominal  tumour,  or  movable  kidney.  The  difficulty 
in  discrimination  is  increased  when  the  lappet  is  swollen,  or  the 
uniting  band  is  thin,  or  the  transverse  furrow  is  so  deep  as  to  permit 
the  colon  or  a  loop  of  small  intestine  to  lie  in  it,  thus  causing  a  line 
of  tympanitic  percussion  between  the  isolated  lappet  and  the  liver 
and  giving  an  impression  that  the  two  are  entirely  separate.  The 
lappet,  however,  usually  moves  with  respiration,  and  as  a  rule  its 
edge  is  found  by  careful  palpation  to  be  continuous  with  the  left 
lobe  of  the  liver. 

II.  Abnormal  Position. — The  various  causes  of  a  misplaced 
liver  have  been  described  (page  468).  Brief  reference  is  here  made  to 
the  movable  or  floating  liver — a  rare  condition.  It  occurs  mainly  in 
middle-aged  or  elderly  women  with  relaxed  abdominal  walls.  There 
may  be  a  sense  of  weight  and  dragging,  with  referred  discomfort  or 
pain  in  the  right  shoulder.  The  condition  is  to  be  diagnosed  by 
finding  the  normal  liver  dulness  absent ;  the  liver,  recognised  by  its 
shape  and  notch,  prolapsed  ;  and  the  practicability  of  replacing  the 
•organ  in  its  normal  site  by  position  or  manipulation. 

III.  Acute  Catarrh  of  the  Bile  Ducts.— A  simple  angio- 
cholitis  not  caused  by  gallstones.  It  is  in  the  great  majority  of 
cases  an  extension  of  a  gastro-duodenitis  (page  777)  to  the  intestinal 
portion  of  the  common  duct. 

(«)  Causes. — It  may  arise  from  dietetic  errors  (most  common), 
•exposure  to  cold,  mental  or  physical  fatigue,  malaria,  influenza,  pneu- 
monia, typhoid  fever,  the  passive  congestion  of  chronic  valvular  dis- 
ease, and  chronic  nephritis.  It  may  be  epidemic.  As  a  rule  it 
-occurs  in  young  persons  as  a  result  of  indigestion. 

{h)  Symptoms.— OccsLSvonoWy  icterus  is  the  only  symptom  present. 
Ordinarily  there  is  anorexia ;  moderate  nausea  and  vomiting,  which 
may  persist  for  3  or  4  days  ;  mild  epigastric  or  right  hypochondriac 
tenderness  ;  constipation,  seldom  diarrhaa ;  fever,  if  present  at  all,  is 
moderate  (101°  to  102°)  ;  and  often  slight  swelling  of  the  liver  and 
perhaps  of  the  spleen.  The  gall  bladder  is  usually  not  palpable. 
The  pulse  and  respiration  are  either  normal  or,  as  happens,  may  be 
much  diminished  in  frequency.  Pruritus  is  not  so  common  as  in 
the  grave  form  of  jaundice  due  to  chronic  obstruction.  The  other 
signs  of  icterus  simplex  (page  80)  are  present.  The  onset  may  be 
with  chill,  headache,  and  severe  vomiting,  especially  in  the  epidemic 
variety.  The  disease  usually  lasts  from  4  to  8  weeks,  seldom  but  2 
■weeks  or  as  long  as  3  months. 


802  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

(c)  Diagnosis. — The  cardinal  symptom  is  jaundice  of  a  moderate 
grade  occurring  in  previously  healthy  young  persons,  without  pain 
and  with  or  without  digestive  disturbances.  The  form  due  to  infec- 
tious diseases,  nephritis,  or  cardiac  disease  is,  of  course,  preceded  and 
accompanied  by  the  symptoms  of  the  causative  illness.  If  the  icterus 
persists  longer  than  3  months  it  may  be  suspected  to  be  due  to  a 
graver  ailment  than  simple  acute  catarrhal  inflammation,  and  the 
patient  should  be  watched  and  examined  with  reference  to  progress- 
ive emaciation,  or  the  evidences  of  impacted  gallstones,  cirrhosis,  or 
carcinoma. 

IV.  Chronic  Catarrh  of  the  Bile  Ducts. — Catarrhal  cholan- 
gitis occurs  in  obstruction  of  the  common  duct,  usually  by  gall- 
stones, less  commonly  by  malignant  disease,  stricture,  or  outside 
pressure.     Osier  recognises  two  groups  : 

{a)  Complete  obstruction  of  the  common  duct,  the  patient  pre- 
senting chronic  and  intense  jaundice  without  fever.  A  history  of 
previous  attacks  of  hepatic  colic  and  slight  or  absent  enlargement  of 
the  gall  bladder  point  toward  obstruction  by  gallstones  rather  than 
by  a  neoplasm. 

{h)  Incomplete  obstruction  of  the  common  duct,  when  due  to  gall- 
stones, presents  recurrent  paroxysms  of  pain,  accompanied  by  chill, 
fever  (103°  to  105°),  and  sweats,  the  hepatic  intermittent  fever  of 
Charcot.  The  chills,  which  are  separated  by  an  apyrexial  interval, 
may  be  very  severe  and  in  their  periodicity  resemble  quotidian,  tertian, 
or  quartan  ague.  Jaundice  may  be  intense  and  persistent,  or  varying 
and  intermittent,  according  to  the  degree  of  obstruction  or  the  ball- 
valve  action  of  the  stone,  and  usually  intensifies  after  each  paroxysm. 
The  attack  may  be  accompanied  by  nausea  and  vomiting.  Bile  may 
be  found  in  the  stools  from  time  to  time ;  the  liver  and  gall  bladder 
are  slightly  or  not  at  all  enlarged;  and  ascites  is  absent.  Steady 
failure  of  the  health  is  not  common.  Each  series  of  attacks  may 
continue  for  days  or  weeks,  and  there  may  be  a  recurrence  of 
a  series  at  varying  intervals,  covering  a  period  of  3  or  4  years. 
Eecovery  may  occur.  It  is  probable  that  the  repeated  attacks 
take  place  especially  when  there  is  a  "ball -valve"  stone  in  the 
ampulla  of  Vater,  the  dilatation  in  the  wall  of  the  duodenum  into 
which  the  common  duct  empties.  The  condition  is  doubtless  due 
to  repeated  infection  by  micro-organisms  contained  in  the  bile^ 
the  infective  process  not  being  sufficiently  intense  to  cause  suppu- 
rative inflammation  (see  V  following),  but  the  latter  may  occur  as 
a  sequel. 

The  diagnosis  requires  the  exclusion  of  malaria  by  the  blood  ex- 
amination.    As   previously  stated,   the   presence   of   a  dilated   gall 


DISEASES   OP  THE  BILE  PASSAGES  803 

bladder  indicates  occlusion  from  other  causes  than  an  impacted  gall- 
stone in  the  common  duct. 

V.  Suppurative  Inflammation  of  the  Bile  Ducts.— Sup- 
purative cholangitis  of  both  larger  and  smaller  ducts  is  usually  due 
to  gallstones,  occasionally  to  cancer  of  the  duct,  worms,  foreign 
bodies,  or  extension  from  suppurative  pylephlebitis.  The  symptoms 
are  frequent  paroxysms  such  as  described  in  IV  preceding,  except 
that  the  fever  is  septic  and  remittent  rather  than  intermittent; 
jaundice,  mild,  or  not  severe;  a  swollen  and  tender  liver  and  a 
moderately  enlarged  gall  bladder ;  leucocytosis ;  progressive  loss  of 
strength,  and  emaciation.  Pain  may  be  slight.  The  general  symp- 
toms assume  a  rapid  septic  or  pygemic  type,  and  death  is  inevitable. 

VI.  Icterus  Neonatorum. — There  are  two  forms,  physiological 
and  pathological. 

(«)  Mild  or  physiological  icterus  occurs  in  about  one  third  of  the 
newborn.  The  skin  and  conjunctivae  are  yellow,  but,  as  a  rule,  the 
urine  does  not  contain  bile,  and  the  faeces  are  of  normal  colour.  It 
disappears  in  from  4  to  14  days. 

{h)  Severe  or  pathological  icterus  may  be  due  to  congenital  oblit- 
eration or  absence  of  the  common  or  hepatic  duct,  syphilitic  hep- 
atitis, or  a  septic  phlebitis  of  the  umbilical  vein.  The  jaundice  is 
marked,  the  urine  bile-stained,  the  stools  clay  coloured,  and  hemor- 
rhages from  the  cord  may  occur.     It  is  an  often  fatal  disease. 

VII.  Stenosis  and  Obstruction  of  the  Bile  Ducts. — Aside 
from  obstruction  by  gallstones,  the  common  duct  may  become 
occluded  from  ulceration  and  adhesion  (rare)  due  to  the  previous 
passage  of  a  calculus ;  or  the  presence  of  parasites  (lumbricoid 
worms,  echinococcus,  distoma  hepaticum)  or  foreign  bodies  (seeds) 
in  the  duct.  It  may  also  be  occluded  by  pressure  from  outside  by 
carcinoma  of  the  pylorus  or  pancreas ;  abdominal  tumours  or  aneurism ; 
enlarged  glands  in  the  hepatic  fissure  secondary  to  malignant  disease 
of  the  stomach  or  other  abdominal  viscera;  and  cicatricial  contrac- 
tion due  to  perihepatitis,  syphilis  of  the  liver,  or  ulcer  of  the  duo- 
denum. 

The  syynjJtoms  are  practically  those  of  a  chronic  obstructive 
jaundice  (pages  79  and  80).  The  icterus  varies  in  intensity,  but  usu- 
ally increases ;  the  liver  is  enlarged,  except  in  cases  of  long  standing, 
when  it  becomes  somewhat  cirrhotic  and  shrunken ;  the  gall  bladder 
is  enlarged  if  the  common  duct  is  obstructed,  except  in  the  case  of 
gallstones ;  there  is  hepatic  and  referred  right-shoulder  pain ;  and 
hepatic  fever— chill,  fever,  and  sweat,  with  gastric  disturbances — 
especially  if  the  obstruction  is  due  to  calculus. 

The  diagnosis  as  to  the  exact  cause  of  the  obstruction  is  often 


804  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

extremely  difficult.  It  depends  on  a  careful  study  of  the  symptoms 
{q.  V.)  of  each  of  the  possible  causative  conditions,  especially  gall- 
stones ;  carcinoma  of  the  head  of  the  pancreas,  or  of  the  pylorus,  or 
the  hepatic  lymph  glands,  perhaps  secondary  to  malignant  disease  of 
the  breast,  stomach,  rectum,  colon,  or  pelvic  organs,  not  omitting  an 
examination  of  the  clavicular  and  other  glands  for  confirmatory  evi- 
dence ;  and  abdominal  tumour  or  aneurism. 

VIII.  Acute  Infectious  Inflammation  of  the  Gall  Blad- 
der.— Acute  cholecystitis  is  due  to  infection  by  a  variety  of  micro- 
organisms, most  commonly  the  Bacillus  coU  communis,  Bacillus 
typhosus,  Pneumococcus,  Staphylococcus,  and  Streptococcus. 

While  it  is  usually  associated  with  the  presence  of  gallstones,  it 
is  not  so  generally  recognised  that  infection  may  take  place  without 
cholelithiasis.  One  may  recognise  then  a  calculous,  and  a  non-calcu- 
lous  or  idiopathic,  form.  The  inflammation  may  be  catarrhal,  suppu- 
rative (empyema  of  the  gall  bladder),  or  phlegmonous ;  resulting,  in 
the  severer  forms,  in  gangrene,  perforation,  localized  peritonitis  and 
abscess,  or  a  general  peritonitis. 

{a)  Symptoms. — Acute  paroxysmal  pain  usually  in  the  right  hypo- 
chondrium,  less  commonly  in  the  epigastrium  or  right  iliac  (appen- 
dical)  region,  is  the  earliest  evidence  of  the  disease.  It  is  shortly 
followed  by  nausea,  vomiting,  abdominal  distention,  rigidity,  and 
tenderness.  The  tenderness  is  at  first  diffused,  becoming  localized, 
but  not  always  over  the  site  of  the  gall  bladder.  Prostration  is 
usually  well  marked  or  severe.  There  may  be  obstinate  constipation 
or  even  an  apparently  complete  intestinal  obstruction,  neither  flatus 
nor  faeces  passing.  In  the  form  due  to  gallstones,  jaundice  is  com- 
mon ;  in  the  non-calculous  variety  it  is  seldom  present.  There  may 
be  comparatively  mild  and  recurring  attacks  of  acute  cholecystitis 
without  the  presence  of  gallstones. 

{h)  Diagnosis. — In  the  form  due  to  calculi  there  is  usually  a  his- 
tory of  hepatic  colic,  followed  by  jaundice  in  a  certain  proportion  of 
cases ;  in  the  non-calculous  variety,  the  fact  that  the  patient  is  con- 
valescing from  pneumonia  or  typhoid  fever,  or  has  had  previous 
symptoms  referable  to  the  gall  bladder,  is  very  suggestive. 

The  diagnosis  is  often  extremely  difficult.  The  symptoms  may 
exactly  simulate  those  of  appendicitis  or  acute  intestinal  obstruction, 
as  the  local  pain  and  tenderness  may  be  elsewhere  than  over  the  gall 
bladder.  The  finding  of  a  distended  gall  bladder  and  the  presence 
of  jaundice,  together  with  a  suggestive  history,  constitute  the  most 
distinctive  evidence  of  cholecystitis.  In  a  certain  proportion  of  cases 
exploratory  operation  will  be  required  to  settle  the  question. 

Extremely  severe  symptoms,  with  evidences  of  local  or  general 


DISEASES  OF  THE  BILE  PASSAGES  805 

peritonitis,  point  to  a  suppurative,  phlegmonous,  or  gangrenous 
cholecystitis,  perhaps  with  perforation  of  the  gall  bladder ;  but  such 
cases,  which  are  fatal  without  surgical  aid,  may  be  attended  by  de- 
ceptively mild  manifestations. 

IX.  Carcinoma  of  the  Gall  Bladder. — This  may  be  primary, 
and,  if  so,  is  associated  with  gallstones  in  about  90  per  cent  of  all 
cases ;  or  secondary  to  disease  in  the  liver  or  neighbouring  organs. 
It  usually  starts  in  the  fundus  of  the  bladder. 

The  symptoms  are  chronic  jaundice,  occurring  in  about  70  per 
cent  of  the  cases ;  persistent  pain  and  tenderness,  subject  to  severe 
exacerbations ;  occasionally  vomiting,  haematemesis,  melaena,  ascites, 
and  fever ;  in  about  two  thirds  of  the  cases  the  presence  of  a  firm, 
tender,  and  uneven  tumour,  which,  unless  adherent,  moves  with  respi- 
ration, and  extends  downward  and  toward  the  umbilicus  from  the 
usual  site  of  the  gall  bladder ;  and  the  development  of  cachexia. 

Carcinoma  may  be  primary  in  the  ducts,  especially  the  common 
duct,  but  this  is  not  common.  There  is  severe  jaundice  and  enlarge- 
ment of  the  gall  bladder,  but  the  diagnosis  is  rarely  made  except  by 
exploratory  operation. 

X.  Gallstones. — Cholelithiasis  occurs  mainly  in  women  (75 
per  cent),  especially  those  who  have  borne  children.  The  patient  is 
usually  between  40  and  60,  rarely  under  35,  years  of  age.  Other 
predisposing  causes  are  excessive  eating,  sedentary  occupation,  con- 
stipation, tight  lacing,  enteroptosis,  and  nephroptosis.  While  small 
concretions  may  form  in  the  liver  itself,  the  great  majority  of  gall- 
stones which  cause  symptoms  originate  in  the  gall  bladder. 

Calculi  may,  and  usually  do,  remain  in  the  gall  bladder  for  an 
indefinite  period  without  giving  rise  to  symptoms.  If  a  calculus 
leaves  the  gall  bladder  and  enters  the  ducts,  the  symptoms  of  hepatic 
colic  usually  arise  ;  if  it  becomes  permanently  impacted  in  the  cystic 
or  common  duct,  the  evidences  of  chronic  obstruction  appear.  Sub- 
sequently ulceration  and  perforation  may  occur  with  the  formation 
of  a  biliary  fistula,  or  the  calculus  may  ulcerate  through  into  the 
intestine  and,  if  of  sufficient  size,  cause  intestinal  obstruction.  The 
symptoms  of  these  various  events  are  as  follows : 

(I)  Hepatic  Colic— («)  Symptoms.— The  attack  is  sudden,  with 
excruciating  cutting  pain,  usually  localized  in  the  right  hypochon- 
drium,  whence  it  may  spread  over  the  abdomen  and  lower  thorax, 
and  in  some  cases  be  referred  to  the  right  shoulder  and  arm.  There 
are  often  vomiting,  drenching  sweats,  a  feeble  and  rapid  pulse,  and 
occasionally  syncope.  Rather  frequently  there  is  a  chill  with  fever 
(101°  to  103"=).  The  liver  may  become  enlarged  and  noticeably  ten- 
der, the  gall  bladder  swollen,  tender,  and  palpable,  and  the  spleen 
53 


806  DIAGNOSIS,   DIRECT   AND  DIFFERENTIAL 

also  may  swell  moderately.  Jaundice  appears  in  about  one  half  of 
the  cases,  usually  within  24  hours  after  the  beginning  of  the  attack 
and  while  the  stone  is  passing  through  the  common  duct.  Ordi- 
narily it  is  slight  and  of  brief  duration,  but  may  be  either  absent  or 
intense,  depending  respectively  on  the  freedom  of  the  passage  or  the 
degree  of  temporary  impaction  of  the  stone.  The  urine  may  contain 
bile  pigment  and  albumin.  Palpitation,  praecordial  oppression,  and 
an  acute  mitral  murmur  have  been  noted. 

The  duration  of  the  attack  is  variable,  lasting  from  a  few  hours 
to  a  week,  or  even  longer,  with  remissions  and  exacerbations,  until 
the  stone  is  finally  expelled.  Possible  but  rare  accidents  are  con- 
vulsions, fatal  syncope,  and  rupture  of  the  duct  followed  by  a  lethal 
peritonitis. 

{h)  Differential  Diagnosis. — If  colic  of  the  type  just  described, 
and  jaundice,  even  if  but  a  trace,  are  present,  the  diagnosis  is  prac- 
tically certain.  A  history  of  previous  attacks  is  very  suggestive.  If 
the  character  and  location  of  the  pain  are  not  distinctive  and  icterus 
is  absent,  a  positive  diagnosis  may  be  extremely  difl&cult.  It  is  of 
great  diagnostic  importance  to  examine  the  stools  for  several  days 
after  the  attack,  in  order,  by  finding  the  stone,  to  confirm  beyond 
doubt  the  nature  of  the  attack.  The  stool  is  placed  in  a  fine-meshed 
sieve  and  water  allowed  to  run  through  until  the  soluble  portions 
have  been  washed  away.  It  is  to  be  discriminated  from  the  follow- 
ing diseases : 

(1)  Acute  Non-calculous  Cholecystitis. — The  symptoms  of  this 
disease  (page  804)  are  so  similar  to  those  of  hepatic  colic  that  in  cer- 
tain cases  they  can  not  be  differentiated  except  by  operation  which 
discloses  the  absence  of  calculi. 

(2)  Eenal  Colic. — Compared  with  gallstone  colic  the  pain  of 
right-side  renal  colic  is  in  the  lower  abdomen,  starting  in  the  lateral 
or  posterior  lumbar  region  and  radiating  downward  into  the  groin, 
inner  aspect  of  thigh,  and  the  testicle.  Frequent  and  painful  urina- 
tion may  be  present,  and  the  urine  contains  red  blood  cells.  The 
calculus  may  be  voided  by  way  of  the  urethra. 

(3)  Gastralgia. — In  this  the  pain  begins  near  the  middle  line 
in  the  epigastrium,  there  is  rarely  chill  or  fever,  jaundice  is  absent, 
and  no  calculus  is  found  in  the  stools.  The  patient  is  usually 
neurotic. 

(4)  Enteralgia. — The  pain  is  in  mid-abdomen,  is  relieved  by  firm 
pressure  and  the  passage  of  flatus,  and  a  history  of  dietetic  errors  is 
usually  obtained. 

(5)  Xervous  Hepatic  Colic. — In  nervous  women  there  may  be 
a  pseudo-biliary   colic  precipitated  or  aggravated  by  fatigue   and 


DISEASES  OF  THE  BILE  PASSAGES  807 

anxiety  or  other  depressing  emotions.  The  liver  may  be  tender,  the 
pain  come  in  paroxysms  or  be  continuous  with  exacerbations,  but 
the  gall  bladder  is  not  swollen,  jaundice  is  absent,  there  is  no  fever, 
and  no  calculus  in  the  stools. 

(II)  Impacted  Gallstones  in  the  Cystic  Duct.— When  a  calculus 
engages  in  the  cystic  duct  and  becomes  impacted  certain  results 
may  ensue,  as  follows  : 

(1)  Dropsy  of  the  Gall  Bladder.— The  distended  organ  can  usu- 
ally be  felt  below  the  costal  margin  as  an  elastic  gourd-shaped,  ovoid, 
or  rounded  tumour,  ordinarily  of  moderate  size,  occasionally  as  large 
as  a  foetal  head,  rarely  of  such  dimensions  as  to  be  mistaken  for  an 
ovarian  tumour.  It  may  not  be  sufficiently  tense  to  be  palpable. 
It  moves  with  respiration.  Gallstone  crepitus  may  be  perceived. 
Jaundice  is  not  present  in  obstruction  of  the  cystic  duct  alone.  If 
the  obstruction  is  recent  the  gall  bladder  contains  bile,  mucus,  and 
perhaps  some  pus ;  if  of  long  standing,  simply  a  clear,  thin  mucous 
jGiuid.  It  may  require  discrimination  from  movable  kidney  {q.  v.) 
and  carcinoma  of  the  gall  bladder  (page  805). 

(2)  Acute  Infectious  Inflammation  of  the  Oall  Bladder.— Acute 
cholecystitis,  either  catarrhal,  suppurative  (empyema),  or  phlegmon- 
ous, with  or  without  perforation  and  subsequent  abscess  or  perito- 
nitis, may  arise  as  a  consequence  of  the  impaction  in  the  cystic  duct. 
For  the  symptoms  see  Cholecystitis  (page  804). 

(Ill)  Impacted  Gallstones  in  the  Common  Duct. — Commonly  the 
stone  lodges  near  the  end  of  the  common  duct,  or  there  may  be  a 
series  of  stones  along  the  duct. 

(a)  Symptoms. — The  distinctive  signs  of  a  stone  impacted  in  the 
common  duct  (Naunyn)  are  the  presence  of  jaundice,  of  variable  in- 
tensity, for  more  than  one  year,  with  the  persistent  or  intermittent 
presence  of  bile  in  the  stools  ;  fever ;  enlargement  of  the  spleen ;  ab- 
sent or  slight  enlargement  of  the  liver  or  distention  of  the  gall  blad- 
der ;  and  the  absence  of  ascites. 

{h)  Results. — The  presence  of  the  stone  causes  a  chronic  catarrhal 
inflammation  of  the  bile  ducts  (cholangitis)  which  may  eventuate  in 
a  suppurative  cholangitis.  Indeed,  the  symptoms  of  impacted  stone 
are  largely  those  of  the  cholangitis  excited  by  its  presence.  Accord- 
ing to  Osier,  three  groups  of  cases  are  recognisable,  which,  with  their 
distinctive  symptoms,  are  as  follows : 

(1)  Complete  obstruction  with  mild  catarrhal  cholangitis  (see  IV, 
(a),  page  802) ;  (2)  incomplete  obstruction  Avith  a  severer  grade  of 
catarrhal  cholangitis  (see  IV  (J),  page  802),  in  which  recovery  is 
possible ;  (3)  incomplete  obstruction  with  suppurative  cholangitis 
(see  V,  page  803),  in  which  death  is  inevitable. 


g08  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

(IV)  Other  Sequelae  and  Complications  of  Gallstones. — The  stone 
may  ulcerate,  with  the  formation  of  a  biliary  fistula,  through  the  gall 
bladder  or  common  or  cystic  ducts  into  the  stomach  (rare) ;  duode- 
num (more  common) ;  colon  (not  uncommon)  ;  abdominal  cavity  (not 
uncommon) ;  bladder  (occasional) ;  lungs  (not  uncommon),  in  which 
case  bile  may  be  coughed  up ;  or  an  external  communication  (most 
common)  may  be  established  in  the  right  hypochondriac  or  epigastric 
regions,  by  which  the  stone  escapes. 

Large  gallstones  which  enter  the  bowel,  and  are  either  discharged 
or  cause  obstruction,  have  usually  ulcerated  into  the  duodenum  or 
colon,  but  in  exceptional  cases  calculi  of  very  considerable  size  have 
passed  through  a  greatly  dilated  common  duct. 

XI.  Hypersemia  of  the  Liver. — This  may  be  active  or  jyas- 
sive.     The  latter  is  by  far  of  the  most  clinical  importance. 

(1)  Active  Hyperaemia. — The  causes  are  overeating  of  rich  food, 
alcoholism,  acute  infections  like  malaria  or  typhoid  fevers,  amenor- 
rhcea,  or  the  sudden  arrest  of  habitual  bleeding  from  hemorrhoids. 
The  symptoms  are  vague,  consisting  of  a  feeling  of  distress  and  ful- 
ness in  the  right  hypochondrium,  especially  after  an  overhearty 
meal,  perhaps  with  slight  tenderness  from  upward  pressure  under 
the  costal  margin. 

(II)  Passive  Congestion. — (1)  Causes. — This  arises  from  any  con- 
dition which  produces  an  obstruction  to  the  flow  of  blood  through 
the  right  heart,  especially  chronic  valvular  disease,  less  commonly 
pulmonary  emphysema  or  cirrhosis ;  or  through  the  inferior  cava,  as 
with  pressure  by  intrathoracic  tumours.  The  ultimate  result  is  a 
"  nutmeg  "  liver. 

(2)  The  symptoms  are  enlargement  of  the  liver,  which  may  be 
very  considerable,  the  lower  border  extending  as  low  down  as  the 
navel.  If  due  to  valvular  disease  and  the  tricuspid  valve  is  incompe- 
tent, the  whole  organ  may  pulsate.  The  swelling  may  increase  or 
diminish  more  or  less  rapidly.  There  may  be  a  feeling  of  weight  and 
discomfort,  and  the  swollen  liver  is  usually  tender.  Slight  jaundice 
is  not  uncommon,  with  clay-coloured  stools  and  bile-tinged  scanty 
urine  of  high  specific  gravity.  There  may  be  an  enlarged  spleen ; 
occasionally  hsematemesis ;  and  in  advanced  cases  ascites,  followed 
perhaps  by  general  cedema.  Gastro-intestinal  disturbances  are  usu- 
ally present. 

XII.  Thrombosis  of  the  Portal  Vein. — In  rare  instances 
clotting  may  occur  in  the  portal  vein  as  a  result  of  hepatic  cirrhosis 
or  syphilis ;  carcinoma  involving  the  vein  ;  circumscribed  peritonitis  ; 
perforation  of  the  vein  by  a  gallstone  (rare) ;  or  pressure  by  tumours. 
The  diagnosis  is  uncertain  and  seldom  made.     An  extremely  abrvpt 


DISEASES  OF  THE  LIVER  AND  BILE  PASSAGES  809 

onset  of  vomiting  of  blood,  intestinal  hemorrhage,  ascites,  and  swell- 
ing of  the  spleen  will  justify  a  strong  suspicion  of  portal  thrombosis, 
especially  if  one  of  the  causative  conditions  be  present. 

XIII.  Abscess  of  the  Liver.  —  Causes.  —  Hepatic  abscess  is 
single  or  multiple,  always  the  result  of  infection.  The  infective  ma- 
terial may  reach  the  liver  by  way  of  the  portal  vein  from  lesions  in 
the  portal  territory  due  variously  to  dysenteric,  typhoid,  or  gastric 
ulcers,  appendicitis,  amoebic  dysentery,  disease  of  the  rectum  or  neck 
of  the  bladder,  pelvic  abscess,  abscess  of  the  spleen,  or  phlebitis  of 
the  umbilical  vein  in  the  newborn.  These  usually  cause  a  suppurar 
live  pylephlebitis  from  which  septic  emboli  arise,  and,  entering  the 
liver,  initiate  abscesses,  tisually  multiple.  The  septic  foci  may  lie 
outside  of  the  portal  area  and  the  infective  material  be  carried  to 
the  right  heart  by  way  of  the  superior  or  inferior  cava,  traverse  the 
lungs  and  left  heart,  and  enter  the  liver  by  way  of  the  hepatic  artery, 
as  in  general  pyaemia,  suppurative  diseases  of  the  bone,  and  suppurat- 
ing wounds  of  the  scalp ;  or  the  infection  may  come  from  the  heart 
itself  as  in  ulcerative  endocarditis.  Earely  it  enters,  against  the 
blood  stream,  by  the  hepatic  veins.  Finally,  infection  may  be  caused 
by  a  cholangitis,  due  to  gallstones  or  parasites  (distoma,  echinococ- 
cus,  roundworms). 

In  the  great  majority  of  cases  abscess  of  the  liver  is  due  to  dysen- 
tery, next  most  frequently  to  appendicitis,  less  often  to  suppurating 
hemorrhoids,  gastric  ulcer,  or  osteomyelitis.  Except  when  of  amoe- 
bic or  dysenteric  origin  the  suppuration  is  usually  multiple. 

Symptoms. — Multiple  hepatic  abscesses  occurring  in  the  course 
of  a  general  pyaemia  may  present  no  distinctive  symptoms  except 
an  enlarged  and  tender  liver  with  slight  jaundice. 

In  general  the  symptoms  of  liver  abscess  comprise  the  following : 
Fever,  which  is  often  high  at  the  outset  (103°  to  105°),  but  may  begin 
insidiously,  soon  becoming  irregular,  intermittent,  or  hectic  in  type, 
and  interrupted  by  periods  of  normal  temperature.  Chills  may  pre- 
cede, and  sweats  often  follow,  the  exacerbations  of  the  fever.  If  the 
case  becomes  chronic,  fever  may  be  absent.  There  is  usually  hepatic 
and  right-shoulder  pain  of  a  dull  aching  character,  increased  and 
dragging  when  the  patient  lies  upon  his  left  side.  There  is  jaun- 
dice, seldom  more  than  a  moderate  muddy  yellowness  of  the  skin 
and  conjunctivae.  Gastric  disturbances,  often  with  alternating  diar- 
rhoea and  constipation,  or  constipation  alone,  are  present.  Ascites 
is  rare.  If  the  abscess  is  sufficiently  large  the  pressure  upon  the 
lung  through  the  diaphragm  may  cause  pleuritic  symptoms.  There 
is  a  progressive  loss  of  flesh  and  strength. 

Upon  examination  the  liver  is  found  to  be  enlarged  and  tender, 


810  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

and  the  enlargement,  especially  if  a  single  abscess  of  considerable 
size  exists  in  the  right  lobe  of  the  liver,  is  upward  and  to  the  right, 
contrary  to  the  findings  in  other  swellings  of  the  liver.  The  upper 
limit  of  liver  dulness  in  such  cases  may  lie  as  high  as  the  fifth  in- 
stead of  the  eighth  rib  in  the  midaxillary  line,  and  at  the  level  of 
the  angle  of  the  scapula  posteriorly.  It  may  project  below  the  costal 
margin  anteriorly  as  much  as  4  inches,  but  in  multiple  abscesses  pal- 
pable swelling  may  be  absent.  If  the  liver  is  accessible,  it  is  found  to 
be  smooth  and  tender,  and,  rarely,  fluctuation  is  obtained.  A  fric- 
tion rub  over  the  hepatic  area  may  be  heard  upon  deep  inspiration  if 
the  perihepatic  peritoneum  is  inflamed.  In  fatal  cases  the  typhoid 
status  usually  develops. 

Complications  and  SequelsB. — The  suppurative  inflammation  may 
involve  the  pleural  cavity  with  or  without  perforation  of  the  dia- 
phragm, and  invade  the  lung.  In  this  case  there  will  be  a  severe 
paroxysmal  cough,  with  dulness,  weak  bronchial  respiration,  and  in- 
creased fremitus  at  the  right  base,  with  the  expectoration  of  a  char- 
acteristic reddish-brown  sputum,  perhaps  containing  the  Ammha 
coll.  The  abscess  may  finally  rupture  into  a  bronchus ;  or  into  the 
stomach  or  intestine,  with  the  passage  of  a  quantity  of  pus  in  the 
stools ;  or  into  the  peritoneal  cavity  with  sequent  peritonitis ;  or  very 
rarely  into  the  pericardium  ;  or  point  and  discharge  externally  (after 
adhesions  have  formed)  below  the  costal  margin  or  in  the  epigastric 
region. 

Differential  Diagnosis. — The  cardinal  symptoms  are :  irregular 
fever  with  chills  and  sweats,  hepatic  pain,  enlargement  and  tender- 
ness of  the  liver,  and  slight  icterus.  In  doubtful  cases  aspiration  of 
the  liver  should  be  done,  which,  if  successful,  affords  a  reddish- 
brown,  gray,  or  creamy  pus  containing  liver  cells,  bile  pigment, 
amoebaB,  or  cocci.  Leucocytosis  is  always  present.  Except  in  trop- 
ical climates,  hepatic  abscess  is  almost  invariably  secondary,  and  in- 
quiry should  be  made  for  the  causative  affections  previously  men- 
tioned.    The  following  conditions  require  to  be  differentiated : 

(1)  Intermittent  Malarial  Fever. — Liver  abscess  in  temperate  or 
malarial  climates  is  usually  diagnosed  as  malaria  because  of  the 
ague-like  paroxysms  attending  it;  but  the  absence  of  the  Plas- 
modium and  the  futility  of  quinine  in  arresting  the  fever  will  rule 
out  malaria.  Moreover,  there  is  no  splenic  enlargement  in  abscess, 
and  there  is  usually  a  history  of  dysentery  or  other  cause  of  intes- 
tinal ulceration. 

(2)  Intermittent  Fever  of  Hepatic  Colic  or  Catarrhal  Cholangitis. 
— In  this  there  is  a  history  of  previous  attacks ;  the  jaundice  is  more 
intense,  and  usually  deepens  after  each  paroxysm  of  chill,  fever,  and 


DISEASES  OF  THE  LIVER  811 

sweat ;  the  duration  is  much  longer,  with  entire  absence  of  fever 
between  the  paroxysms ;  and  there  is  no  serious  impairment  of  the 
general  health, 

(3)  Typhoid  Fever. — The  diarrhoea,  delirium,  rapid  pulse,  and 
other  symptoms  of  the  typhoid  status  which  often  attend  the  later 
stages  of  liver  abscess  may  closely  simulate  typhoid  fever,  but  chills, 
sweats,  irregular  fever,  meteorism,  and  bronchitis  are  less  common  ; 
rose  spots  and  a  positive  Widal  reaction  are  absent ;  and  there  is  usu- 
ally a  preceding  history  of  dysentery.  Js'evertheless,  hepatic  abscess 
may  complicate  typhoid  fever. 

(4)  Suppurative  Pleurisy. — In  the  cases  where  an  empyema  is 
due  to  and  coexists  with  hepatic  abscess,  a  correct  appreciation  of 
the  true  condition  is  impossible,  unless  the  characteristic  brownish- 
red  sputa  are  present,  or  an  examination  of  aspirated  pus  from  the 
pleural  cavity  reveals  liver  cells  and  bile  pigment,  thus  proving  the 
hepatic  origin  of  the  empyema.  The  Amoeba  coli  may  be  found  in 
the  sputum  or  pus.  A  large  right-side  empyema,  by  which  the  liver 
is  pushed  down  and  apparently  enlarged,  may  so  closely  simulate 
liver  abscess  that  a  differential  diagnosis  is  extremely  difficult.  The 
upper  line  of  flatness  in  empyema  lies  at  a  higher  point  than  in 
abscess  and  may  change  position  with  movement ;  bulging  of  the 
affected  side  is  common  ;  the  cough  and  dyspnoea  are  more  marked ; 
there  is  a  history  of  previous  tuberculous  disease,  or  a  pneumonia  or 
serous  pleurisy;  and  the  earliest  symptoms  are  pulmonary  rather 
than  intestinal  or  abdominal. 

Prognosis. — The  mortality  is  from  50  to  60  per  cent.  Death 
usually  occurs  in  from  6  weeks  to  3  months.  In  solitary  abscesses 
operation  may  give  favourable  results. 

XI Y.  Cirrhosis  of  the  Liiver. — Causes. — Chronic  alcoholism 
(50  per  cent  of  all  cases),  syphilis,  chronic  heart  or  lung  diseases 
causing  passive  hepatic  congestion,  chronic  inflammation  of  the  bile 
ducts  or  obstruction  by  gallstones,  and  other  but  minor  causes. 

Varieties. — Two  clinical  forms  are  recognised,  the  atrophic  (or 
alcoholic)  and  the  hypertrophic. 

(I)  Atrophic  (Alcoholic)  Cirrhosis.— /^mp^oms.— Occurs  mainly 
in  men,  about  40  years  of  age  or  over.  So  long  as  the  collateral  cir. 
culation  compensates  for  the  obstruction  caused  by  the  contracting 
connective  tissue,  to  the  portal  circulation,  the  disease  may  be  latent. 
When  passive  portal  congestion  occurs  the  early  symptoms  are  usu- 
ally those  of  a  chronic  gastric  catarrh,  anorexia,  furred  tongue,  nau- 
sea, and  vomiting.  Later,  sometimes  early,  there  may  be  epistaxis, 
haematemesis,  or  bleeding  from  dilated  veins  of  the  esophagus,  intes- 
tinal hemorrhage,  or  bleeding  hemorrhoids.    Ascites,  often  becoming 


812  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

enormous,  usually  ensues,  with  sequent  great  oedema  of  the  legs  and 
genitals.  Jaundice,  if  present  at  all,  is  slight.  The  urine  is  scanty 
and  high  coloured,  of  high  specific  gravity,  loaded  with  urates,  and 
often  contains  bile  pigment.  Fever  is  uncommon,  but  may  be  pres- 
ent (100°  to  102°)  during  advanced  stages. 

The  face,  often  ruddy  at  first,  becomes  pallid,  sallow,  and  pinched. 
There  is  usually  progressive  loss  of  flesh,  and  the  emaciation  of  the 
thorax  and  upper  extremities  contrasts  strongly  with  the  distended 
abdomen  and  (edematous  legs.  The  presence  of  the  caput  Medusse 
and  other  distended  veins  of  the  abdomen  (mammary,  epigastric) 
may  be  noted.  The  liver  is  at  first  somewhat  enlarged,  but  later 
becomes  smaller,  although — a  fact  to  be  noted — the  reduction  in 
size  may  be  slight.  Its  firm  lower  edge  may  be  felt  under  the  costal 
margin  if  the  ascites  will  permit,  and  its  surface  is  hard,  sometimes 
finely  granular.  The  spleen  is  usually  enlarged  and  palpable.  After 
tapping,  the  area  of  liver  dulness  is  found  to  be  diminished  in  its 
vertical  diameter.  In  any  stage  of  the  disease  intense  headache, 
amaurosis,  noisy  delirium,  convulsions,  stupor,  or  coma  may  develop, 
closely  simulating  and  usually  supposed  to  be  the  cerebral  symptoms 
of  uraemia,  but  due  to  a  toxic  agent  as  yet  unknown. 

The  duration  of  the  disease  may  cover  many  years. 

Diagnosis. — The  cardinal  symptoms  are  a  history  of  alcoholism, 
the  presence  of  ascites,  and  the  detection  of  a  firm,  perhaps  a  small, 
liver.  The  occurrence  of  hsematemesis  or  melaena  and  enlargement 
of  the  spleen  will  tend  to  confirm  the  diagnosis.  It  may  be  impos- 
sible to  distinguish  the  initial  enlargement  of  a  cirrhotic  liver  from 
a  fatty  liver ;  and  in  rare  instances  cancer  and  cirrhosis  are  associ- 
ated, as  proved  at  autopsy.  The  syphilitic  origin  of  the  disease  may 
be  suspected  if  there  is  an  indubitable  history  or  unmistakable  signs 
of  previous  syphilis,  or  if  the  liver  is  irregular  in  shape. 

(II)  Hypertrophic  Cirrhosis. — This  form  occurs  mainly  in  men 
under  40  years  of  age ;  occasionally  in  children ;  and  there  is  not 
usually  an  alcoholic  history  (Osler).  Its  duration  varies  from  4  to 
10  years.     The  cause  of  the  disease  is  practically  unknown. 

Symptoins. — There  is  jaundice,  usually  slight.  The  liver  is  uni- 
formly increased  in  size  and  the  enlargement  is  often  visible ;  its 
edge  is  smooth,  firm,  hard,  and  may  extend  downward  to  the  level 
of  the  umbilicus,  and  its  surface  is  smooth ;  the  spleen  is  enlarged, 
hard,  and  readily  palpated.  There  are  attacks  of  pain  in  the  region 
of  the  liver,  slight  or  severe,  sometimes  accompanied  by  nausea  and 
vomiting  and  followed  by  an  increase  of  the  jaundice,  but  the  gall 
bladder  is  not  swollen.  The  urine  contains  bile  pigment,  but  the 
stools  remain  dark.     There  may  be  slight  fever,  and  a  marked  leuco- 


DISEASES  OF  THE  LIVER  813 

cytosis  is  not  uncommon.  In  children  the  enlargement  of  the  spleen 
may  be  very  considerable.  There  may  be  hemorrhages,  purpura,  and 
itching  or  bronzing  of  the  skin.  At  any  time  during  the  course  of 
the  disease  delirium  and  high  fever  with  a  grave  form  of  jaundice 
may  develop.  In  contradistinction  to  atrophic  cirrhosis,  ascites  and 
dilated  abdominal  veins  do  not  occur. 

Diagnosis. — In  amyloid  liver  jaundice  is  absent.  In  carcinoma 
of  the  liver  the  spleen  is  not  enlarged,  there  may  be  ascites,  the 
patient  is  over  40,  and  the  liver  is  nodular  and  irregular, 

XY.  Fatty  Liver. — Two  varieties  are  recognised, /a^^^  infiUror 
tion  and  fat ti/  degeneration. 

(I)  Fatty  Infiltration. — This  may  be  present  as  a  part  of  a  gen- 
eral obesity  ;  or,  on  the  other  hand,  because  of  interference  with  oxi- 
dation, may  supervene  in  the  course  of  chronic  wasting  diseases  like 
pulmonary  tuberculosis,  carcinoma,  grave  anaemia,  malarial  cachexia, 
or  syphilis.  A  fatty  cirrhotic  liver  may  be  found  as  the  result  of 
chronic  alcoholism.  Aside  from  the  evidence  derived  from  physical 
examination,  the  general  symptoms  are  not  distinctive,  being  com- 
monly those  of  the  causative  disease  or  condition.  There  is  no 
jaundice  whatever,  although  the  stools  may  be  pale,  and  ascites  does 
not  occur.  The  liver  is  found  to  be  greatly  enlarged,  smooth,  and 
painless,  often  reaching  as  far  down  as  the  umbilicus.  The  spleen 
remains  of  normal  size. 

The  presence  of  general  obesity  suggests  but  may  interfere  with 
the  physical  detection  of  this  condition.  It  is  easily  recognised  in 
thin  subjects.  By  comparison  the  amyloid  liver  is  of  firmer  con- 
sistence, and  usually  associated  with  enlargement  of  the  spleen  and 
albuminuria.  The  physical  characteristics  of  the  lucaemic  liver 
resemble  those  of  the  fatty  liver,  but  a  blood  examination  will  read- 
ily make  the  discrimination. 

(II)  Fatty  Degeneration. — May  be  due  to  alcoholism,  carcinoma, 
phthisis,  chronic  dysentery,  profound  anaemia,  acute  specific  infec- 
tions, poisoning  by  phosphorus,  arsenic,  or  chloroform,  and  forms  an 
essential  feature  of  acute  yellow  atrophy.  The  slighter  degrees  of 
fatty  degeneration  are  clinically  unrecognisable.  The  symptoms  of 
the  grave  forms  are  those  of  acute  yellow  atrophy  (page  816)  or  phos- 
phorus poisoning. 

XVI.  Amyloid  Liver. — Occurs  most  frequently  as  a  result  of 
chronic  suppuration  in  tuberculous  disease  of  the  bones,  especially 
of  the  hip  joint  or  vertebrae ;  next  most  commonly  it  is  due  to  syph- 
ilis, particularly  syphilitic  ulceration  of  the  rectum  and  disease  of 
the  bones.  Less  often  it  is  associated  with  rachitis,  carcinoma,  and 
infectious  fevers.     The  symptoms  are  not  distinctive.     The  liver  is 


814  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

uniformly  and  greatly  enlarged,  smooth,  solid,  firm,  and  not  tender. 
The  margin  is  usually  rounded,  but  may  be  sharp  and  firm.  The 
spleen  also  is  enlarged  from  associated  amyloid  disease.  Jaundice 
is  absent,  the  stools  may  be  light  coloured  but  contain  bile,  and  there 
is  no  ascites  or  other  evidence  of  portal  obstruction.  As  an  amyloid 
kidney  usually  coexists,  the  urine  often  contains  serum  albumin,  and 
also  serum  globulin,  with  abundant  casts. 

The  diagnosis,  except  in  the  rare  instances  when  the  amyloid 
liver  is  not  enlarged,  is  readily  made.  The  cardinal  symptoms  com- 
prise a  great  and  steady  enlargement  of  the  organ,  in  conjunction 
with  chronic  suppuration,  syphilis,  or  chronic  phthisis. 

XVII.  Carcinoma  of  the  Liver. — This  occurs  most  commonly 
in  men,  seldom  under  40  years  of  age,  very  rarely  in  children.  It  is 
next  in  frequency  to  carcinoma  of  the  stomach  and  uterus ;  usually 
secondary,  mainly  to  primary  disease  in  the  portal  territory,  especial- 
ly of  the  stomach  and  rectum,  or  to  mammary  carcinoma.  Carci- 
noma of  the  gall  bladder  has  already  been  described  (page  805). 

{a)  Symptoms. — The  disease  may  be  latent  except  for  an  indefi- 
nite ill  health.  Progressive  emaciation  and  loss  of  strength  may  be 
the  earliest  symptoms.  There  are  usually  anorexia,  nausea,  and 
vomiting.  Jaundice,  ordinarily  slight,  sometimes  intense,  is  present 
in  50  per  cent  of  cases.  Dull  pain  or  uneasiness  in  the  right  hypo- 
chondrium  or  shoulder  is  usually  present,  but  may  be  lacking.  As- 
cites is  not  common,  occurring  in  but  a  small  proportion  of  cases. 
The  spleen  is  seldom  enlarged.  Fever,  usually  moderate  (100°  to 
102°),  is  not  infrequent  during  the  later  stages ;  rarely  chills  and 
high  intermittent  fever  may  occur.  A  marked  cachexia  with  anaemic 
cedema  of  the  feet  and  legs  almost  invariably  appears  toward  the 
end  of  the  disease ;  and  at  the  same  period  toxic  symptoms,  head- 
ache, delirium,  stupor  or  coma,  may  supervene. 

Physical  examination  shows  enlargement  of  the  superficial  veins 
and  distention  of  the  upper  portion  of  the  abdomen.  If  the  emacia- 
tion is  marked,  the  nodular  character  of  the  enlarged  liver  may  be 
evident  by  inspection.  The  organ  is  found  to  be  greatly  increased 
in  size,  its  margin  lying  perhaps  below  the  navel,  and  moving  with 
respiration.  Usually  the  liver  is  hard,  irregular,  and  nodulated,  each 
nodule  sometimes  presenting  a  characteristic  depression  or  umbilica- 
tion  in  its  centre.  When  the  growth  is  mainly  in  the  left  lobe  the 
latter  may  resemble  a  distinct  epigastric  tumour.  In  rare  cases  the 
liver  is  uniformly  enlarged  and  smooth,  lacking  nodulation.  The 
duration  of  the  disease  is  from  3  to  15  months,  rarely  2  years. 

(Jb)  Differential  Diagnosis. — The  cardinal  symptom  of  hepatic  car- 
cinoma is   the  enlarged  nodular  liver  with  cachexia.     Previous  or 


DISEASES  OP  THE  LIVER  8I5 

present  carcinoma  of  other  organs  (stomach,  intestine,  rectum,  mam- 
mary gland),  with  jaundice  and  perhaps  ascites,  confirm  the  diagno- 
sis.    Age  and  heredity  are  suggestive. 

(1)  If  the  liver  is  diffusely  carcinomatous  and  the  enlargement  is 
smooth  and  uniform,  a  variety  sometimes  encountered,  it  may  require 
differentiation  from  amyloid  or  fatty  liver.  The  presence  of  jaun- 
dice, the  rapid  increase  in  the  size  of  the  organ,  and  the  develop- 
ment of  a  marked  cachexia  will  pronounce  for  malignant  disease. 

(2)  The  large  nodulated  hydatid  liver  may  resemble  that  of  car- 
cinoma, but  in  the  former  the  duration  of  the  disease  is  much  longer, 
the  wasting  and  anaemia  are  much  less  marked,  the  nodules  are 
softer,  jaundice  is  more  common,  aspiration  may  enable  the  finding 
of  booklets,  and  finally  it  is  of  rare  occurrence. 

(3)  The  large  syphilitic  amyloid  liver  containing  irregular  or 
rounded  projecting  gummata  may  be  difficult  to  separate,  as  the 
jaundice  may  be  marked  and  the  organ  greatly  enlarged.  But  the 
history  or  evidences  of  syphilis,  the  longer  duration  of  the  disease, 
and  the  slighter  degree  of  impairment  of  the  general  health  will 
negative  malignant  disease. 

(4)  Hypertrophic  cirrhosis  in  the  early  stages  can  not  always  be 
distinguished  from  carcinoma.  Eeliance  must  be  placed  upon  smooth 
and  painless  enlargement  of  the  liver,  the  presence  of  an  enlarged 
spleen,  and  the  non-appearance  of  the  cancerous  cachexia. 

(5)  Whether  the  malignant  disease  of  the  liver  is  sarcoma  rather 
than  carcinoma,  as  sometimes  happens,  can  not  be  decided  unless 
there  is  a  primary  sarcoma  elsewhere.  The  primary  growth  is  usu- 
ally a  melano-sarcoma  of  the  eye,  lymph  glands,  or  skin,  and  if  sec- 
ondary deposits  occur  in  the  liver  there  may  be  melanuria,  which, 
with  the  presence  of  the  original  tumour  and  the  very  rapid  increase 
in  the  size  of  the  liver,  may  enable  a  diagnosis. 

It  is  hardly  possible  to  determine  positively  whether  carcinoma 
of  the  liver  is  primary  or,  as  usual,  secondary,  unless  the  primary 
growth  can  be  discovered. 

XVIII.  Perihepatitis. — Eeference  is  here  made  to  a  chronic 
inflammation,  with  great  thickening  (capsulitis)  of  the  fibrous  en- 
velope (Glisson's  capsule)  of  the  liver.  Acute  inflammation  of  the 
peritoneal  covering  of  the  liver,  including  subphrenic  abscess,  is 
described  under  diseases  of  the  peritoneum  {q.  v.). 

Chronic  capsulitis  (Glissonian  cirrhosis)  is  divided  (Osler)  into 
two  groups  :  one,  in  adults,  with  recurring  ascites  and  evidences  of 
interstitial  nephritis,  without  jaundice,  and  which  can  not  be  dis- 
tinguished from  atrophic  cirrhosis  of  the  liver ;  the  other  forming  a 
part  of  a  widespread  fibroid  process  which  includes    perihepatitis. 


816  DIAGNOSIS,   DIRECT  AXD  DIFFERENTIAL 

perisplenitis,  proliferative  peritonitis,  adherent  pericardium,  and  in- 
durative mediastinitis.  The  liver  may  be  rounded,  smooth,  and 
readily  grasped,  resembling  the  spleen,  and  there  is  persistent  ascites. 

XIX.  Acute  Yellow  Atrophy. — A  rare  disease  attended  by  a 
rapid  necrosis  of  the  liver  cells.  It  occurs  with  the  greatest  fre- 
quency in  pregnant  women  between  20  and  30  years  of  age.  The 
condition  is  almost  exactly  that  which  is  produced  by  phosphorus 
poisoning. 

Symptoms. — The  initial  symptoms  are  malaise,  headache,  anorexia, 
nausea,  and  vomiting,  followed  in  a  few  days  by  jaundice,  the  condi- 
tion resembling  a  simple  gastro-duodenal  catarrh.  In  from  1  to  3 
weeks  from  the  onset  cerebral  symptoms,  delirium,  muscular  trem- 
bling, perhaps  convulsions,  drowsiness,  coma,  and  persistent  vomiting 
become  manifest.  At  this  time  the  jaundice  deepens.  There  may 
be  subcutaneous  or  mucous-membrane  hemorrhages.  There  may  or 
may  not  be  moderate  fever.  There  is  no  bile  in  the  clay-coloured 
stools ;  the  urine  is  bile-stained,  contains  albumin,  fatty  casts,  and 
quite  frequently  leucin  and  tyro  sin.  The  typhoid  status  usually  de- 
velops with  dry  tongue,  rapid  pulse,  coma,  and  death.  Physical 
examination  shows  a  progressive  decrease  in  the  area  of  hepatic  dul- 
ness,  and  its  replacement  by  tympanicity. 

Diagnosis. — The  cardinal  symptoms  are  jaundice,  vomiting,  delir- 
ium, hemorrhages,  with  leucin  and  tyrosin  in  the  urine,  and  atrophy 
of  the  liver.  It  is  to  be  remembered  that  severe  cerebral  symptoms 
may  occur  during  the  course  of  any  grave  jaundice. 

In  phospliorus  poisoni)ig,  which  yellow  atrophy  resembles,  the 
onset  is  sudden,  the  gastric  symptoms  more  prominent,  the  nervous 
symptoms  are  less  marked  and  appear  at  a  later  period,  and  the 
urine  does  not  contain  leucin  or  tyrosin.  Moreover,  there  may  be  a 
history  of  the  ingestion  of  rat  paste  or  match  heads. 

The  symptoms  of  hypertrophic  cirrhosis  may,  in  some  respects, 
exactly  simulate  those  of  yellow  atrophy,  but  enlargement  instead  of 
shrinkage  of  the  liver,  the  absence  of  leucin  and  tyrosin,  and  the  fre- 
quent pyrexia  will  speak  for  the  former. 

XX.  Syphilis  of  the  Liver. — See  page  740. 

XXI.  Leucaemic  Liver. — See  Index. 

XXII.  Hydatids  of  the  Liver. — See  Index. 

X.    DISEASES   OF   THE    PANCREAS 

{For  the  examination  of  the  pancreas,  see  pages  470  and  471) 

I.  Acute  Pancreatitis. — Of  this  3  forms  are  recognised :  hem- 
orrhagic, suppurative,  and  gangrenous. 


DISEASES  OF  THE   PANCREAS  817 

(I)  Hemorrliagic  Pancreatitis. — Occurs  mainly  in  adult  males. 
Predisposing  causes  are  injury,  alcoholism,  gallstones,  severe  chronic 
gastro-duodenitis,  and  chronic  mercurialism. 

(a)  Symptoms. — The  onset  is  sudden,  with  deep-seated  violent  and 
colicky  pain  in  the  upper  portion  of  the  abdomen,  soon  followed  by 
nausea  and  persistent  vomiting,  constipation,  abdominal  distention, 
perhaps  limited  to  the  epigastrium,  and  meteorism.  The  tempera- 
ture may  be  subnormal  at  first,  later  there  is  moderate  fever,  perhaps 
beginning  with  a  chill.  Deep  pressure  over  the  upper  abdomen  or 
epigastric  region  may  reveal  circumscribed  resistance.  Tender  points 
(fat  necrosis)  may  be  found  scattered  over  the  abdominal  wall.  De- 
lirium, dyspnoea,  hiccough,  fatty  diarrhoea,  and  albuminuria  may  be 
present.  Symptoms  of  collapse  rapidly  supervene,  and  death  occurs 
from  the  2d  to  the  4th  day  of  the  disease,  or  even  sooner. 

{b)  Differential  Diagnosis. — The  cardinal  symptoms  (Fitz)  com- 
prise a  sudden,  violent,  deep-seated  pain  in  the  epigastrium,  fol- 
lowed by  vomiting  and  collapse,  and  in  24  hours  by  a  circumscribed 
epigastric  swelling,  tympanitic  or  resistant,  with  slight  fever,  consti- 
pation, tenderness  over  the  course  of  the  pancreas,  and  tender  spots 
in  the  abdomen.     Few  correct  diagnoses  are  made  intra  vitam. 

Most  commonly  the  disease  is  mistaken  for  acute  intestinal  ob- 
struction, or  peritonitis  due  to  perforation  of  a  duodenal  or  gastric 
ulcer.  Symptoms  pointing  to  obstruction  rather  than  pancreatitis 
are  general  abdominal  distention,  visible  peristalsis  of  the  intestinal 
coils,  and  faecal  vomiting,  although  obstruction  high  up  in  the  in- 
testine and  manifesting  itself  by  local  signs  in  the  epigastrium  is  not 
common.  But  the  most  acute  diagnostician  may  be  tripped.  Ulcer 
of  the  stomach  or  duodenum  occurs  usually  in  younger  persons ;  there 
is  a  history  of  chlorosis  or  anaemia,  pain  after  eating,  and  haemateme- 
sis  or  intestinal  hemorrhage.  In  gallstone  colic  there  is  seldom 
severe  collapse  or  prostration,  the  pain  is  in  the  right  hypochon- 
drium,  and  jaundice  is  often  present.  Xevertheless,  gallstones  and 
pancreatitis  may  coexist.  Corrosive  poisoning  can  be  discriminated 
by  the  history  and  perhaps  by  an  examination  of  the  vomitus. 

The  prognosis  is  almost  invariably  bad. 

(II)  Suppurative  Pancreatitis.— Occurs  mainly  in  men.  The  dis- 
ease may  set  in  acutely  with  severe  epigastric  pain,  hiccough,  vomit- 
ing, chills  and  irregular  fever,  tympanites,  constipation,  slight  jaun- 
dice, and  splenic  swelling,  ending  fatally  within  a  week ;  or  it  may 
continue  for  3  or  4  weeks  with  irregular  chills  and  fever,  and  steady 
loss  of  flesh  and  strength,  finally  ending  in  death ;  or  it  may  become 
chronic,  lasting  several  months  or  a  year,  with  progressive  weakness 
and  emaciation,  and  either  continuous  moderate  fever  or  occasional 


818  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

attacks  of  pain  and  vomiting,  followed  by  fever  and  delirium.  There 
may  be  fatty  diarrhoea,  jaundice,  and  glycosuria.  The  abscess  may 
perforate  into  the  peritoneal  cavity,  stomach,  or  duodenum,  or  cause 
portal  thrombosis.  The  diagiiosis  of  pancreatic  abscess  can  not  be 
made  unless  it  forms  a  palpable,  deep-seated  mass  in  the  epigastrium, 
the  presence  of  which,  in  association  with  the  symptoms  described, 
may,  in  rare  instances,  suggest  the  diagnosis. 

(Ill)  Gangrenous  Pancreatitis. — This  is  usually  a  sequel  of  hem- 
orrhage (see  II,  folloAving),  or  of  (I)  and  (II)  just  described,  the 
pancreas  becoming  necrotic.  The  symptoms  are  the  same  as  those 
of  hemorrhagic  pancreatitis,  except  that  chills  and  fever  are  usual, 
jaundice  may  occur,  and  the  duration  is  from  10  days  to  3  weeks. 
Death  is  the  ordinary  termination,  although  the  necrotic  pancreas  has 
been  discharged  by  way  of  the  rectum  with  subsequent  recovery. 

II.  Hemorrhage  into  the  Pancreas. — Occurs  mainly  in 
adults  over  40  years  of  age.  The  si/m^jtoms  comprise  a  sudden  onset, 
during  perfect  health,  of  severe,  sharp,  or  colicky  pain  in  the  upper 
abdomen,  accompanied  by  nausea  and  obstinate  vomiting.  The  pa- 
tient rapidly  becomes  depressed,  restless,  and  anxious,  with  a  cold, 
sweating  skin.  The  pulse  is  small  and  rapid,  becoming  later  running 
and  imperceptible.  The  temperature  is  normal  or  subnormal,  the 
abdomen  becomes  distended  and  tender,  especially  over  its  upper  por- 
tion.    Collapse,  syncope,  and  death  follow  within  24  hours. 

III.  Chronic  Pancreatitis. — The  organ  becomes  hard,  and 
often  contracted,  as  a  result  of  interstitial  fibrous  overgrowth.  The 
most  frequent  cause  is  an  extension  into  the  pancreatic  duct  of  a 
chronic  gastro-duodenitis  or  catarrh  of  the  bile  passages  ;  next  most 
frequently  it  is  a  result  of  alcoholism  and  syphilis.  It  is  often  asso- 
ciated with  diabetes. 

The  symptoms  are  not  distinctive.  There  may  be  evidences  of 
chronic  catarrhal  gastritis  with  occasional  attacks  of  deep-seated  pain 
in  the  epigastric  region,  faintness,  anxiety,  and  moderate  fever. 
Jaundice,  due  to  pressure  upon  the  common  bile  duct  by  the  fibroid 
changes  in  the  head  of  the  pancreas,  may  be  present,  so  also  fatty 
diarrhoea,  and  fat  and  sugar  in  the  urine.  A  sense  of  resistance  over 
the  epigastrium  has  been  observed.  Xevertheless  an  ante-mortem 
diagnosis  is  rarely,  if  ever,  possible  without  exploratory  operation. 

IV.  Carcinoma  of  the  Pancreas. — This  occurs  principally  in 
men  over  40  years  of  age ;  is  usually  primary ;  and  most  commonly 
involves  the  head  of  the  organ.     It  is  not  a  frequent  disease. 

Symptoms. — The  symptoms  are  not  distinctive.  There  is  continu- 
ous dull,  occasionally  paroxysmal  and  radiating,  pain  in  the  epigas- 
trium.    Nausea,  vomiting,  and  dyspeptic   symptoms   are   common. 


DISEASES  OF  THE   PANCREAS  819 

From  pressure  by  the  enlarged  head  of  the  pancreas  upon  the  end  of 
the  common  duct  intense  and  permanent  jaundice  may  arise,  with 
swelling  of  the  liver  and  gall  bladder ;  upon  the  portal  vein,  ascites ; 
upon  the  thoracic  duct,  chylous  ascites ;  upon  the  pylorus,  gastrec- 
tasia ;  upon  the  inferior  cava,  cedema  of  the  lower  half  of  the  body ; 
upon  the  left  ureter,  hydronephrosis.  The  stools  are  clay  coloured, 
and  fatty  diarrhoea  and  diabetes  may  be  present  but  are  not  common. 
There  is  very  rapid  emaciation  and  cachexia.  In  about  one  third  of 
the  cases  a  deep-seated  epigastric  tumour  can  be  felt,  which  lying,  as 
it  does,  directly  upon  the  aorta,  may  present  a  distinctly  transmitted 
pulsation,  perhaps  a  hruit.  The  prognosis  is  almost  invariably  unfa- 
vourable, but  cases  have  recovered  after  operation. 

Diagnosis. — This  is  difficult  and  not  often  made.  The  significant 
symptoms  are  epigastric  pain,  rapid  emaciation,  the  late  onset  of 
intense  and  permanent  jaundice  with  dilatation  of  the  gall  bladder, 
and  the  presence  of  a  deep-seated,  immovable,  and  hard  epigastric 
tumour.     It  requires  to  be  separated  from  the  following : 

(1)  Carcinoma  of  the  Pylorus. — Compared  to  carcinoma  of  the 
pancreas,  a  pyloric  growth  is  readily  movable ;  the  stomach  is  usually 
dilated ;  there  may  be  coffee-ground  vomitus  and  melaena ;  jaundice, 
ascites,  glycosuria,  and  fatty  diarrhoea  are  generally  absent ;  HCl  is 
absent,  lactic  acid  present,  in  the  stomach  contents ;  and,  finally,  the 
duration  is  much  longer  than  that  of  carcinoma  of  the  pancreas. 

(2)  Carcinoma  of  the  Transverse  Colon. — In  this  the  tumour  is 
not  so  deep-seated,  it  is  movable,  evidences  of  intestinal  obstruction 
are  generally  present,  and  there  is  no  jaundice. 

(3)  Aneurism  of  the  Abdominal  Aorta. — The  history,  the  expan- 
sile pulsation,  and  the  absence  of  cachexia,  will  vouch  for  aneurism 
rather  than  carcinoma. 

V.  Pancreatic  Cysts. — {a)  Causes. — These  cysts  are  usually 
either  traumatic,  inflammatory,  or  retention  cysts ;  the  latter  due  to 
plugging  of  the  duct  of  Wirsung  by  calculi,  or  occlusion  of  the  smaller 
ducts  by  the  contraction  of  a  chronic  interstitial  pancreatitis. 

{h)  Symptoms. — In  the  traumatic  cases  the  onset  may  be  sudden, 
with  pain,  vomiting,  and  peritonitic  symptoms;  in  inflammatory 
cases  either  gradual  after  dyspeptic  attacks  with  colicky  pain  sug- 
gestive of  gallstones,  or  more  rapid  Avith  symptoms  of  intestinal 
obstruction.  The  more  chronic  retention  cysts  may  give  rise  to  no 
symptom  until  they  attain  a  very  considerable  size. 

Frequently  there  are  attacks  of  colicky  pain,  sometimes  referred 
to  the  left  hypochondrium  and  left  shoulder,  with  nausea,  vomiting, 
and  steady  enlargement  of  the  abdomen.  Fatty  diarrhoea  and  saliva- 
tion are  rare,  glycosuria  and  albuminuria  not  infrequent,  and  from 


820  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

the  pressure  of  large  tumours  jaundice,  ascites,  and  dyspnoea  may 
become  manifest.  A  decided  loss  of  weight  has  been  noted  in  a 
number  of  cases.  Constipation  is  common,  and  there  may  be  recur- 
ring intestinal  hemorrhages. 

The  elastic,  perhaps  fluctuating,  smooth,  or  lobulated  cystic  tumour 
is  found  in  the  upper  abdomen,  usually  in  the  middle  line.  In  the 
majority  of  cases  it  reaches  the  abdominal  wall  between  the  stomach 
and  the  colon,  the  former  having  been  thrust  upward.  More  rarely 
it  lies  above  the  stomach  or  below  the  colon  ;  still  more  infrequently, 
when  springing  from  the  tail  of  the  pancreas,  it  is  discovered  in  the 
left  hypochondrium.  It  is  fixed,  moves  slightly,  if  at  all,  with  res- 
piration, and  may  be  so  large  as  to  fill  the  abdomen.  The  cyst  may 
develop  rapidly,  but  as  a  rule  the  growth  is  slow  and  chronic,  and  it 
may  exist  for  many  years,  in  the  majority  for  from  2  to  4  years. 

(c)  Diagnosis. — This  rests  upon  the  finding  of  a  tumour  with  the 
characteristics  Just  described.  The  cyst  may  be  aspirated  and  the 
contents  examined.  Inflation  of  the  stomach  and  the  colon  will  aid 
in  determining  the  exact  location  of  the  cyst.  It  requires  differen- 
tiation from  hydronephrosis  {q.  v.)  or  renal  cysts  {q.  v.),  a  greatly 
dilated  gall  bladder  (page  467),  or,  if  very  large,  from  an  ovarian 
cyst.  The  prognosis,  if  the  condition  is  correctly  diagnosed  and 
operated,  is  good. 

VI.  Pancreatic  Calculi. — These  rare  formations  may  lead  by 
their  presence  to  chronic  pancreatitis,  cysts,  suppurative  pancreatitis, 
or  carcinoma.  A  diagnosis  may  be  attempted  if,  without  Jaundice, 
there  are  attacks  of  colic,  due  to  the  passage  of  the  calculus  through 
the  main  duct,  the  pain  extending  along  the  left  costal  margin  and 
through  to  the  back,  with  glycosuria  and  fatty  diarrhoea.  If  calculi 
composed  of  calcium  carbonate  or  phosphate  can  be  recovered  from 
the  stools  subsequent  to  the  attack  the  diagnosis  is  confirmed. 
Ordinarily  a  diagnosis  of  gallstone  colic  is  made. 

XI.    DISEASES    OF    THE    PERITONEUM 

I.  Acute  Diffuse  Peritonitis.— Causes. — Earely  this  is  pri- 
mary or  idiopathic,  occurring  as  a  terminal  event  in  chronic  nephri- 
tis, arteriosclerosis,  or  gout.  Ordinarily  it  is  secondary,  arising  by 
extension  from  an  inflamed  organ  covered  by  peritoneum,  or  from 
perforation  of  a  similarly  covered  hollow  organ,  or  from  rupture  of 
an  abscess  into  the  peritoneal  cavity.  Peritonitis  from  perforation 
may  be  due  to  typhoid,  cancerous,  tuberculous,  simple,  or  stercoral 
ulcer  of  the  stomach  or  intestine,  or  to  perforation  of  the  appendix 
or  gall  bladder ;  from  rupture  of  a  purulent  collection,  to  appendical 
abscess,  pyosalpinx,  ovarian  abscess,  retroperitoneal  abscess,  empye- 


DISEASES  OF  THE  PERITONEUM  821 

ma  of  the  gall  bladder,  and  abscess  of  the  liver,  spleen,  or  pancreas. 
It  may  arise  by  extension  from  any  of  the  inflammations  just  men- 
tioned, without  perforation  or  rupture.  It  may  form  a  part  of  sep- 
ticfemia  or  pyaemia,  or  be  due  to  cancer  or  tuberculosis  of  the 
abdominal  viscera.  The  infective  organisms  are  various,  but  those 
of  most  frequent  occurrence  are  the  Bacillus  coli  communis  (in  peri- 
tonitis from  perforation  of  the  intestinal  tract),  the  Staphylococcus 
aureus  (post-operative  and  puerperal),  and  the  Streptococcus  pyogenes 
(idiopathic  or  terminal). 

Symptoms. — If  the  patient  is  already  gravely  ill,  particularly  when 
a  stuporous  condition  is  present,  or  when  a  localized  peritoneal  ab- 
scess causes  a  slow-spreading  general  peritonitis,  the  onset  may  be 
gradual  and  insidious,  the  symptoms  of  the  primary  disease  over- 
shadowing those  of  the  peritoneal  involvement. 

Ordinarily  the  initial  symptom  is  a  chilly  feeling  or  a  marked 
rigour,  with  a  rise  of  temperature,  vomiting,  and  intense  abdominal 
pain.  The  pain  may  at  first  be  local  and  correspond  to  the  seat  of 
the  primary  lesion,  but  soon  becomes  diffused  and  general.  Except 
when  due  to  perforation  of  a  gastric  ulcer,  when  it  is  referred  to  the 
chest,  back,  or  shoulder,  the  greatest  pain  is  below  the  navel.  The 
abdomen  is  excessively  tender,  soon  becomes  distended  and  tympa- 
nitic, in  rare  cases  remaining  flat  and  rigid,  and  the  abdominal  mus- 
cles are  firmly  contracted.  As  the  pain  is  increased  by  pressure  or 
movement,  the  patient  lies  upon  the  back  with  the  knees  draAvn  up, 
in  order  to  minimize  the  tension  of  the  abdominal  walls  ;  the  respira- 
tion is  costal,  and  talking,  coughing,  vomiting,  and  straining  to 
empty  the  bladder  or  bowel  are  avoided,  so  far  as  possible,  because 
contraction  of  the  diaphragm  is  painful.  The  vomiting  is  usually 
persistent,  first  of  the  stomach  contents,  then  of  yellowish  bile-con- 
taining fluid,  finally,  of  a  greenish  fluid.  Very  seldom  the  vomitus 
is  brownish  black,  with  an  odour  suggestive  of  a  faecal  origin.  Con- 
stipation is  usual,  but  a  brief  initial  diarrhoea  may  occur.  The  pulse 
is  rapid  (110  to  160),  small,  often  wiry;  the  respirations  are  acceler- 
ated (30  to  40).  In  extremely  severe  cases  the  temperature  may  be 
normal  or  subnormal ;  ordinarily  it  is  moderately  elevated ;  exception- 
ally, and  especially  at  the  onset,  it  may  be  high  (104°  to  105°),  with  a 
cool  surface.  The  urine  is  scanty,  high  coloured,  and  contains  a 
large  excess  of  indican.  There  may  be  frequent  urination,  less  com- 
monly retention.  More  or  less  marked  symptoms  of  collapse  often 
become  manifest  at  an  early  period.  The  gray  face  bears  an  expres- 
sion of  anxiety,  the  nose  is  pinched,  the  eyes  sunken,  the  cheeks  col- 
lapsed, and  the  lips  cyanotic.  The  skin  is  cool  and  clammy,  the 
hands  and  feet  cold  and  wet. 
54 


822  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Physical  examination  reveals  in  the  majority  of  cases  a  rigid,  mo- 
tionless, greatly  distended  abdomen,  universally  tympanitic  on  per- 
cussion. In  rare  instances,  particularly  if  the  abdominal  muscles  are 
strong  and  well-developed,  there  may  be  a  flat  and  rigid  abdomen 
throughout  the  course  of  the  disease.  Prolonged  auscultation  shows^ 
in  consequence  of  intestinal  paresis,  an  absence  of  the  usual  gurgling 
or  splashing  sounds,  and  possibly  the  presence  of  friction  sounds 
during  respiration.  If  the  meteorism  is  sufficiently  great  the  splenic 
dulness  is  obliterated ;  so  also  with  hepatic  dulness,  except  in  the 
midaxillary  line,  at  which  point  it  may  still  be  found.  If  the  re- 
maining hepatic  dulness  disappears  when  the  patient  is  turned  on 
the  left  side  the  presence  of  free  air  or  gas  in  the  peritoneal  cavity 
(pneumo-peritoneum)  may  be  inferred.  Owing  to  the  upward  press- 
ure upon  the  diaphragm  the  apex  beat  may  be  found  in  the  4th  in- 
terspace, farther  to  the  left  than  normal.  If  the  patient  lives  long 
enough  the  signs  of  peritoneal  effusion  become  manifest. 

Duration  and  Prognosis. — Usually  terminates  in  death  from  ex- 
haustion, the  duration  varying,  according  to  acuteness  and  severity,. 
from  2  to  10  days.  Cardiac  paralysis  is  occasionally  responsible  for 
a  sudden  lethal  ending. 

Diagnosis. — The  cardinal  symptoms  of  a  classical  case  are  sudden 
severe  abdominal  pain,  increasing  abdominal  distention,  tenderness, 
and  gradual  effusion,  with  persistent  vomiting,  fever,  and  symptoms 
of  collapse.  Always  suspect  and  look  for  evidences  of  appendicitis, 
especially  in  young  adults ;  for  puerperal  infection,  gonorrhoea,  sal- 
pingitis, ovarian  or  pelvic  abscess,  in  women ;  for  perforated  gastric 
ulcer ;  and  for  walking  typhoid  fever  with  perforation,  especially  in. 
young  and  vigorous  persons. 

The  diagnosis  is  at  times  extremely  difficult  if,  as  may  happen  in 
typhoid  fever,  or  when  the  patient  is  stuporous  or  comatose,  the 
symptoms  are  insidious  and  not  very  distinctive.  There  may  be  sim- 
ply an  increase  of  the  already  existing  meteorism,  a  more  marked 
tenderness,  and  an  intensification  of  the  evidences  of  collapse  or 
prostration,  with  perhaps  a  higher  level  of  temperature.  Occasional 
errors,  both  positive  and  negative,  are  inevitable.  The  following  dis- 
eases may  require  differentiation : 

(1)  Acute  Entero-colitis. — See  page  778. 

(2)  Intestiiial  Obstruction. — See  page  794. 

(3)  Embolism  of  the  Superior  Mesenteric  Artery. — See  page  797. 

(4)  Acute  Hemorrhagic  Pancreatitis. — See  page  817. 

(5)  Rupture  of  an  Ectopic  Gestation. — See  page  787. 

(6)  '■'■Hysterical  Peritonitis.''^ — This  neurosis,  which  in  several 
personal  cases  has  been  one  of  the  varying  features  of  mucous  colic 


DISEASES  OF  THE   PERITONEUM  S23 

(page  799),  may  exactly  simulate  true  diffuse  peritonitis  in  its  abrupt 
onset  with  severe  abdominal  pain  and  rigidity,  great  tenderness,  and 
marked  meteorism,  with  vomiting,  diarrhoea,  frequent  urination,  and 
even  evidences  of  collapse.  It  is  said  that  fever  may  also  be  present. 
If  characteristic  hysterical  symptoms  are  associated  the  diagnosis  is 
ordinarily  clear.  Otherwise  the  usual  absence  of  fever,  the  exag- 
gerated intensity  of  the  local  signs  in  comparison  with  the  general 
condition,  and  a  final  recovery,  will  suggest  the  neurotic  nature  of 
the  affection.  Recurrences  may  take  place.  Nevertheless  mistakes 
will  occur,  at  least  in  the  first  attack. 

II.  Acute  Localized  Peritonitis.  —The  symptoms  of  circum- 
scribed peritonitis  resemble  those  of  the  diffuse  form  except  in  de- 
gree. The  pain  and  tenderness  is  limited  to  the  neighbourhood  of 
that  part  of  the  peritoneum  which  is  involved ;  the  vomiting  and 
meteorism  may  be  slight  or  absent ;  constipation  is  usually  present, 
but  is  easily  overcome ;  and  the  collapse  symptoms  are  moderate  or 
slight.  If,  as  often  happens,  the  inflammatory  focus  is  walled  off 
from  the  general  peritoneal  cavity  by  protective  adhesions,  the  con- 
stitutional symptoms  may  disappear  and  the  local  signs  be  reduced 
to  those  indicative  of  adhesions  or  of  a  thick-walled  pus  sac — an 
encapsulated  abscess.  The  three  varieties  of  localized  peritonitis 
which  are  of  especial  interest  to  the  student  of  internal  medicine  are 
appendicular  abscess  (page  784),  pelvic  peritonitis  from  salpingitis  or 
ovaritis  (page  787),  and  suij^hrenic  peritonitis. 

Subphrenic  Peritonitis. — An  inflammation,  usually  suppurative, 
of  the  peritoneum  covering  the  right  and  left  lobes  of  the  liver,  or  of 
the  lesser  cavity  of  the  peritoneum,  together  with  that  of  the  adja- 
cent portions  of  the  diaphragm. 

{a)  Causes. — The  majority  of  subphrenic  abscesses  are  due  to  per- 
foration of  a  gastric  ulcer,  next  most  commonly  to  the  upward  exten- 
sion of  an  appendical  inflammation,  then  to  perforation  of  a  duodenal 
ulcer.  Less  frequently  the  origin  is  from  extension  of  a  pneumonic 
infection  or  perforation  of  an  empyema  through  the  diaphragm, 
malignant  disease  of  the  stomach  or  liver,  rupture  of  an  hepatic, 
perinephritic,  or  pancreatic  abscess,  diseases  of  the  gall  bladder,  or 
trauma.  The  majority  of  abscesses  due  to  perforation  of  a  gastric  or 
duodenal  ulcer  contain  air,  forming  a  subphrenic  pyopneumothorax. 

{b)  Symptoms.— k.&  the  great  majority  of  cases  are  due  to  perfora- 
tion of  a  gastric  ulcer  the  onset  is  usually  abrupt,  with  severe  epi- 
gastric or  hypochondriac  pain  and  tenderness ;  vomiting  usually  of 
bile-stained,  sometimes  of  bloody,  fluid ;  and  rapid,  embarrassed,  or 
painful  respiration.  Soon  afterward  the  symptoms  indicative  of  sup- 
puration become  manifest— chills,  sweats,  irregular  fever,  and  loss  of 


824  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

flesh  and  strength.  At  a  later  period  the  abscess  may  perforate  the 
diaphragm  into  the  pleural  cavity  and  establish  a  communication 
with  a  bronchus,  an  event  indicated  by  severe  and  paroxysmal  cough 
and  profuse  purulent  expectoration. 

The  physical  signs  are  very  often  perplexing.  Ordinarily  they 
simulate  those  of  an  empyema.  When  the  abscess  is  on  the  right 
side.,  lying  between  the  liver  and  diaphragm,  there  may  be  visible 
bulging  and  deficient  mobility  of  the  right  hypochondriac,  and  some- 
times of  the  epigastric,  region.  The  liver  is  pushed  downward,  its 
lower  edge  reaching  even  to  the  level  of  the  navel.  If  the  abscess 
does  not  contain  air  there  is  an  apparent  vertical  and  upward  increase 
of  hepatic  dulness,  perhaps  to  the  4th  rib,  above  which  is  normal  or 
slightly  tympanitic  pulmonary  resonance.  If  the  abscess  contains 
air  there  will  be  a  zone  of  tympanitic  percussion  between  the  area 
of  dulness  (or  flatness)  and  the  area  of  pulmonary  resonance ;  a 
change  in  the  posture  of  the  patient  will  alter  the  position  of  the 
line  of  flatness ;  and  a  succussion  sound,  limited  to  the  subdiaphrag- 
matic area  (Janeway),  may  be  heard  upon  shaking  the  thorax.  There 
is  an  absence  of  respiratory  murmur,  voice  sounds,  and  vocal  fremi- 
tus over  the  area  of  dulness  or  of  tympanicity ;  while  over  the  lung, 
which  is  compressed  by  pressure  transmitted  through  the  diaphragm, 
the  respiration  may  be  normal,  broncho-vesicular,  or  even  bronchial 
in  quality.  Friction  sounds,  due  to  an  associated  dry  or  fibrinous 
pleurisy,  may  be  heard  over  the  complementary  pleura.  These  phys- 
ical signs  may  lie  at  and  be  limited  to  a  lower  level  of  the  thorax 
than  one  would  expect  in  an  empyema,  a  finding  which,  if  present,  is 
a  somewhat  suggestive  fact  from  a  diagnostic  point  of  view ;  but  if 
there  is  a  large  amount  of  air  in  the  abscess  the  diaphragm  may  be 
pushed  up  to  the  3d  or  even  to  the  2d  rib,  with  physical  signs  exactly 
like  those  of  pneumothorax  {q.  v.). 

When  the  abscess  is  contained  in  the  lesser  peritoneal  cavity  and 
lies  between  the  diaphragm  above  and  the  spleen,  stomach,  and  left 
lobe  of  the  liver  below,  which  is  the  case  in  the  large  majority  of 
subphrenic  abscesses  caused  by  perforation  of  the  stomach  or  duo- 
denum, the  physical  signs  are  upon  the  left  side.  If  the  abscess  con- 
tains air  the  signs 'are  exactly  those  of  a  left  pneumothorax. 

If  the  lesser  cavity  contains  a  large  quantity  of  pus  (or  other 
fluid),  a  tumour  may  be  formed  in  the  left  hypochondriac,  epigas- 
tric, and  umbilical  regions.  The  colon  invariably  lies  below,  never 
above  or  in  front  of  the  tumour.  The  tumour  apparently  changes 
in  size  and  shape,  according  to  the  character  of  the  contents  of  the 
stomach,  which  latter  viscus  lies  between  the  fluid  collection  and 
the  anterior  abdominal  wall.     If  the  stomach  contains  fluid,  the  size 


DISEASES  OF  THE  PERITONEUM  825 

and  area  of  dulness  of  the  tumour  are  apparently  increased  ;  if  it  is 
distended  with  gas,  the  dulness  is  replaced  by  a  tympanitic  percus- 
sion sound  and  the  tumour  may  elude  palpation. 

Occasionally  milder,  fibrinous  and  non-suppurative,  perihepatic 
peritonitis  may  be  met  with,  occurring  in  the  course  of  acute  or 
chronic  inflammations  of  the  liver,  or  a  pleurisy,  or  following  a  blow, 
indicated  by  localized  moderate  pain  and  tenderness,  with  friction 
sounds  over  the  epigastrium  or  in  the  right  hypochondrium,  corre- 
sponding to  the  exposed  area  of  hepatic  dulness. 

(c)  Diagjiosis. — The  condition  is  obscure  and  often  escapes 
recognition.  It  is  usually  diagnosed  as  an  empyema,  pneumotho- 
rax, or  pyopneumothorax.  Elfusion  into  the  lesser  peritoneum  is 
frequently  judged  to  be  a  cyst  of  the  pancreas. 

Information  of  value  may  be  gleaned  from  the  history.  If  the 
earliest  symptoms  are  (upper)  abdominal  in  location  and  character 
(severe  pain,  vomiting),  the  presumption  leans  toward  a  subphrenic 
inflammation ;  if  thoracic  (cough,  pleuritic  pain)  it  points  toward 
an  empyema.  The  latter,  however,  may  cause  the  former  by  perfora- 
tion, or  per  contra.  In  suspected  cases  of  subphrenic  abscess  aspira- 
tion should  be  done  in  the  7th  or  8th  space  in  the  midaxillary  line. 
It  is  stated  that  if  the  fluid  flows  more  freely  during  inspiration  it  is 
indicative  of  its  location  below  the  diaphragm,  the  descent  of  which 
during  inspiration  increases  the  intra-abdominal  pressure  while  pro- 
ducing a  negative  intrathoracic  pressure. 

{d)  Terminations  and  Prognosis.— The  prognosis  of  subphrenic 
abscess  is  very  grave,  but  depends  largely  upon  an  early  recognition 
of  the  condition  and  prompt  operation.  In  rare  cases  the  pus  dis- 
charges by  way  of  the  abdominal  wall  or  the  lungs,  or  still  more 
infrequently  undergoes  absorptive  and  other  changes. 

III.  Chronic  Peritonitis. — Of  this  there  are  several  varieties: 
adhesive;  proliferative,  in  which  the  peritoneum  is  greatly  thick- 
ened, with  but  little  adhesion ;  cancerous ;  tuberculous,  and  hemor- 
rhagic.    The  process  may  be  local  or  general. 

(I)  Chronic  Local  Peritonitis.— This  is  usually  of  the  adhesive 
variety,  occurring  as  a  result  of  acute  or  chronic  inflammation  of  the 
abdominal  viscera,  mainly  of  the  spleen,  liver,  intestines  (especially 
the  appendix),  or  mesentery;  or  of  the  pelvic  organs.  The  points 
of  attachment  of  the  adhesions,  which  may  be  short,  or  long  and 
bandlike,  vary  according  to  the  locality  and  the  viscus  affected. 
Thus  the  spleen  and  liver  may  be  adherent  to  the  diaphragm,  and 
coils  of  intestine  to  each  other,  to  the  abdominal  wall,  or  to  the 
mesentery.  In  the  greater  proportion  of  cases  no  symptoms  arise. 
Intestinal  adhesions  may,  however,  cause  internal  strangulation  and 


826  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

obstruction,  or  give  rise  to  more  or  less  constant  and  severe  col- 
icky pain.  The  latter  condition,  if  correctly  diagnosed,  usually  by 
exploratory  operation,  may  be  relieved  by  separation  of  the  adhe- 
sions. 

(II)  Chronic  Diffuse  Peritonitis. — Causes. — Most  commonly  tuber- 
culous ;  less  often  a  sequel  of  acute  simple  inflammation ;  rarely 
cancerous ;  or  may  arise  from  chronic  cardiac,  hepatic,  or  intestinal 
disease.  The  proliferative  form  is  most  frequently  associated  with 
chronic  alcoholism,  occasionally  with  chronic  nephritis. 

Symptoms. — For  those  of  tuberculous  peritonitis,  see  page  732. 

The  disease  may  be  entirely  latent.  The  symptoms  are  often 
obscure  and  indefinite.  There  may  be  vague  abdominal  discomfort, 
burning  sensations,  or  actual  colicky  pain,  either  with  constipation 
or  diarrhoea.  There  may  be  irregular  slight  fever,  with  loss  of  flesh 
and  strength.  More  or  less  ascites,  or  one  or  more  collections  of 
encysted  fluid,  may  be  present ;  and  occasionally  there  is  jaundice 
from  pressure  upon  the  common  bile  duct.  As  in  acute  peritonitis, 
but  in  lesser  degree,  there  may  be  abdominal  distention  with  rigidity. 
Sacs  of  fluid  and  adherent  intestinal  coils  may  cause  tumourlike 
masses ;  and  the  omentum  may  be  rolled  and  puckered  into  a  trans- 
verse cylindrical  mass  between  the  stomach  and  the  colon.  The 
physical  signs  are  obviously  variable,  and  the  exact  significance  of 
the  dull  or  tympanitic,  ill-defined  swellings,  which  may  be  found,  is 
often  diflBcult  to  determine. 

IV.  Carcinoma  of  the  Peritoneum. — This  is  usually  second- 
ary to  malignant  disease  of  the  liver,  stomach,  or  pelvic  viscera; 
much  less  frequently  it  is  primary. 

Symptoms. — These  are  a  persistent  ascites  with  loss  of  flesh  and 
cachexia.  Fever  may  or  may  not  be  present.  If  the  abdominal 
effusion  is  moderate  or  is  removed  by  tapping,  multiple,  somewhat 
large,  irregular  nodules  may  be  found  by  palpation ;  so  also  the 
transverse  roll  of  puckered  omentum,  although  this  occurs  as  well  in 
tuberculous  and  proliferative  peritonitis.  Secondary  umbilical  nod- 
ules or  hardening  may  be  present,  and  the  inguinal  glands  may  be 
implicated.  The  fluid  may  be  hemorrhagic  and  contain  significant 
cells  or  cell  groups. 

Diagnosis. — If  there  is  primary  malignant  disease  of  the  stomach, 
liver,  uterus,  ovaries,  or  rectum  (for  which  search  should  always  be 
made),  the  nature  of  the  peritoneal  involvement  is  evident.  If, 
however,  the  peritoneum  is  primarily  affected,  and  no  antecedent 
local  carcinoma  can  be  found,  the  diagnosis  becomes  difficult  or  im- 
possible, as  the  physical  signs  previously  described  are  common  to 
chronic  peritonitis,  whether  carcinomatous,  tuberculous,  or  prolifer- 


DISEASES  OF   THE  PERITOKEUM  827 

ative,  or  to  hydatids  of  the  peritoneum.  Carcmomatous  disease  oc- 
curs usually  in  persons  past  middle  life  ;  there  is  a  marked  cachexia ; 
and  nodules  or  indurations  about  the  navel,  or  enlargement  and  indu- 
ration of  the  inguinal  glands,  point  to  carcinoma.  Tuberculous  peri- 
tonitis occurs  mainly  in  children  or  before  middle  life ;  the  cachexia 
is  not  marked,  suppurative  inflammation  of  the  navel,  with  a  fistu- 
lous opening,  is  more  common  than  induration,  and  evidences  of 
tuberculous  disease  may  be  found  elsewhere.  Hydatids  of  the  perito- 
neum may  exactly  simulate  the  numerous  nodules  of  carcinoma,  and, 
unless  hydatid  fremitus  can  be  obtained  or  the  aspirated  fluid  con- 
tains booklets,  the  diagnosis  may  be  difficult  or  impossible. 

V.  Ascites. — Causes. — Pressure  upon  the  end  branches  of  the 
portal  vein  within  the  liver,  as  in  hepatic  cirrhosis,  syphilis,  carci- 
noma, or  chronic  passive  congestion ;  or  upon  the  vein,  before  it 
enters  the  liver,  by  new  growths,  carcinoma,  abscess,  or  chronic 
peritonitis  involving  the  transverse  fissure  or  gastro-hepatic  omen- 
tum ;  or  pressure  by  aneurism,  abdominal  or  ovarian  tumours,  or  the 
enlarged  spleen  of  leucaemia  or  malaria ;  and  chronic  simple,  tuber- 
culous, or  carcinomatous  peritonitis.  Ascites  may  be  a  part  of  a 
general  cedema  due  to  chronic  cardiac  disease,  pulmonary  cirrhosis 
or  emphysema,  nephritis,  anaemia,  or  the  malarial,  cancerous,  or  syphi- 
litic cachexiae. 

Character  of  the  Fluid. — The  fluid  may  be  hemorrhagic  in  tuber- 
culosis and  carcinoma  of  the  peritoneum,  occasionally  in  cirrhosis. 
In  non-inflammatory  ascites  the  fluid  usually  has  a  sp.  g.  of  1.015  or 
below,  with  2.5  per  cent  or  less  of  albumin  ;  in  peritonitis,  1.018  or 
over,  with  4.5  per  cent  or  more  of  albumin.  Chylous  or  chyloid 
ascites  (page  651)  occurs  in  carcinoma,  perforation  of  the  thoracic 
duct,  filariasis,  and  perhaps  under  an  exclusive  milk  diet  (Osler). 

Diagnosis. — See  page  433. 

VI.  Retroperitoneal  Sarcoma.— According  to  the  summary 
by  Steele,  Lobstein's  cancer  occurs  more  frequently  in  males  (6 
to  4) ,  either  during  the  first  10  years  of  life  or  between  40  and  50 
years  of  age.  In  90  per  cent  of  the  cases  the  tumour  (rarely  larger 
than  a  man's  head)  originates  in  the  lumbar  region  or  the  central 
portion  of  the  posterior  abdominal  wall  at  the  attachment  of  the 
mesentery. 

(rt)  Symptoms.— These  at  first  consist  of  indefinite  digestive  dis- 
turbances, such  as  constipation,  diarrhoea,  nausea,  anorexia,  colicky 
pains,  or  dragging  sensations  in  the  abdomen.  Later  there  are 
oedema  and  neuralgic  pains  in  the  legs,  genitalia,  abdominal  walls, 
and  lumbar  region  (at  first  unilateral),  and  due  to  pressure  upon  the 
iliac  veins  and  the  sacral  and   lumbar  plexuses.     Finally,  cachexia 


828  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

and  the  evidences  of  partial  or  complete  obstruction  of  the  small  in- 
testine become  manifest. 

Physical  Signs. — At  first  it  is  simply  possible  to  recognise  the 
presence  of  a  deep-seated  tumour,  but  as  the  growth  increases  in 
size  the  colon  (inflated,  if  necessary)  will  be  recognised  to  lie  upon 
its  anterior  surface.  The  tumour  may  be  central,  lying  in  mid- 
abdomen,  or  be  found  to  the  right  or  left  of  the  median  line,  and 
may  fluctuate  and  be  movable  or  move  with  respiration,  but  is  or- 
dinarily immovable  and  solid.  In  central  tumours  there  is  a  dull 
area  surrounded  by  a  zone  of  tympany. 

{h)  Diagnosis. — (Edema  of  the  legs  and  neuralgic  pain  in  the 
legs  and  lumbar  region,  evidences  of  intestinal  obstruction,  the  find- 
ing of  a  tumour  at  or  to  one  side  of  the  navel,  and  the  presence  of 
the  colon  over  the  anterior  surface  of  the  neoplasm,  indicate  the 
retroperitoneal  origin  of  the  latter.  The  rapid  growth  of  the  tumour 
(average  duration  between  8  and  9  months)  and  the  appearance  of 
cachexia  indicate  its  malignant  nature.  It  is  often  impossible, 
especially  in  the  later  stages,  to  distinguish  retroperitoneal  sarcoma 
from  tumours  of  the  kidney  and  suprarenal  capsules  or  other 
growths  lying  behind  the  peritoneum,  except  by  an  exploratory 
incision. 


SECTION  in 
DISEASES   OF   THE   RESPIRATOEY  SYSTEM 

{See,  in  Part  I,  Larynx  {pages  238  to  2JtS) ;  Voice  {pages  2^3  to  246) ;  Congh  {pages 

256  to  259) ;  Sputum  {pages  259  to  263  and  pages  596  to  603) ;  Physical 

Examination  of  Lungs  and  Pleurce  {pages  382  to  422) 

I.   DISEASES   OF  THE   NOSE 

{See  also  pages  211  to  218) 

I.  Acute  Nasal  Catarrh. — {a)  Causes. — An  acute  coryza  or 
rhinitis  may  be  an  initial  symptom  of  an  infection  like  influenza  or 
measles;  more  commonly  it  is  primary — a  "cold  in  the  head."  Its 
epidemic  and  contagious  character  is  so  marked  that  it  probably 
depends  upon  germ  infection.  The  chief  predisposing  causes  are 
exposure  to  cold,  variable  weather,  and  inhalation  of  irritating 
vapours. 

(J)  Symptoms. — There  is  chilliness,  headache,  slight  fever  (100° 
to  101°),  and  sneezing,  with  quickened  pulse,  dry  skin,  and  thirst. 
Some  backache  and  general  aching  are  not  uncommon.     The  nasal 


DISEASES  OF  THE  NOSE  §29 

mucous  membrane  swells  so  that  mouth-breathing  is  imperative,  and 
there  is  a  thin  acrid  discharge  from  the  nostrils.  The  eyes  water, 
the  senses  of  smell  and  taste  are  impaired,  the  pharynx  is  reddened, 
the  throat  is  sore  and  the  neck  stiff,  and  slight  dysphagia  may  be 
present.  Herpes  of  the  nose  and  lips  is  common.  The  larynx  may 
be  involved,  causing  hoarseness ;  the  trachea  and  bronchi,  cough ; 
the  Eustachian  tubes,  slight  deafness.  In  a  day  or  two  the  nasal 
discharge  increases,  becomes  thicker  and  muco-purulent,  and  in  5  or 
6  days  the  swelling  of  the  mucosa  and  the  associated  symptoms  sub- 
side.    The  coryzal  discharge  persists  for  a  week  or  two  longer. 

(c)  Diagnosis. — Ordinarily  easy,  but  the  possibility  that  it  is  the 
initial  coryza  of  measles  or  influenza  is  to  be  borne  in  mind. 

II.  Chronic  Nasal  Catarrh. — Caused  by  recurring  attacks 
of  acute  coryza,  syphilis,  rarely  tuberculosis.  Three  forms  may  be 
recognised  :  simple,  hypertrophic,  and  atrophic. 

Symptoms. — (a)  Simple  Chronic  Catarrh. — There  is  a  special 
liability  to  "  catching  cold,"  the  mucous  membranes  readily  become 
congested  and  swollen,  with  consequent  occasional  stenosis,  and 
there  is  an  overabundant  thick  secretion.  If  this  condition  persists 
it  becomes : 

(b)  Hy2)ertrophic  Rhinitis. — The  lower  turbinals  are  swollen  and 
enlarged,  there  is  constant  hawking  to  remove  the  thick  secretion 
from  the  upper  pharynx,  and  the  patient  becomes  a  mouth-breather 
to  a  varying  extent.  In  the  majority  of  cases  the  pharyngeal  mucosa 
and  adenoid  tissues  are  coincidently  affected,  constituting  a  chronic 
naso-pharyngeal  catarrh.  The  voice  becomes  nasal,  and  varying  de- 
grees of  deafness  are  common.  (See  also  Mouth-Breathing,  page 
163;  Adenoids,  page  756;  and  Chronic  Pharyngitis,  page  754.) 

(c)  Atrophic  Rhinitis. — This  may  be,  but  is  by  no  means  neces- 
sarily, a  sequence  of  the  hypertrophic  form.  The  horrible  and  dis- 
gusting odour  (ozena),  which  is  the  principal  symptom  of  the  dis- 
ease, is  met  with  also  as  an  evidence  of  syphilis,  disease  of  the  nasal 
bones,  glanders,  and  foreign  bodies.  The  sense  of  smell  is  abolished. 
On  inspection,  the  nasal  mucosa  is  seen  to  be  shrunken  and  atrophied, 
with  a  resultant  unusual  roominess  of  the  nasal  chambers.  The 
thick  purulent  secretion  coating  the  membrane  dries  into  yellowish- 
green  adherent  crusts,  which  emit  the  offensive  odour. 

III.  Hay  Fever.— («)  Causes.— A  neurotic  idiosyncrasy  must 
be  predicated,  together  with  an  unusually  irritable  nasal  mucosa. 
The  exciting  causes  are  many,  comprising  the  pollen  of  various 
plants,  dusts,  emanations  from  feathers,  etc.;  and  occasionally  a 
strong  suggestion  appears  to  be  a  causative  factor.  According  to 
season  two  forms  have  been  recognised  :  the  "  June  "  or  "  rose  "  cold 


8^  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

in  the  spring,  and  the  "  hay  asthma  "  or  "  hay  fever  "  which  occurs 
during  August  and  September. 

(b)  Symptoms. — The  disease  begins  suddenly,  and  often  shows  a 
curious  punctuality  in  the  date  of  its  annual  recurrences.  The 
symptoms  are  those  of  a  severe  coryza  with  a  profuse  watery,  rarely 
muco-purulent,  discharge.  The  eyes  are  reddened  and  watery,  with 
itching  lids.  The  senses  of  taste,  smell,  and  hearing  are  much  im- 
paired. Cough,  sometimes  very  severe,  and  excited  by  a  tickling 
sensation  in  the  larynx  and  pharynx,  is  a  frequent  concomitant. 
There  may  be  slight  chilliness,  fever,  disturbed  sleep,  poor  appetite, 
and  a  sense  of  weakness.  Not  infrequently  attacks  occur  which  are 
identical  with  bronchial  asthma;  or  the  asthmatic  attack  may  alter- 
nate with  the  coryza.  The  symptoms  vary  from  day  to  day  in  sever- 
ity, and  the  entire  attack  usually  covers  from  4  to  6  weeks. 

IV.  Epistaxis. — See  page  215. 

II.    DISEASES    OF   THE    LARYNX 

(See  also  pages  238  to  S43,  243  to  246,  arid  256  to  259) 

I.  Acute  Catarrhal  Laryngitis. — («)  Causes. — Cold,  excess- 
ive use  of  the  voice,  inhalation  of  irritating  vapours,  injury,  foreign 
bodies,  swallowing  of  corrosive  poisons  or  very  hot  fluids.  May  be 
primary,  more  commonly  associated  with  an  acute  naso-pharyngeal 
catarrh. 

{h)  Symptoms. — The  voice  is  hoarse,  husky,  or  completely  lost ; 
there  is  a  sensation  of  tickling  in  the  larynx,  with  a  frequent  dry 
cough ;  and  there  may  be  a  feeling  of  constriction  with  moderate 
dysphagia,  and  slight  tenderness  on  grasping  the  larynx.  Examina- 
tion shows  a  reddened  and  swollen  laryngeal  mucosa,  affecting  par- 
ticularly the  ary-epiglottic  folds.  The  vocal  cords  are  pinkish, 
swollen,  and  lack  their  normal  mobility.  A  moderate  mucous  secre- 
tion coats  the  affected  portions.  In  rare  instances  oedema  of  the 
glottis  may  supervene.  As  a  rule  there  is  but  slight  fever.  Very 
severe  cases  may  present  marked  dysphagia,  incessant  and  distressing 
cough,  and  intense  dyspnoea. 

(c)  Diagnosis. — Ordinarily  the  diagnosis  is  easy,  particularly  if 
the  patient  is  of  an  age  to  permit  a  laryngoscopic  examination.  The 
latter  will  rule  out  nervous  aphonia  and  glottic  oedema. 

II.  Acute  Laryngitis  with  Spasm  of  the  Glottis.— In  the 
vast  majority  of  instances  it  is  this  condition  which  in  children  con- 
stitutes "spasmodic  croup,"  the  laryngitis  occurring  alone  or  as  a 
part  of  an  acute  naso-pharyngeal  catarrh.  The  spasmodic  attack 
almost  always  occurs  after  the  first  sleep,  and  in  many  cases  is  pre- 
ceded by  the  symptoms  of  a  slight  "  cold."    Usually  between  10  and 


DISEASES  OP  THE  LARYNX  831 

12  P.  M.  the  child  awakes  with  a  brazen,  croiipy  cough,  husky  or 
whispering  voice,  dyspnoea,  stridulous  respiration,  congested  face, 
and  great  restlessness.  Under  treatment  the  spasmodic  element  sub^ 
sides,  the  child  falls  asleep  and  wakes  the  next  morning  either  well 
or,  as  is  more  commonly  the  case,  still  with  a  croupy  cough  and 
other  evidences  of  a  mild  catarrh  of  the  larynx.  The  attacks  may 
recur  with  diminishing  intensity  for  3  or  4  subsequent  nights. 

It  seldom  happens  that  laryngismus  stridulus  is  mistaken  for 
spasmodic  croup,  as  in  the  former  there  is  an  absence  of  fever, 
corjza,  and  antecedent  hoarseness ;  but  in  the  absence  of  patches  on 
the  pharynx,  swollen  cervical  glands,  and  a  satisfactory  inspection 
(difficult  or  impossible  in  infants  and  very  young  children),  it  may 
be  hard  to  exclude  membranous  or  diphtheritic  laryngitis  except  by 
the  lapse  of  time,  which  in  the  latter  case  will  disclose  the  signs  of  a 
progressive  laryngeal  stenosis.  I  have  seen  a  case  of  scarlet  fever 
requiring  intubation,  and  another  of  severe  catarrhal  laryngitis  re- 
quiring tracheotomy,  but  in  neither  of  which  was  there  oedema  or 
false  membrane. 

III.  Ckronic  Laryngitis.— (a)  Causes.— Eesvilts  from  repeated 
acute  attacks,  especially  in  those  who  speak  much  in  public  or  in  the 
open  air ;  too  much  smoking ;  and  chronic  alcoholism. 

(5)  Symptofns.— The  voice  is  husky,  hoarse,  or  rough,  and  in 
severe  cases  an  almost  complete  aphonia  may  occur.  Cough  is  usu- 
ally present,  either  slight  or  severe  and  paroxysmal,  and  is  due  to  a 
frequent  sensation  of  irritation  or  tickling  in  the  larynx.  Rarely  is 
there  pain.  It  is  often  associated  with  chronic  pharyngitis,  and  may 
be  caused  by  nasal  stenosis.  Laryngoscopic  examination  will  show 
a  slightly  swollen  and  but  moderately  reddened  mucous  membrane, 
with  distention  of  the  mucous  glands  of  the  epiglottis  and  ventricles. 
Superficially  eroded  spots  are  occasionally  seen. 

IV.  (Edema  of  the  Larjmx.— («)  Causes. — Very  rarely  it  fol- 
lows acute  laryngitis.  It  occurs  in  connection  vrith  erysipelas,  diph- 
theria, scarlet  fever,  typhus  and  typhoid  fevers,  and  acute  phlegmo- 
nous inflammations  of  the  pharynx,  neck,  and  floor  of  the  mouth ; 
syphilitic  or  tuberculous  laryngitis ;  with  the  general  oedema  of  acute 
or  chronic  nephritis  and  chronic  heart  disease  ;  or  from  pressure  by 
intra-thoracic  growth  or  aneurism. 

(h)  Symptoms. — The  chief  symptom  is  a  rapidly  developing  dysp- 
noea, with  increasing  huskiness  and  final  extinction  of  the  voice. 
The  respiration  may  be  stridulous. 

(c)  Diagnosis. — In  addition  to  the  presence  of  one  of  the  causa- 
tive affections  and  the  quick  oncoming  of  dyspnoea,  the  laryngoscope, 
or  palpation,  or  even  simple  inspection  with  the  tongue  fully  de- 


832  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

pressed,  will  reveal  great  swelling  of  the  epiglottis  and  ary-epiglottic 
folds.  The  condition  is  very  fatal  in  the  absence  of  prompt  surgical 
treatment. 

V.  Tuberculous  Liaryngitis. — In  the  great  majority  of  cases 
this  is  secondary  to  pulmonary  tuberculosis,  with  which  it  occurs  as  a 
complication  in  from  18  to  30  per  cent. 

(«)  Symptoms. — The  earliest  symptom  is  a  huskiness  or  hoarse- 
ness of  the  voice,  which  may  eventuate  in  aphonia  and  mere  whis- 
pering. Sooner  or  later  there  is  dysphagia,  Avhich  may  be  so  marked 
that  any  attempt  to  swallow  causes  excruciating  pain,  perhaps  cough 
and  suffocation.  Cough  is  frequent,  ineffectual,  and  painful.  The 
severer  symptoms  are  seen  particularly  when  there  is  extensive 
ulceration  and  destruction  of  the  epiglottis  and  ulceration  in  the 
pharynx.  In  the  early  stage  the  mucous  membrane  of  the  larynx  is 
thickened  and  pale ;  later,  the  broad,  gray,  ill-defined  tuberculous 
ulcers  appear,  particularly  on  the  posterior  surface  of  the  epiglottis, 
the  ary-epiglottic  folds,  the  false  and  the  true  cords.  The  latter 
are  thickened  and  eroded. 

{V)  Diagnosis. — In  the  presence  of  ascertained  pulmonary  tuber- 
culosis the  diagnosis  of  tuberculous  laryngitis  is  rarely  difficult.  If 
the  lung  symptoms  are  indefinite  it  may  be  confused  with  syphilitic 
laryngitis,  but  the  absent  history  of  the  latter  disease,  the  negative 
result  of  the  therapeutic  test  (mercury  and  iodides),  and  the  finding 
of  tubercle  bacilli  in  some  of  the  secretion,  which  may  be  removed 
from  the  ulcers  if  necessary,  will  decide  its  tuberculous  nature. 

VI.  Syphilitic  Laryngitis. — This  is  a  frequent  secondary  or 
tertiary  symptom,  and  occurs  also  in  the  hereditary  form. 

[a)  Symptoms. — These  are  hoarseness,  aphonia,  and  dysphagia.  If 
secondary,  the  lesion  is  an  erythema,  perhaps  with  superficial  ulcera- 
tion and  the  evidences  of  a  mild  catarrhal  laryngitis.  If  tertiary, 
small  submucous  gummata  are  present,  which  may  ulcerate  deeply, 
often  causing  necrosis  and  exfoliation  of  the  laryngeal  cartilages,  or 
slowly  heal.  In  either  case  the  contraction  of  the  resulting  scar  or 
fibrous  tissue  may  produce  stenosis  of  the  larynx. 

(Z»)  Diagnosis. — This  depends  upon  the  history  and  especially 
upon  the  coexisting  evidences  of  the  causative  disease  (see  also  V 
preceding).  The  laryngeal  lesions  of  inherited  syphilis  appear  in  the 
majority  of  cases  within  the  first  year  of  life ;  less  commonly  at  12  to 
15  years  of  age. 

VII.  Tumours  of  the  Larynx. — A  tumour  of  the  larynx 
should  be  remembered  as  a  possible  cause  of  hoarseness,  aphonia,  or 
other  alterations  in  the  voice ;  or  of  cough,  dyspnoea  (sometimes 
sudden),  and  dysphagia.     Laryngoscopic  examination  will  reveal  the 


DISEASES  OP  THE  LARYNX  AND  BRONCHI  833 

growth,  seated  as  a  rule  upon  the  vocal  cords.     As  the  treatment  is 
surgical,  special  works  should  be  consulted  for  further  information. 

VIII.  Laryngismus  Stridulus.— A  spasm  of  the  laryngeal 
adductors  occurring  in  children  usually  between  6  months  and  5  years 
of  age.  It  is  unattended  by  cough,  hoarseness,  or  other  evidence  of 
laryngitis,  and  is  a  neurosis,  seen  most  commonly  in  association  with 
rickets,  less  frequently  with  tetany  {q.  v.).  At  one  time  it  was  pre- 
sumed to  be  due  to  enlargement  of  the  thymus  gland,  and  was  called 
"  thymic  asthma."  It  is  to  be  distinguished  from  the  spasm  of  the 
glottis  which  may  occur  in  connection  with  many  laryngeal  affections. 
In  popular  parlance  it  is  variously  called  "  holding  the  breath,"  "  fit 
of  passion,"  or  "child-crowing." 

The  attack  comes  on  often  as  the  child  wakes  from  sleep,  either 
at  night  or  in  the  daytime.  The  breathing  ceases,  the  face  becomes 
congested  and  cyanotic,  and  the  seizure  terminates  suddenly  with  a 
high-pitched  crowing  inspiration.  There  may  be  convulsive  move- 
ments of  the  hands  and  feet  (carpo-pedal  spasm),  or,  less  frequently, 
general  convulsions.  The  paroxysm  may  be  repeated  a  number  of 
times  during  24  hours.  Death  during  the  attack  is  a  very  rare  con- 
sequence. The  absence  of  coryza,  cough,  hoarseness,  or  fever,  together 
with  the  character  and  frequency  of  the  attacks,  will  serve  to  sepa- 
rate it  from  spasmodic  croup. 

IX.  Paralyses  of  the  Larynx.— See  pages  240  to  243. 

III.    DISEASES    OF  THE    BRONCHI 

I.  Acute  BroncMtis. — Acute  catarrhal  inflammation  of  the 
bronchial  mucosa  is  usually  bilateral,  and  affects  mainly  the  first  and 
second  divisions  of  the  tubes.  It  is  often  epidemic,  and  probably 
due  to  a  microbic  infection.  Affecting  the  bronchioles  ("  capillary 
bronchitis  "),  it  is  simply  a  part  of  a  broncho-pneumonia. 

(a)  Causes. — Usually  a  downward  extension  of  an  acute  naso- 
pharyngeal catarrh  caused  by  cold,  and  occurs  as  a  symptom  in 
influenza,  measles,  typhoid  fever,  malaria,  pertussis,  and  bronchial 
asthma.  Very  young,  elderly,  and  debilitated  persons  are  particu- 
larly liable ;  so  also  are  certain  individuals. 

(b)  Symptoms.— Usually  there  is  a  coryza,  with  chilliness,  slight 
hoarseness,  soreness  of  the  throat,  a  feeling  of  weakness  and  oppres- 
sion, and  some  general  aching  of  the  back  and  limbs.  There  is  slight 
fever  (100  °  to  101  °  ),  but  in  severe  cases  it  may  rise  to  103  °,  with  a  cor- 
responding frequency  of  the  pulse.  The  bronchitic  symptoms  proper 
are  substernal  soreness,  rawness,  tightness  or  oppression ;  cough,  at 
first  dry,  rough,  and  irritating,  often  occurring  in  severe  paroxysms, 


834  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

and  by  its  violence  causing  muscular  pain  and  soreness  along  the 
costal  margins.  In  from  one  to  three  or  four  days  the  cough  loosens 
and  expectoration  appears,  at  first  scanty  and  mucous,  later  abun- 
dant and  muco-purulent,  with  great  relief  to  the  patient. 

The  breathing,  except  in  children  or  in  severe  cases  with  fever  in 
adults,  is  not  increased  in  rapidity,  and  there  is  rarely  dyspnoea 
unless  the  smaller  tubes  are  involved.  Palpation  and  percussion  are, 
as  a  rule,  negative.  Auscultation  in  the  initial  stage  reveals  sibilant 
and  sonorous  rales,  which  in  the  stage  of  abundant  secretion  are 
replaced  by  fine  and  coarse  moist  or  bubbling  rales.  The  breath 
sounds  may  be  somewhat  harsh. 

(c)  Course  and  Duration. — In  otherwise  healthy  adults  the  fever 
disappears  within  a  week,  and  at  the  end  of  two  weeks  convalescence 
is  established,  although  a  moderate  loose  cough  and  expectoration 
may  persist  for  a  week  or  two  longer.  But  in  the  very  old,  the  very 
young,  or  in  persons  debilitated  from  any  cause,  the  inflammation  may 
extend  to  the  bronchioles  and  air  cells  constituting  a  broncho- 
pneumonia (page  844). 

{d)  Differential  Diagnosis. — At  the  onset,  in  sudden  and  severe 
cases,  bronchitis  may  simulate  lobar  pneumonia,  but  the  absence  of 
the  physical  signs  of  consolidation,  as  well  as  the  milder  grade  of 
disturbance,  will  soon  decide  against  the  graver  disease.  The  de- 
velopment of  broncho-pneumonia  during  the  course  of  an  acute 
bronchitis  is  usually  indicated  by  the  finding  of  numerous  fine  and 
subcrepitant  rales,  with  patches  of  slight  dulness  and  weak  or  distant 
bronchial  breathing,  especially  at  the  bases  of  the  lungs.  It  is  well 
to  bear  in  mind  that  an  acute  bronchitis  may  be  the  initial  symptom 
of  measles  or  pertussis.  The  physical  signs  of  acute  miliary  tuber- 
culosis of  the  lungs  may  at  the  beginning  closely  resemble  those  of 
an  acute  bronchitis. 

II.  Chronic  Bronchitis. — This  is  usually  associated  with  em- 
physema, and  not  uncommonly  there  are  dilatations  of  the  bronchial 
tubes  (bronchiectases). 

{a)  Causes. — Occasionally  due  to  repeated  attacks  of  acute  bron- 
chitis, but  occurs  much  more  commonly  as  a  result  of  chronic  valv- 
ular disease,  chronic  alcoholism,  rheumatism,  gout,  chronic  nephri- 
tis, syphilis,  chronic  pulmonary  disease,  or  aortic  aneurism.  It  affects 
mainly  elderly  persons,  and  the  symptoms  are  aggravated  during  the 
winter  months. 

{h)  Varieties. — Certain  clinical  varieties  are  recognised. 

(1)  The  most  common  form  occurs  in  elderly,  often  gouty,  men, 
and  is  associated  with  emphysema,  heart  disease,  arteriosclerosis,  and 
highly  acid  urine  containing  a  trace  of  albumin.     The  cough  may 


DISEASES  OF  THE   BRONCHI  835 

occur  only  in  the  morning  or  at  night,  with  free  expectoration.    The 
general  health  may  be  unimpaired  for  years. 

(2)  Dry  catarrh  occurs  in  elderly  persons,  is  associated  with  em- 
physema and  characterized  by  violent  paroxysms  of  cough,  with  no, 
or  but  little  and  tenacious,  expectoration. 

(3)  Bronchorrhcea,  a  profuse  watery  or  thin  and  purulent,  rarely 
thick,  expectoration,  may  attend  chronic  bronchitis  in  the  old  or  the 
young,  and  in  the  former  may  be  ultimately  associated  with  bronchi- 
ectasis and  putrid  bronchitis. 

(4)  A  form  of  chronic  bronchitis  occurring  particularly  in  women 
has  been  described  by  Osier.  It  comes  on  between  20  and  30  years  of 
age,  and  may  persist  without  impairment  of  the  general  health. 

(c)  Symptoms. — Cough,  frequently  paroxysmal,  worse  in  the  morn- 
ing and  at  night,  is  the  most  constant  symptom,  often  disappearing 
in  summer  and  returning  in  the  winter.  The  amount  of  expectora- 
tion yaries;  rarely  there  is  none,  more  commonly  it  is  more  or  less 
abundant  and  muco-purulent  or  decidedly  purulent,  occasionally 
thin  and  serous.  Fever  is  rarely  present,  and  substernal  pain  is 
uncommon!  although  there  may  be  soreness  along  the  costal  margins 
if  the  cough  is  violent  and  paroxysmal.  There  may  be  some  dysp- 
noea on  exertion. 

The  physical  examination  usually  shows  an  enlarged  chest  with 
deficient  expansion,  due  to  associated  emphysema.  The  percussion 
note  is  normal,  hyperresonant,  or  slightly  tympanitic.  Auscultation 
reveals  prolonged,  usually  low-pitched  and  wheezy,  expiration  over 
both  lungs,  with  bilateral  fine  and  coarse,  dry  and  moist,  rales.  Ex- 
ceptionally there  may  be  slight  dulness  or  impaired  resonance  with 
fine  crepitations  at  the  bases,  due  to  a  certain  amount  of  oedema 
and  passive  congestion.  The  physical  signs  in  some  cases  may  be 
negative. 

{d)  Diagnosis.— This  is  usually  easy.  The  heart,  arteries,  and 
urine  should  be  examined  in  order  to  ascertain  whether  the  bron- 
chitis is  secondary  to  cardio-vascular  or  renal  disease. 

'There  are  certain  cases  which  suggest  pulmonary  tuberculosis, 
but  the  discrimination  can  generally  be  made  by  the  absence  of  the 
fever,  circumscribed  consolidation,  and  emaciation,  which  attend 
phthisis,  as  well  as  a  failure  to  find  tubercle  bacilli  in  the  sputum. 

III.  Putrid  Bronchitis.— (a)  Causes.— In  rare  cases  this  is 
primary,  following,  or  alternating  with,  a  chronic  bronchitis,  but  in 
the  large  majority  of  instances  it  is  indicative  of  bronchiectasis,  gan- 
grene, abscess,  empyema  with  perforation  of  the  lung,  pulmonary 
actinomycosis,  or  decomposition  of  the  material  contained  in  phthis- 
ical cavities. 


836  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

(b)  Symptoms. — The  sputum  has  a  fetid  and  disgusting  odour, 
is  usually  copious,  thin,  and  grayish,  and  on  standing  separates  into 
two  layers,  the  upper  a  greenish  fluid  covered  with  frothy  mucus, 
the  lower  consisting  of  a  thick  sediment  in  which  may  be  found  pea- 
sized  gray  or  yellow  masses  (Dittrich's  plugs),  composed  of  bacteria, 
pus,  leptothrix,  fat  crystals,  and  detritus.  The  physical  signs  vary 
according  to  the  associated  or  causative  conditions  {q.  v.). 

Fetid  bronchitis,  when  an  event  in  the  ordinary  chronic  form, 
may  be  announced  by  irregular  chills,  high  fever,  and  a  greater  de- 
gree of  general  weakness,  caused  by  septic  absorption  from  the  decom- 
posing secretion.  Abscess,  gangrene,  pneumonia,  or  metastatic  cere- 
bral abscess  may  result,  or  the  affection  settle  back  into  the  usual 
course  of  a  chronic  bronchitis,  with  or  without  the  persistence  of 
the  offensive  character  of  the  sputum. 

IV.  Bronchiectasis. — The  dilatation  may  be  cylindrical  or  sac- 
cular, usually  partial  and  often  bilateral ;  but,  especially  in  congeni- 
tal cases,  may  be  general  and  unilateral,  involving  all  the  bronchia 
of  one  lung. 

{a)  Causes. — Occurs  most  commonly  in  connection  with  chronic 
bronchitis  and  emphysema,  chronic  phthisis,  broncho-pneumonia  in 
children,  adhesive  pleurisy,  or  interstitial  pneumonia ;  and  occlusion 
of  a  bronchus,  by  foreign  bodies  or  by  the  pressure  of  a  tumour  or 
aneurism,  whereby  the  accumulated  secretion  distends  the  tubes. 
Very  rarely  it  is  a  congenital  anomaly. 

(J)  Symptoms. — Small  bronchiectases,  such  as  occur  in  chronic 
bronchitis,  emphysema,  and  phthisis,  may  not  give  rise  to  suggestive 
symptoms,  and  the  condition  may  be  quite  unsuspected. 

If  there  are  one  or  more  saccular  dilatations  of  considerable  size, 
the  characters  of  the  cough  and  expectoration  are  distinctive.  The 
cough  is  paroxysmal,  usually  occurs  in  the  morning,  and  is  due  to 
the  accumulation  of  secretion  in  one  or  more  large  sacs.  When  filled, 
the  cavity  overflows  either  spontaneously  or  because  of  a  change  of 
X)osition,  thus  irritating  the  adjoining  healthy  mucosa  and  exciting 
cough.  After  the  sac  is  emptied  a  period  of  quiescence  succeeds 
until  a  reaccumulation  takes  place.  The  expectoration  is  copious, 
and  a  large  quantity  is  discharged  in  a  short  time.  On  standing,  the 
gi*ay  or  grayish-brown  sputum  separates  into  two  layers,  the  upper 
thin,  mucoid,  and  covered  by  a  brownish  froth,  the  lower  consisting 
of  a  thick  granular  sediment  containing  pus  cells,  granular  debris, 
fatty-acid  crystals,  and  occasionally  red  cells  and  haematoidin  crys- 
tals. Nummular  masses  are  not  common,  nor  are  elastic  fibres  found 
unless  the  walls  of  the  dilatation  are  ulcerated.  The  sputum  usually 
has  a  peculiar  sour  or  stale  odour;  occasionally  it  is  extremely  offen- 


DISEASES  OF  THE   BRONCHI  837 

sive  because  of  the  presence  of  a  putrid  bronchitis  (III,  preceding). 
Hemorrhage  may  occur;  fever  and  dyspnoea  are  not  common,  except 
as  caused  by  a  coexisting  thoracic  affection. 

The  physical  examination  may  be  negative  unless  there  are  saccu- 
lar dilatations  sufficiently  large  and  superficial  to  afford  the  signs  of 
cavity.  If  the  sac  is  empty  there  are  tympanitic  percussion,  pectoril- 
oquy, and  cavernous  or  amphoric  respiration,  with  occasional  metal- 
lic rales.  If  the  sac  contains  fluid  the  percussion  note  is  dull,  and 
loud  gurgling  rales  are  heard. 

(c)  Diagnosis. — Moderate  dilatations  are  not  recognisable,  but  if 
there  is  evidence  of  a  cavity  at  the  base  of  the  affected  lung  in 
chronic  interstitial  pneumonia  or  chronic  pleurisy,  it  is  a  bronchiec- 
tasis. (1)  Compared  with  a  phthisical  cavity,  a  saccular  dilatation 
lies,  as  a  rule,  toward  the  base  rather  than  the  apex  of  the  lung,  the 
signs  persist  but  do  not  increase,  the  sputa  are  rarely  nummular, 
the  tubercle  bacillus  is  absent,  there  is  usually  no  fever  and  but  little 
loss  of  flesh  and  strength,  and  the  previous  history  is  not  that  of 
pulmonary  tuberculosis.  (2)  Actinomycosis  of  the  lung  may  give 
rise  to  conditions  which  closely  resemble  bronchiectasis,  but  an  ex- 
amination of  the  sputum  will  enable  the  differentiation.  (3)  A  local- 
ized empyema  which  has  perforated  the  lung  and  established  com- 
munication with  a  bronchus  is  discriminated  with  difficulty  from 
bronchiectasis,  but  there  is  usually  a  history  of  an  acute  pleurisy, 
with  a  sudden  onset  of  recurring  paroxysms  of  cough  and  expecto- 
ration. Pulmonary  abscess  {q.  v.)  and  pulmonary  gangrene  (g.  v.) 
are,  as  a  rule,  readily  distinguished  from  bronchial  sacculations. 

(d)  Prognosis. — In  rare  instances  cerebral  abscess  and  pulmonary 
abscess  or  gangrene  may  occur.  Pulmonary  osteo-arthropathy  may 
follow.  Ordinarily  the  condition,  although  incurable,  permits  a  long 
and  fairly  comfortable  life. 

V.  Fibrinous  Bronchitis. — A  rare  disease,  acute  or  chronic, 
attended  by  the  formation  and  expulsion  of  fibrinous  casts  (Fig. 
214,  page  599)  of  a  bronchus  and  its  branches.  It  occurs  most  fre- 
quently in  males  (2  to  1)  between  20  and  40  years  of  age,  and  in  the 
spring  months.  It  is  sometimes  hereditary,  and  a  certain  epidem- 
icity  has  been  noted.  It  is  frequently  associated  with  tuberculosis, 
less^  frequently  with  chronic  pleurisy,  herpes,  impetigo,  and  pemphi- 
gus, and  occasionally  the  attacks  coincide  with  the  menstrual  period. 
Its  causation  is  unknown. 

(«)  Symptoms.— Yevj  rarely  the  disease  is  acute,  beginning  with 
chills  and  high  fever,  and  followed  by  dyspnoea,  violent  paroxysms  of 
cough,  and  occasionally  haemoptysis. 

More  commonly  the  attack  comes  on  like  an  ordinary  severe 
55 


838  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

bronchitis.  Fever  is  not  always  present.  The  cough  becomes  vio- 
lent and  paroxysmal,  and  there  are  dyspnoea  and  a  varying  degree  of 
cyanosis.  Usually  in  a  few  hours,  sometimes  days,  expectoration 
occurs,  the  sputa,  often  blood-stained,  containing  rounded  ball-like 
masses,  which,  when  unravelled,  prove  to  be  casts  of  a  secondary  or 
tertiary  bronchus  with  its  terminal  branches.  Hasmoptysis,  some- 
times profuse,  may  accompany  or  follow  the  expulsion  of  the  casts. 
With  the  discharge  of  the  mould  the  cough  and  dyspnoea  sub- 
side, perhaps  only  to  return  in  1  or  2  days,  and  thus  continue  for 
a  week  or  longer.  The  attacks  may  recur  at  intervals  of  weeks, 
months,  or  years,  or  there  may  be  but  one  attack  in  a  lifetime. 
In  some  instances  the  recurrences  have  a  definite  and  regular  period 
of  intermission.  The  same  bronchus  is  usually  involved  at  each 
attack. 

The  physical  signs  are,  as  a  rule,  those  of  a  severe  bronchitis.  If 
a  large  bronchus  is  obstructed  there  may  be  diminished  vocal  frem- 
itus, weak  or  absent  respiration,  and  deficient  expansion  or  inspira- 
tory retraction  of  the  lower  ribs  over  the  affected  side.  Dulness 
may  be  present  if  the  lung  area  supplied  by  the  plugged  bronchus  is 
collapsed. 

{b)  Diagnosis  and  Prognosis. — The  diagnosis  depends  entirely 
upon  the  discovery  of  the  casts.  They  may  require  to  be  distin- 
guished from  the  casts  of  diphtheria  by  bacteriological  examina- 
tion. 

The  prognosis  is  usually  favourable,  although  the  disease  may 
cover  a  period  varying  from  5  to  15  years.  Extremely  acute  attacks 
may  prove  fatal. 

VI.  Bronchial  Obstruction. — (a)  Causes. — This  may  be  due 
to  foreign  bodies  in  the  bronchia  and  to  thickening  of  the  bron- 
chial walls  by  inflammation  or  neoplasm,  or  to  external  pressure 
upon  a  bronchus  by  abnormal  thoracic  masses  such  as  mediastinal 
or  pulmonary  tumour  or  abscess,  aneurism,  enlarged  bronchial  or  me- 
diastinal glands,  hydatids,  and  large  pleural  effusions  or  pleural  neo- 
plasms. 

(b)  Symptoms. — Obstruction  of  the  smaller  bronchi  does  not  give 
rise  to  appreciable  symptoms.  If  a  main  or  large  bronchus  is  closed 
there  will  be  marked  dyspnoea,  perhaps  with  inspiratory  retraction  of 
the  lower  sternum  and  lower  ribs  and  intercostal  spaces,  particularly 
upon  the  affected  side.  The  larynx  will  move  with  respiration,  but 
to  a  much  slighter  extent  than  when  the  obstruction  is  at  the  glottic 
opening.  The  physical  examination  reveals  deficient  expansion  upon 
the  affected  side,  diminished  vocal  fremitus,  a  normal  percussion 
sound,  diminished  or  absent  respiratory  murmur,  and,  possibly,  large 


DISEASES  OF  THE  BRONCHI  839 

and  small  dry  rdles  at  the  narrowed  or  obstructed  point.  Later  there 
may  be  dulness  if  the  lung  collapses.  It  is  necessary  to  exclude 
laryngeal  stenosis  by  visual  examination. 

VII.  Bronchial  Astluna.— The  pathology  of  this  disease  is 
unsettled.  Some  regard  it  as  a  pure  neurosis,  a  spasm  of  the  bron- 
chial muscles ;  others  as  a  neurotic  hyperaemia  and  swelling  of  the 
bronchial  mucosa,  with  an  exudate  of  mucin.  It  is  probable  that 
the  second  view  applies  to  the  majority  of  cases.  It  may  alternate 
with  neuralgia  and  epilepsy. 

(a)  Causes. — An  underlying  and  peculiar  irritability  of  the  nerv- 
ous system  or  bronchial  muscles  and  mucosa,  akin  to  that  in  hay 
fever,  must  be  predicated.  The  exciting  causes  are  extraordinarily 
diverse.  An  attack  may  be  precipitated  by  the  inhalation  of  dusts 
or  odours  from  certain  flowers  or  plants  or  emanations  from  animals. 
In  one  locality  or  climate  attacks  will  occur,  in  others  there  is  per- 
fect freedom  from  the  seizures.  Strong  emotions,  fatigue,  indiscre- 
tions in  diet,  and,  more  rarely,  the  presence  of  intestinal  parasites, 
or,  in  women,  pelvic  disease,  may  be  responsible.  Diseases  of  the 
upper  air-passages,  such  as  nasal  polypi,  hypertrophic  rhinitis,  and 
chronically  enlarged  tonsils,  are  often  strongly  predisposing  causes. 
A  frequent  initial  event  is  an  acute  bronchitis. 

The  disease  often  begins  in  childhood.  It  is  more  common  in 
men  than  in  women  (2  to  1) ;  half  of  the  cases  are  hereditary ;  and 
it  occurs  rather  more  frequently  in  winter  and  spring  than  in  the 
summer,  unless  associated  with  hay  fever. 

(J)  Symptoms.— The  attack  may  begin  abruptly,  but  in  about  50 
per  cent  of  cases  there  are  various  premonitory  symptoms,  such  as 
anxiety,  depression,  nervousness,  irritability,  vertigo,  drowsiness, 
headache,  neuralgia,  chilly  feelings,  substernal  tightness,  polyuria,  or 
flatulence  and  digestive  disturbances. 

Ordinarily  the  paroxysm  commences  at  night,  often  during  sleep ; 
less  commonly  while  awake,  or  during  the  day.  There  is  a  sense  of 
breathlessness,  with  thoracic  oppression  and  constriction,  soon  de- 
veloping into  the  most  intense  dyspnoea.  The  patient  may  rush  to 
the  window  for  air,  or  sit  up,  placing  his  hands  on  the  bed  or  the  arms 
of  a  chair  in  order  to  gain  additional  support  for  the  extraordinary 
muscles  of  respiration.  Cyanosis  soon  appears,  the  face  is  anxious 
and  wet  with  perspiration,  the  hands  and  feet  are  cold,  the  tempera- 
ture subnormal,  and  the  pulse  frequent  and  small.  .The  attack 
reaches  its  height  in  from  a  few  minutes  to  several  hours,  at  which 
time  the  dyspncea  lessens,  and  there  is  often  a  violent  fit  of  coughing 
and  the  raising  of  a  tenacious  and  scanty  expectoration,  with  great 
relief  to   the   patient.     The   eosinophiles  in   the  blood   are   much 


840  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

increased  during  the  attacks,  constituting  from  25  to  50  per  cent  of 
the  total  differential  leucocyte  count. 

Physical  examination  during  the  attack  reveals  a  distended  chest, 
as  the  lungs  are  overfull  of  air  which  can  not  be  expired.  Moreover, 
as  the  thorax  is  thus  in  the  inspiratory  position,  its  movements,  in 
spite  of  the  violent  respiratory  efforts,  are  extremely  limited,  and 
the  diaphragm  is  lowered  and  almost  immobile.  The  respirations 
are  normal  or  decreased  in  frequency ;  inspiration  is  short  and  quick ; 
the  expiration  is  prolonged  and  wheezy  because  of  the  difficulty 
in  expelling  the  previously  inspired  air  through  the  narrowed  tubes — 
an  expiratory  dyspnoea.  Percussion  is  normal  or  hyperresonant.  On 
auscultation  a  multitude  of  sonorous  and  sibilant  rales  are  heard, 
during  both  inspiration  and  expiration.  Toward  the  close  of  the 
attack,  and  during  its  course  if  bronchitis  coexists,  moist  rales  of 
various  sizes  are  perceived. 

The  sputum  in  the  early  stage  of  the  attack  is  expectorated  with 
great  difl&culty  and  contains  rounded  gelatinous  pellets,  an  examina- 
tion of  which  will,  in  every  case  of  true  bronchial  asthma,  reveal  the 
presence  of  Curschmann's  spirals  (Fig.  215,  page  599).  Late  in  the 
attack  the  sputum  is  muco-purulent  and  the  spirals  disappear.  Ley- 
den's  crystals  and  eosinophiles  may  also  be  found, 

(c)  Course^  Duration^  and  Prognosis. — The  attacks  may  be  re- 
peated for  from  2  to  5  or  6  nights,  with  or  without  wheezy  cough  and 
respiration  during  the  intervals.  The  set  of  paroxysms  may  recur  at 
intervals  of  a  month  or  a  year,  more  or  less.  If  the  recurrences  are 
frequent,  severe,  and  long  continued,  emphysema,  right-heart  dilata- 
tion, and  chronic  bronchitis  usually  ensue,  with  permanent  dyspncea 
and  wheezy  asthmatic  respiration,  the  purely  spasmodic  seizures 
ceasing  or  diminishing  in  frequency  and  intensity. 

However  alarming  the  appearance  of  the  patient,  death  never 
takes  place  during  the  attack.  On  the  other  hand  the  disease  is 
essentially  chronic,  although  there  may  be  prolonged  periods  of  free- 
dom. Death  may  occur  in  old  cases  from  the  resultant  emphysema 
and  cardiac  lesions. 

{d)  Diagnosis. — This  is  usually  easy.  The  dyspnoea  (the  so-called 
asthma)  of  renal  and  cardiac  disease  is  not  attended  by  the  dry, 
sonorous,  and  piping  rdles  and  other  physical  signs  of  true  asthma, 
although  fine,  moist  crepitations  may  be  heard ;  nor  is  the  subjective 
dyspnoea  of  hysteria.  In  glottic  spasm  or  abductor  paralysis  the 
dyspnoea  is  distinctly  of  the  inspiratory  type,  voice  changes  may  be 
present,  and  the  multitudinous  dry  rales  of  asthma  are  conspicuously 
absent. 


DISEASES  OF  THE  LUNGS  841 


IV.    DISEASES    OF    THE    LUNGS 

I.  Pulmonary  Congestion. — Two  forms  are  recognised  :  active 
and  passive. 

(1)  Active  Congestion. — In  the  great  majority  of  cases  active 
hyperaemia  is  a  symptom  or  associated  condition  in  connection  with 
certain  pulmonary  diseases,  such  as  bronchitis,  pneumonia,  tubercu- 
losis, or  pleurisy.  In  certain  instances  it  is  possible  that  it  may  occur 
as  a  primary  and  independent  affection,  which  may  quickly  disappear 
or  be  followed  by  oedema,  or,  in  rare  cases,  by  reason  of  its  intensity, 
terminate  in  death.  This  condition  results  from  drunkenness  and 
exposure  to  severe  cold  or  great  heat,  or  from  violent  exertion. 

The  symptoms  are  rapid  breathing,  cough,  blood-tinged  frothy 
sputa,  somewhat  harsh  respiration,  with  fine  moist  rdles,  and  an 
absence  of  fever,  unless  some  febrile  or  inflammatory  condition 
coexists.  The  diagnosis  of  this  condition,  aside  from  pulmonary 
oedema  and  abortive  pneumonia,  must  be  made  with  caution. 

(II)  Passive  Congestion. — Of  passive  hyperaemia  two  varieties  are 
recognised  :  mechanical  and  hypostatic. 

{a)  Mechanical  Congestion. — (1)  Causes. — In  the  vast  majority  of 
cases  passive  hyperaemia  is  a  result  of  affections  of  the  left  heart, 
especially  mitral  stenosis  or  incompetency,  or  of  emphysiema.  In 
rare  instances  it  is  due  to  pressure  by  tumours.  The  essential  ele- 
ment in  either  case  is  the  presence  of  an  obstacle  to  the  return  of 
the  blood  to  the  left  ventricle,  with  resulting  chronic  congestion 
(brown  induration)  of  the  lungs. 

(3)  Symptoms. — Dyspnoea,  cough,  and  the  expectoration  of  frothy, 
often  blood-stained,  sputa  containing  "  heart-disease  cells "  (page 
S98).  Haemoptysis  may  occur.  So  long  as  the  compensation  of 
valvular  defects  is  unbroken  these  symptoms  do  not  appear. 

{b)  Hypostatic  Congestion. — (1)  Causes. — In  general  it  occurs  in 
fevers  and  conditions  of  great  debility  attended  by  feebleness  of  the 
heart,  and  is  favoured  by  a  prolonged  dorsal  position.  It  is  common 
in  long-continued  typhoid  fever ;  paralyses,  especially  cerebral ;  pro- 
longed coma  ;  abdominal  tumours,  tympanites,  or  ascites  ;  and  wast- 
ing diseases  like  tuberculosis  and  carcinoma. 

(2)  Symptoms. — Subjective  and  rational  symptoms  are  usually 
lacking,  but  physical  examination  will  disclose,  over  the  bases  pos- 
teriorly, slight  dulness,  weak,  or  harsh,  perhaps  broncho-vesicular, 
respiration,  and  moist  rales.  The  vocal  fremitus  may  or  may  not 
be  increased.  If  patches  of  broncho-pneumonia  exist  the  breathing 
may  be  truly  bronchial. 


84:2  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

II.  Pulmonary  (Edema. — {a)  Causes. — This  condition — an 
effusion  of  serum  from  the  distended  capillaries  into  the  alveoli  and 
their  walls — is  almost  invariably  secondary  to  the  various  forms  of 
pulmonary  congestion,  inflammation,  abscess,  infarction,  or  tubercu- 
losis. The  oedema  may  be  local,  in  the  immediate  neighbourhood  of 
a  circumscribed,  usually  inflammatory,  lesion ;  or  general.,  arising 
from  causes  similar  to  those  which  produce  congestion,  or  con- 
stituting a  terminal  event  in  states  of  great  debility.  The  factors 
which  appear  to  be  instrumental  in  causing  the  transudation  are 
increased  tension  in  the  pulmonary  vessels,  increased  fluidity  of  the 
blood,  an  abnormal  permeability  of  the  vessel  walls  due  to  nutritive 
changes,  and  left  ventricular  weakness. 

The  diseases  with  which  oedema  is  most  commonly  associated  are 
pneumonia ;  the  cachexias,  especially  that  due  to  carcinoma ;  grave 
or  fatal  anaemias ;  acute  and  chronic  nephritis  ;  acute  specific  fevers 
with  heart  weakness ;  cardiac  valvular  disease  ;  and  cerebral  apo- 
plexy or  injuries. 

(J)  Symptoms. — The  onset  of  this  condition  may  be  extremely 
sudden,  especially  in  nephritis.  More  commonly  there  is  simply  an 
Increase  in  the  manifestations  of  the  pre-existing  causative  disease. 

The  symptoms  of  pulmonary  oedema  are  increasing  dyspnoea, 
cyanosis,  cough,  and  an  abundant,  frothy,  watery,  rarely  tenacious, 
expectoration,  which  may  be  blood-stained  if  congestion  is  also  pres- 
ent. Fever  is  absent  unless  the  oedema  is  due  to  some  inflammatory 
or  other  febrile  condition.  The  physical  signs  are  impaired  reso- 
nance or  slight  dulness  over  the  bases,  with  absent  or  weak,  perhaps 
broncho-vesicular,  breath  sounds.  There  are  abundant  large  and 
small  rales,  of  an  unusually  liquid  character,  over  the  involved  areas. 

(c)  Diagnosis. — This  depends  mainly  upon  the  presence  of  numer- 
ous unusually  moist  rales,  both  large  and  small,  and  slight  dulness 
at  the  bases,  particularly  if  the  temperature  is  normal. 

III.  Broncho-pulm.onary  Hemorrhage  {Hemoptysis). — See 
page  261. 

IV.  Piihnonary  Hem.orrhage  or  Infarction. — Under  this 
head  may  be  included  pulmonary  apoplexy  (diffuse  infiltration),  and 
embolism  or  infarction. 

(I)  Diffuse  Hemorrhagic  Infiltration. — In  septicaemia  or  pyaemia, 
excessively  severe  or  malignant  fevers,  and  in  certain  diseases  of  the 
brain  there  may  be  an  extensive  infiltration  of  the  lungs  with  blood. 
If  the  patient  lives,  pneumonia,  abscess,  or  gangrene  results.  This 
condition  is  not  common  and  the  symptoms  are  indefinite.  There 
may  be  dyspnoea,  cyanosis,  haemoptysis,  and  collapse  symptoms  with 
signs  of  rapid  pulmonary  consolidation. 


DISEASES  OF  THE  LUNGS  843 

(II)  Pulmonary  Embolism  and  Thrombosis.— Circumscribed  infarc- 
tions are  due  to  stasis,  thrombosis,  or  embolism  of  some  of  the 
branches  of  the  pulmonary  artery,  whereby  the  vessels  are  blocked 
and  characteristic  wedge-shaped  hemorrhagic  areas  or  infarcts  result. 
Emboli  may  be  non-septic  or  septic. 

Causes. — Non-septic  embolism  arises  most  commonly  from 
chronic  cardiac  disease,  especially  mitral  stenosis,  or,  less  frequently, 
regurgitation.  Thrombi  may  form  in  the  right  auricle  or  in  the 
systemic  veins  and,  either  entire  or  disintegrated  into  smaller  por- 
tions, become  emboli;  or  thrombosis  or  stasis  take  place  in  the 
branches  of  the  pulmonary  artery  itself. 

Septic  emboli  originate  from  a  gangrenous  or  a  sappnratiye  focus, 
such  as  exists  in  pyaemia,  and  as  they  are  practically  masses  of  patho- 
genic bacteria,  pulmonary  gangrene  or  metastatic  abscesses  will 
result  from  their  lodgment  in  the  lung. 

Symptoms. — (1)  Of  Non-septic  Embolism. — If  the  embolus  is  suf- 
ficiently large  to  occlude  a  main  branch  of  the  pulmonary  artery 
sudden  death  may  occur.  If  a  medium-sized,  but  still  large,  branch 
is  the  seat  of  the  obstruction  there  will  be  cough,  haemoptysis,  men- 
tal anxiety,  intense  dyspnoea,  syncope,  and  perhaps  coma  and  convul- 
sions. If  the  smallest  branches  are  involved  there  may  be  no  recog- 
nisable symptoms ;  or  there  may  be  moderate  dyspnoea,  cough,  and 
slight  haemoptysis ;  or  the  expectoration,  especially  at  the  onset, 
may  consist  of  a  small  quantity  of  nearly  pure  blood  or  a  gelatinous 
bloody  mucus,  the  blood  subsequently  disappearing.  It  is  not,  at 
first  certainly,  the  rusty  sputum  of  a  pneumonia.  Cough  and  haem- 
optysis occurring  during  the  course  of  chronic  cardiac  disease  is 
very  suggestive  of  embolism,  although  the  spitting  of  blood  may 
result  from  passive  congestion. 

The  physical  signs  in  slight  infarctions  are  negative.  If  the  in- 
farction is  large  and,  as  is  usually  the  case,  occupies  the  lower  lobe, 
there  will  be  near  the  base  circumscribed  dulness,  increased  fremitus 
and  voice  sounds,  broncho-vesicular  or  bronchial  breathing,  and  moist 
rales— i.  e.,  the  evidences  of  a  strictly  limited  consolidation.  There 
may  be  pleural  friction  accompanied  by  transient  pain. 

(3)  Of  Septic  Embolism.— If  the  first  metastasis  of  a  gangrenous 
or  suppurative  focus  is  to  the  lungs,  the  earlier  symptoms  caused  by 
the  septic  embolus  will  resemble  those  just  described  as  being  caused 
by  a  non-septic  plug,  followed  in  due  time  by  the  evidences  of  pulmo- 
nary abscess  {q.  v.)  or  gangrene  {q.  v.).  Occurring  as  a  part  of  an 
already  existing  pyaemia,  the  symptoms  are  those  of  the  causative 
disease  plus  the  physical  signs  of  a  primary  consolidation,  with  sub- 
sequent abscess  or  gangrene. 


84i  DIAGNOSIS,    DIRECT   AND  DIFFERENTIAL 

Diagnosis. — The  sudden  onset  of  dyspnoea  and  pleuritic  pain, 
the  expectoration  of  a  moderate  quantity  of  blood  or  bloody  mucus, 
the  appearance  of  the  physical  signs  of  a  circumscribed  consolida- 
tion at  the  base,  without  fever,  together  with  the  presence  of  chronic 
heart  disease  or  other  acknowledged  causative  condition,  will  enable 
a  diagnosis. 

PkoCtNOSIS. — In  small  non-septic  infarcts  not  unfavourable;  in 
septic  infarcts,  grave. 

V.  Lobar  Pneumonia. — See  page  712. 

VI.  Broncho-pneumonia. — An  infectious  inflammation  of  the 
terminal  bronchi  and  their  communicating  air  cells. 

Causes. — The  disease  may  he  primary,  the  previous  health  having 
been  good ;  or  secondary  to  some  antecedent  disease.  Broncho-pneu- 
monia attacks  especially  the  very  young,  three  fourths  of  the  pneu- 
monias in  children  under  5  years  of  age  being  of  this  variety ;  the 
very  old,  especially  if  they  are  the  subjects  of  some  chronic  and  weak- 
ening ailment;  or  the  debilitated  of  any  age.  It  is  most  common 
among  the  poorer  classes  because  of  insanitary  surroundings.  Kickets 
and  chronic  diarrhoea  also  predispose. 

(1)  The  primary  cases  are  usually  due  to  cold  and  exposure. 

(2)  The  secondary  cases  follow  acute  bronchitis  and  the  infec- 
tious fevers,  especially  measles,  whooping  cough,  diphtheria,  scarlet 
fever,  erysipelas,  and  smallpox.  "  Aspiration  "  pneumonia  is  of  this 
type,  and  is  secondary  to  the  inhalation  of  particles  of  food  or  drink, 
an  accident  which  may  occur  when  the  larynx  is  insensitive,  as  in 
the  coma  of  cerebral  apoplexy,  uraemia,  or  other  condition  attended 
by  prolonged  unconsciousness.  It  may  follow  operations  on  the 
mouth,  nose,  and  trachea,  or  the  inhalation  of  ether ;  or  haemoptysis ; 
or  occur  in  connection  with  cancer  of  the  larynx  or  esophagus ;  or 
result  from  the  aspiration  of  the  secretion  from  a  bronchiectatic 
cavity  or  a  purulent  pleurisy  which  has  perforated  the  lung.  In  all 
these  cases  infective  or  irritant  particles  enter  the  bronchial  tubes. 

(3)  The  bacteriology  of  broncho-pneumonia  is  of  interest.  Xo  one 
organism  is  responsible  for  the  disease.  Among  those  which  are 
most  commonly  found  are  the  Pneumococcus  Janceolatus,  Streptococ- 
cus pyogenes,  Staphylococcus  aureus  et  alhus,  the  influenza  bacillus 
(Pfeiffer's),  and  the  bacillus  of  diphtheria.  As  a  rule  the  infection 
is  a  mixed  one,  at  least  two  varieties  coexisting.  The  most  constant 
organism  in  the  primary  form  of  the  disease  is  the  pneumococcus, 
which  may  exist  alone  ;  in  the  secondary  form  the  streptococcus,  usu- 
ally in  combination  with  one  of  the  other  organisms. 

Symptoms  and  Clinical  Varieties.— The  mode  of  onset  varies.  If 
there  has  been  no  antecedent  disease  and  the  attack  is  primary,  it 


DISEASES  OF  THE   LUNGS 


845 


begins  abruptly  with  a  chill  and  a  rapid  rise  in  temperature,  resem- 
bling, in  this  respect,  a  lobar  pneumonia.  On  the  other  hand,  if  there 
is  a  pre-existing  bronchitis,  either  simple  or  specific,  of  the  larger 
tubes,  the  onset  is  less  abrupt  and  there  is  rarely  a  distinct  chill. 

In  either  case  the  typical  symptoms  are  cough,  which  may  be  vio- 
lent and  painful ;  dyspnoea  and  rapid  respiration  (40  to  60  to  80),  with 
an  expiratory  moan ;  fever,  varying  from  102°  to  104°  ;  rapid  pulse  and, 
after  a  time,  cyanosis.  The  physical  signs  at  first  are  simply  those  of 
a  bronchitis  of  the  smallest  tubes,  abundant  sibilant  and  subcrepitant 
rales  without  dulness;  later,  and  depending  upon  the  presence  of 
patches  of  consolidation,  there  may  be  slight  dulness  with  harsh  or 
broncho-vesicular  respiration,  especially  at  the  bases  and  on  either 
side  of  the  spine.  If  the  consolidated  areas  are  sufficiently  numerous 
and  confluent  the  dulness  may  be  decided,  the  breathing  may  be  bron- 
chial, the  vocal  fremitus  distinctly  increased,  and  marked  bronchoph- 
ony be  present.  In  cases  of  extensive  consolidation  there  may  be  in- 
spiratory retraction  of  the  lower  sternum  and  lower  ribs,  indicative 
of  deficient  lung  expansion. 

There  are  certain,  sometimes  considerable,  variations  in  the  symp- 
toms and  clinical  type  of  the  disease  which  demand  consideration. 

(1)  In  severe  cases,  the  sensitiveness  of  the  nerve  centres  having 
been  decreased  as  an  effect  of  poisoning  by  carbon  dioxide,  the  dysp- 
noea and  cyanosis  steadily  increase,  the  cough  lessens,  the  respirations 
are  shallow  and  ineffectual,  although  rapid,  and  the  rales  become 
larger  and  moister.  The  patient  is  drowsy  but  not  quiet,  and  death 
ensues  from  cardiac  weakness,  especially  of  the  overdistended  and 
labouring  right  ventricle.  This  type  of  the  disease  is  the  suffocative 
catarrh  of  the  old  writers. 


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Chart  XXII. — Temperature  curve  of  prolonged  broncho-pneuinoiiia ;  recovery  (Holt). 


(2)  The  extremely  remittent  type  of  the  fever  in  many  cases  of 
broncho-pneumonia,  especially  in  children,  is  noteworthy,  as  the  fre- 
quency of  its  occurrence  is  not  always  appreciated,  and  from  a  cer- 
tain resemblance  to  the  temperature  curve  of  malaria  a  diagnosis  of 
the  latter  disease  may  be  made  (Chart  XXII). 


846  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

(3)  The  primary  form  in  infants  and  young  children  sets  in 
abruptly,  with  high  fever.  The  physical  signs  are  those  of  a  some- 
what circumscribed  moderate  consolidation  rather  than  of  a  diffuse 
bronchitis,  and  the  disease  bears  a  close  resemblance  to  a  lobar  pneu- 
monia.    Indeed,  it  frequently  terminates  by  crisis. 

(4)  The  primary  form  in  adults  may  begin  like  a  severe  and  acute 
bronchitis,  but  the  fever,  prostration,  cough,  and  dyspnoea  are  more 
marked  than  in  a  bronchitis,  and  the  expectoration  is  tenacious  and 
rusty  or  blood-stained. 

(5)  As  with  lobar  pneumonia  in  children,  so  with  broncho-pneu- 
monia, especially  if  the  onset  is  sudden,  the  initial  symptoms  may  be 
predominantly  cerebral  (delirium,  drowsiness,  convulsions,  coma),  or 
gastro-intestinal  (nausea,  vomiting,  more  rarely  diarrhoea),  the  pul- 
monary symptoms  and  signs  being  masked,  or  not  appearing  until 
several  days  have  elapsed. 

(6)  The  secondary  form  begins  as  a  bronchitis,  oftentimes  grad- 
ually. If  during  convalescence  from  an  acute  infection,  especially 
measles  or  pertussis,  there  is  an  increase  in  the  fever  with  cough, 
dyspnoea,  and  rapid  breathing,  the  presence  of  broncho-pneumonia  is 
assured,  even  though  physical  examination  reveals  nothing  but  fine 
moist  rales  at  the  bases  or  diffused  through  both  lungs,  without  evi- 
dences of  consolidation. 

(7)  Certain  mild  cases  are  seen  in  adults  which  are  not  commonly 
recognised  as  broncho-pneumonia.  Following  a  severe  ordinary  acute 
bronchitis  of  the  larger  tubes  in  otherwise  healthy  persons,  the  cold 
may  in  common  parlance  "  hang  on  "  for  more  than  the  ordinary  2 
or  3  weeks.  There  is  an  irritative  cough  with  scanty  expectoration, 
slight  fever  (99.5°  to  101°),  and  although  the  patient  may  continue  at 
his  ordinary  vocation,  he  feels  poorly,  his  appetite  is  impaired,  and 
his  sleep  is  restless.  A  careful  physical  examination  will  reveal  cir- 
cumscribed areas  where  fine  subcrepitant  rales  may  be  heard  upon 
rather  deep  breathing,  perhaps  with  a  slightly  harsh  respiratory  mur- 
mur and  intensified  voice  sounds.  The  percussion  note  is  normal. 
Under  rest  in  bed  and  other  appropriate  treatment  recovery  occurs 
usually  in  a  week  or  ten  days. 

Duration. — This  is  extremely  variable.  Very  severe  cases,  espe- 
cially in  children,  may  prove  fatal  in  from  3  to  6  days.  The  duration 
of  the  common  type  of  broncho-pneumonia  ending  in  recovery  varies 
from  1  to  3  weeks ;  in  some  instances  the  disease  is  protracted  to  6 
or  8  weeks,  rarely  even  to  10  or  12  weeks.  Death  or  recovery  may 
occur  at  any  time.     As  a  rule  the  decline  of  the  fever  is  by  lysis. 

Tenninations. — These  are  resolution ;  suppuration  or  gangrene, 
practically  only  in  the  aspiration  or  deglutition  pneumonia  of  which 


DISEASES  OP  THE  LUNGS  847 

they  are  common  sequelae ;  and  chronic  interstitial  pneumonia,  espe- 
cially if  the  original  broncho-pneumonia  is  tuberculous. 

Differential  Diagnosis. — The  cardinal  symptoms  are  fever,  usually 
remittent,  cough,  dyspnoea,  rapid  respiration,  and  bilateral  fine  or 
subcrepitant  rdles,  with  or  without  evidences  of  moderate  or  patchy 
consolidation.  A  patient  with  fever,  rapid  breathing,  and  a  chest  so 
full  of  large  and  small  moist  rales  on  both  sides  that  the  respiratory 
murmur  can  not  be  heard,  has  broncho-pneumonia.  Atypical  cases 
are  most  common  in  infants.  Under  3  years  of  age  broncho-pneu- 
monia is  of  much  more  frequent  occurrence  than  lobar  pneumonia. 

The  differential  diagnosis  is  mainly  between  primary  broncho- 
pneumonia with  extensive  confluent  consolidations  and  lobar  pneu- 
monia (page  712),  or  the  protracted  cases  of  broncho-pneumonia  and 
the  broncho-pneumonic  form  of  tuberculosis  (page  72(3).  As  capil- 
lary bronchitis  is  broncho-pneumonia,  nothing  need  be  said  regard- 
ing a  discrimination  between  them. 

Prognosis. — Broncho-pneumonia  is  always  a  grave  disease.  In 
children  of  the  better-housed  classes  the  mortality  varies  from  10  to 
30  per  cent ;  in  hospitals  and  among  the  very  poor,  from  30  to 
50  per  cent.  The  primary  cases  have  a  good  prognosis  ;  the  fatality 
is  greatest  in  the  secondary  forms.  Aspiration  or  deglutition  broncho- 
pneumonia, because  of  its  frequent  termination  in  abscess  or  gangrene 
of  the  lung,  usually  causes  death. 

VII.  Chronic  Interstitial  Pneumonia. — More  or  less  local- 
ized, but  often  extensive,  fibroid  changes  occur  in  the  lungs  in  every 
case  of  pulmonary  tuberculosis,  abscess,  tumour,  hydatids,  emphysema, 
and  pleurisy.  Excluding  these,  there  is  a  diffuse  cirrhosis,  usually 
affecting  an  entire  lung,  less  frequently  both  lungs,  which  is  here 
considered. 

(a)  Causes.— GhiomG  (diffuse)  interstitial  pneumonia  may  in  rare 
cases  be  a  sequel  of  acute  lobar  pneumonia,  more  commonly  of  a 
broncho-pneumonia;  or  may  result  from  compression  of  the  lung 
and  extension  of  fibrous  tissue  from  a  chronic  pleurisy ;  or  be  a  con- 
sequence of  syphilis ;  or  arise  from  the  pressure  of  a  new  growth,  or 
an  aneurism,  or  a  foreign  body  in  a  bronchus.  A  special  form  due  to 
the  inhalation  of  dust  is  described  elsewhere  (see  Pneumonokoniosis). 

{h)  Si/mpioms.— There  is  a  chronic  cough,  with  slight  dyspnoea 
often  present  only  on  exertion.  The  cough  may  be  slight  or  severe, 
with  a  moderate  or  profuse  muco-purulent  expectoration.  Haemop- 
tysis is  not  uncommon.  As  the  bronchial  tubes  are  apt  to  become 
dilated,  the  special  symptoms  and  signs  of  bronchiectasis  (page  836) 
may  be  superadded.  The  disease  is  extremely  chronic,  and  may  be 
protracted  for  from  10  to  20  years  or  longer,  with  but  moderate  loss 


848  DIAGNOSIS,    DIRECT   AND  DIFFERENTIAL 

of  flesh  and  strength,  the  patient  remaining  able  to  perform  light 
manual  labour. 

In  advanced  cases  the  physical  signs  are  :  Marked  retraction,  ap- 
proximation of  the  ribs,  and  deficient  or  absent  expansion  of  the 
aifected  side,  with  compensatory  enlargement  of  the  opposite  healthy 
side.  The  spine  is  curved,  with  its  concavity  toward  the  diseased 
lung,  and  the  shoulder  on  the  same  side  droops.  The  heart  is  drawn 
over  by  the  shrinking  lung,  and,  when  the  left  lung  is  diseased  and 
retracted,  the  heart  is  uncovered  and  there  is  a  wide,  visible  impulse 
in  the  2d,  3d,  and  4th  interspaces.  The  vocal  fremitus  is  increased, 
unless  there  is  considerable  thickening  of  the  pleura,  when  it  is 
diminished  or  absent.  The  percussion  note  is  dull,  flat,  or  wooden, 
except  over  bronchiectatic  cavities,  which,  if  present,  will  cause  a 
tympanitic  or  amphoric  note.  Over  the  apex  and  in  the  axilla  the 
breath  sounds  are  broncho-vesicular  or  bronchial ;  over  bronchiectases, 
cavernous,  or  amphoric ;  over  the  base,  weak,  distant,  or  absent. 
Large  and  small,  dry  or  moist,  rales,  and  quite  frequently  rubbing 
and  creaking  friction  sounds,  are  present.  Over  the  healthy  lung 
there  may  be  hyperresonance  and  exaggerated  respiration.  The  pul- 
monary second  sound  is  accentuated  and  murmurs  may  develop, 
especially  at  the  tricuspid  valve,  when  the  right  ventricle  begins  to 
fail  because  of  the  extra  work  imposed  upon  it. 

Death  may  result  from  intercurrent  disease  ;  from  profuse  haemop- 
tysis ;  from  cardiac  failure  ;  or  from  gradual  asthenia. 

(c)  Differential  Diagnosis. — Practically  the  only  disease  from 
which  it  requires  differentiation  is  pulmonary  tuberculosis,  with 
fibroid  changes  so  extensive  (fibroid  phthisis)  that  the  symptoms  and 
physical  signs  of  the  two  conditions  are  identical.  If  both  lungs  are 
affected  it  speaks  for  tuberculosis,  but  the  only  absolute  evidence  is 
the  finding  of  tubercle  bacilli  in  the  sputum. 

VIII.  Pneumonokoniosis. — (a)  Nature  and  Causes. — This  i& 
a  chronic  interstitial  pneumonia  due  to  the  inhalation  of  dusts  inci- 
dent to  special  employments.  According  to  the  cause,  certain  varie- 
ties are  recognised — anthracosis,  or  coal-miner's  disease ;  chalicosis,. 
"  stonecutter's  phthisis  "  or  "  grinder's  rot,"  caused  by  the  inhalation 
of  mineral  dust,  in  stonecutters,  millstone  makers,  and  grinders  of 
cutlery ;  and  siderosis^  caused  by  the  inhalation  of  metallic  particles 
by  workers  in  iron  (especially),  also  in  brass  and  bronze.  Fibrosis 
may  be  due  further  to  the  breathing  of  vegetable  dusts  by  grain 
shovellers,  and  workers  in  cotton,  flax,  and  tobacco. 

{h)  Symptoms. — These  come  on  gradually  after  years  of  exposure 
to  the  causative  environment.  The  earliest  symptoms  and  signs 
are  those  of  a  chronic  bronchitis,  then  of  associated  emphysema,. 


DISEASES  OF  THE  LUNGS  849 

and  finally  of  chronic  interstitial  pneumonia,  with  or  without  bron- 
chiectasis. In  the  later  stages  the  lungs  may  become  tuberculous  and 
the  signs  of  ulcerative  cavities  become  manifest. 

(c)  Diagnosis. — This  depends  upon  the  history  of  long-continued 
inhalation  of  dust ;  the  presence  of  chronic  bronchitis,  emphysema, 
and  fibrosis ;  and  particularly  upon  an  examination  of  the  sputum. 
In  anthracosis  it  is  black ;  in  siderosis  it  is  of  a  reddish  colour ;  in 
chalicosis  the  microscope  reveals  the  shining  angular  particles  of 
silica.  Whether  the  process  has  become  tuberculous  must  be  ascer- 
tained by  an  examination  for  tubercle  bacilli. 

(d)  Prognosis. — In  the  early  stages  favourable  if  the  patient  can 
leave  his  obnoxious  employment.  Otherwise,  and  in  advanced  cases, 
the  prognosis  is  grave,  although  the  disease  is  very  chronic. 

IX.  Phthisis  Pulmonalis. — See  pages  726  to  731. 

X.  Pulmonary  Atelectasis.  —  («)  Causes.  —  Collapse  of  the 
lungs — a  partial  or  entire  disappearance  of  air  from  the  alveoli  by 
compression  of  the  lung  or  absorption  of  the  air — may  be  congenital 
or  acquired.  The  congenital  variety  occurs  in  the  newborn  or  pre^ 
maturely-born  infant,  as  a  result  of  deficient  breathing  power  or  ob- 
struction of  the  air  passages.  An  acquired  atelectasis  may  be  due  to 
obstruction  caused  by  the  formation  of  mucus  in  bronchitis  of  the 
smaller  tubes ;  to  compression  of  the  lung  by  large  pleural  or  peri- 
cardial effusions  or  pneumothorax,  thoracic  aneurism  or  tumour,  or 
great  enlargement  of  the  heart ;  to  the  weakened  respiratory  action 
caused  by  various  paralyses ;  to  upward  pressure  upon  the  diaphragm 
by  abdominal  effusion,  tumour,  or  meteorism ;  or  to  thoracic  de- 
formities. 

{h)  Symptoms. — These  are  rarely  distinctive,  as  the  condition 
occurs  usually  in  combination  with  broncho-pneumonia,  especially 
in  the  milder  forms  of  the  latter  which  constitute  the  "grippy 
chest." 

If  the  areas  of  collapse  are  small  there  is  no  dulness,  the  respira- 
tory sounds  are  weak  or  absent,  and  at  the  end  of  inspiration  there 
are  localized  fine  or  subcrepitant  rules,  often  with  little  or  no  fever. 
Larger  areas  may  present  a  weak  broncho-vesicular  or  bronchial 
breathing  Avith  appreciable  dulness ;  and  if  the  collapse  is  extensive, 
as  in  the  atelectasis  of  the  ncM^born,  the  respiration  is  rapid,  there  is 
cyanosis,  the  lower  half  of  the  chest  is  retracted  during  inspiration, 
the  extremities  are  cold,  and  there  may  be  muscular  twitching  or 
even  convulsions. 

XI.  Emphysema. — This  term  embraces  interstitial  emphysema, 
the  form  in  which  there  is  a  rupture  of  the  air  cells,  the  contained  air 
passing  into  the  interlobular  tissues ;  and  vesicular  emphysema,  in 


850  DIAGNOSIS,   DIRECT   AND   DIFFERENTIAL 

which  there  is  overdistention  of  the  air  cells  and  atrophy  of  their 
walls.     The  following  varieties  are  recognised  : 

(I)  Interstitial  Emphysema. — This  is  due  to  wounds  of  the  lung ;  or 
to  rupture  of  air  cells  during  a  violent  fit  of  coughing,  or  straining 
in  childbirth  or  at  stool,  or  during  convulsions.  The  condition  can 
not  be  recognised  unless  the  air  travels  from  a  rupture  at  the  root  of 
the  lung  along  the  trachea  to  the  tissues  of  the  neck,  causing  sub- 
cutaneous emphysema ;  or  an  air  sac  ruptures  into  the  pleura  with 
the  consequent  formation  of  a  pneumothorax  in  otherwise  healthy 
persons.  A  friction  sound  of  a  crumpling  character  resembling  that 
heard  in  pleurisy  is  claimed  to  be  somewhat  characteristic  of  inter- 
stitial emphysema. 

(II)  Hypertrophic  Emphysema. — The  lungs  are  enlarged  because  of 
the  atrophy  and  great  distention  of  the  air  cells. 

[a)  Causes. — A  congenital  and  often  hereditary  weakness  of  the 
lung  tissue,  probably  a  defective  development  of  the  elastic  fibres, 
must  be  predicated,  after  which  a  persistently  high  intra-alveolar  air 
tension  accomplishes  the  dilatation.  The  disease  may  follow  chronic 
bronchitis,  whooping  cough,  and  bronchial  asthma,  all  of  which  cause 
increased  intrapulmonary  pressure  ;  so  also  with  heavy  lifting,  blow- 
ing on  wind  instruments,  and  glass-blowing. 

(b)  Symptoms. — The  disease,  in  nearly  all  instances,  begins  insidi- 
ously, often  in  early  childhood.  In  a  well-developed  case  there  is 
dyspnoea,  which  may  be  constant  or  perhaps  felt  only  on  exertion, 
often  with  wheezy  breathing  and  laboured  expiration.  Cyanosis  is 
very  common,  and  may  be  extreme  although  the  patient  is  about. 
Cough  and  frequent  attacks  of  bronchitis,  often  of  an  asthmatic 
character,  sometimes  with  severe  cyanosis,  are  common.  Ultimately 
the  cough,  like  the  bronchitis,  becomes  persistent  and  chronic. 
The  cough  may  for  some  years  disappear  during  the  summer  and 
return  in  the  winter.  Intercurrent  paroxysms  of  spasmodic  asthma 
are  not  uncommon.  The  temperature  is  usually  subnormal  and  the 
surface  of  the  body  noticeably  cool.  The  pulse  is  weak  but  not  rapid. 
As  a  result  of  the  obstruction  to  the  flow  of  blood  through  the  lungs 
the  right  ventricle  may  become  hypertrophiod,  followed  in  course  of 
time  by  dilatation,  tricuspid  insufficiency,  and  consequent  widespread 
passive  congestion  in  the  systemic  veins.  There  may  be  a  slow  loss 
of  strength  and  flesh. 

The  physical  signs  in  a  well-marked  case  are  quite  distinctive. 
Inspection  shows  the  emphysematous  chest  (Fig.  232).  The  expan- 
sion is  greatly  lessened,  the  principal  movement  of  the  chest  is  ver- 
tical, the  upper  abdomen  retracts  during  inspiration,  and  the  expira- 
tory movement  is  prolonged.     The  sterno-mastoid  muscles  are  promi- 


DISEASES  OP  THE  LUNGS  35 1 

nent  and  hypertrophied.  The  neck  veins  are  distended,  perhaps 
pulsating.  The  apex  beat  is  usually  not  palpable,  but  there  is  com- 
monly a  marked  epigastric  pulsation  and  systolic  shock  over  the  ensi- 
form  appendix.  The  vocal  fremitus  is  lessened.  The  percussion  note 
throughout  is  abnormally  clear  and  hyperresonant,  at  times  slightly 
tympanitic.  The  normal  limits  of  pulmonary  resonance  are  extended 
in  every  direction,  the  cardiac 
dulness  is  lessened  or  disap- 
pears, the  upper  limits  of  he- 
patic and  splenic  dulness  are 
lowered  by  one  or  two  inter- 
spaces, and  there  is  resonance 
extending  to  an  unusually 
high  level  above  the  clavicles, 
often  with  supraclavicular 
bulging.  The  characteristic 
auscultatory  finding  is  that 
of  a  greatly  prolonged,  low- 
pitched,  often  wheezy,  expir- 
atory sound,  while  the  inspir- 
atory element  is  short,  weak, 
or  even  absent.     Large  and 

small,  dry  or  moist,  rales,  due  ^.g.  222.-Einphy8einatou8  chest 

to  a  coexisting  bronchitis,  are    ' 

often  heard,  and  may  be  so  abundant  as  to  obscure  the  respiratory 
murmur.  Over  those  portions  of  the  lung  which  are  not  greatly 
distended  there  may  be  exaggerated  or  harsh  breathing.  Vocal  reso- 
nance may  be  increased,  diminished,  or  absent.  The  pulmonary 
second  sound  is  usually  accentuated,  and  the  signs  of  right  ventricu- 
lar hypertrophy  and  dilatation  or  tricuspid  insuflficiency  {q.  v.)  may 
be  found. 

An  acute  vesicular  emphysema  may  develop  quite  suddenly,  dur- 
ing attacks  of  angina  pectoris  and  the  pseudo-asthmatic  seizures 
of  cardiac  disease,  because  of  the  combination  of  violent  inspira- 
tions with  cyanosis  and  pulmonary  congestion.  Percussion  shows 
a  great  increase  in  the  volume  of  the  lungs,  and  upon  auscultation 
there  are  prolonged  expiration  and  universally  distributed  sibilant 
rales. 

(c)  Course  and  Prognosis. — With  the  exception  of  the  rare  acute 
form,  the  course  of  tlie  disease  is  essentially  chronic  and  progressive. 
It  is  incurable,  although  not  inconsistent  with  a  long  life.  Frequent 
attacks  of  bronchitis  aggravate  the  disease,  and  death  may  occur 
from  an  intercurrent  pneumonia  or  the  development  of  pulmonary 


852  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

phthisis.     The  right  heart  sequelae — dropsy,  haemoptysis,  or  acute 
dilatation  and  cyanosis — may  terminate  life. 

{d)  Diagnosis. — The  symptoms  and  physical  signs  in  a  well- 
marked  case  are  usually  sufficiently  distinctive  to  avoid  mistakes. 
It  may  require  discrimination  from  the  following  conditions : 

(1)  Chronic  Bronchitis. — Hypertrophic  emphysema  is  separated 
from  simple  chronic  bronchitis  by  the  dyspnoea,  the  altered  shape  of 
the  chest,  the  hyperresonance,  and  the  low-pitched  and  prolonged 
expiration  characteristic  of  the  former. 

(2)  Pneumothorax. — This  is  usually  unilateral  and,  as  a  rule,  of 
sudden  development  and  urgent  character.  The  percussion  note  is 
of  a  distinctly  tympanitic  quality  rather  than  simply  hyperresonant, 
coin  percussion  elicits  the  bell  sound,  and  there  is  a  line  of  flat- 
ness at  the  base  of  the  lung.  Auscultation  reveals  amphoric  respi- 
ration without  vesicular  quality,  and  there  may  be  metallic  tinkling 
and  succussion  sounds.  Nevertheless  the  so-called  spontaneous 
pneumothorax  may  result  from  the  rupture  of  an  emphysematous 
bleb. 

(3)  Pleurisy  with  Effusion. — The  hyperresonant  or  slightly  tym- 
panitic (Skodaic)  percussion  sound  over  a  lung  compressed  by  a  pleu- 
ritic effusion  may  suggest  emphysema,  but  the  unilateral  flatness, 
the  fever,  and  other  evidences  of  pleural  inflammation  should  pre- 
vent such  a  mistake. 

(III)  Atrophic  Emphysema. — Senile  or  small-lunged  emphysema 
is  a  primary  atrophy  of  the  lungs,  the  air  cells  coalescing  to  form  a 
series  of  large  vesicles.  The  chest  is  small  and  the  intercostal  spaces 
narrowed  by  the  increased  obliquity  of  the  ribs  consequent  upon  the 
diminution  in  the  volume  of  the  lungs,  a  condition  directly  opposite 
to  that  which  obtains  in  hypertrophic  emphysema.  The  subjects 
have  had,  for  years,  chronic  bronchitis,  winter  cough,  and  dyspnoea, 
and  present  an  old  and  withered  appearance. 

(IV)  Compensatory  Emphysema. — When  there  is  deficient  expan- 
sion of  one  lung  or  a  portion  of  a  lung,  the  other  lung  or  a  part  of 
the  same  lung  will  expand  to  compensate  for  the  areas  which  have 
ceased  to  functionate.  Thus  one  lung  becomes  the  seat  of  a  com- 
pensatory emphysema  when  its  companion  is  crippled  by  cirrhosis, 
lobar  pneumonia,  a  large  pleural  effusion,  or  a  pneumothorax. 
Localized  vicarious  emphysema  occurs  in  the  neighbourhood  of 
broncho-pneumonic  areas  and  tuberculous  deposits  or  scars,  and 
especially  at  the  anterior  margins  of  the  lung  if  extensive  pleural 
adhesions  prevent  its  expansion.  The  condition  is  occasionally  to 
be  recognised  by  the  local  finding  of  some  of  the  physical  signs 
which  are  indicative  of  general  emphysema. 


DISEASES  OF  THE  LUNGS  853 

XII.  Abscess  of  the  Liung. — («)  Causes. — An  acute  suppura- 
tive pneumonia  caused  by  pyogenic  organisms,  usually  the  Strepto- 
coccus pyogenes,  or  the  Staphylococcus^  less  commonly  by  the  Piieu- 
mococciis^  Bacillus  typhosus,  or  other  specific  germ.  The  suppura- 
tion may  be  diffuse ;  more  commonly  one  or  more  abscess  cavities  are 
formed.  Abscesses,  usually  small  and  multiple,  occasionally  large, 
may  f oIIoav  a  lobar  or  broncho-pneumonia,  but,  aside  from  suppurative 
infiltration,  this  is  a  rare  sequence,  except  with  inhalation  or  deglu- 
tition pneumonia  (including  foreign  bodies),  in  which  it  is  common. 
The  causative  organisms  may  reach  the  lung  in  infective  emboli 
during  the  course  of  pysemia,  puerperal  septicaemia,  purulent  osteo- 
myelitis, or  ulcerative  endocarditis,  with  or  without  the  production 
of  infarcts.  The  abscess  may  result,  by  extension  or  perforation, 
from  a  purulent  pleurisy,  or  the  perforation  of  an  hepatic  abscess  or 
suppurating  hydatid  cyst. 

{b)  Symptoms  and  Diagnosis. — If  the  abscess  follows  inspiration- 
pneumonia  and  is  of  sufficient  size,  the  condition  is  easy  of  recog- 
nition. There  will  be  a  chill,  high  fever,  and  sweating;  physical 
examination  reveals  the  signs  of  a  cavity,  and  an  examination  of  the 
expectoration  will  afford  characteristic  findings.  The  sputum  is 
yellow  or  greenish,  with  an  odour  which  is  offensive  but  not  putrid 
like  that  of  gangrene,  and  contains  particles  of  lung  tissue  and 
elastic  fibres,  often  in  large  numbers.  If  the  abscess  is  too  small  to 
cause  cavity  signs,  or  if,  as  in  septic  embolism,  there  are  multiple 
small  abscesses,  the  physical  signs  are  indefinite  and  the  symptoms 
are  overshadowed  by  those  of  the  general  pyaemia.  In  the  non- 
pyaemic  cases  ulcerative  endocarditis  of  the  left  heart  and  septic 
nephritis  may  occur  as  secondary  infections,  in  which  case  the  symp- 
toms of  these  lesions  will  supervene. 

(c)  Prognosis. — As  a  rule  death  follows.  In  the  abscesses  re- 
sulting from  pneumonia  there  are  occasional  recoveries,  and  if  the 
abscess  is  single  and  accessible,  surgical  aid  may  avail. 

XIII.  Gangrene  of  the  Lxing. — This  results  from  infection  of 
a  necrotic  area  in  the  lung  by  the  organisms  of  putrefaction,  plus  an 
abnormal  vulnerability  of  the  tissues. 

(«)  Causes.— DxohetQ^  in  particular,  and  general  debility  from 
long-continued  fevers,  predispose.  It  may  be  a  consequence  of  lobar 
pneumonia,  tuberculous  or  bronchiectatic  cavities,  and  hemorrhagic 
infarctions;  or  of  the  lodgment  of  foreign  bodies  in  the  bronchi, 
especially  particles  of  food,  or  infective  particles  from  disease  of 
the  upper  air  passages,  as  in  deglutition  or  inhalation  pneumonia ;  or 
the  perforation  of  a  carcinomatous  ulcer  of  the  esophagus  into  the 
lung  or  bronchus ;  or  be  due  to  pressure  upon  the  bronchi  by  aneu- 
56 


854  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

rism  or  tumour ;  or  obstruction  of  the  pulmonary  artery  by  embolism 
or  pressure.  An  embolus  from  a  gangrenous  area  elsewhere  may  in- 
itiate it.  It  may  also  result  from  the  direct  extension  of  disease  of 
the  ribs  or  of  the  necrotic  changes  attending  malignant  growths  of 
the  esophagus  or  stomach.  It  is  obvious  that  in  the  majority  of 
these  cases  there  is  death  of  the  part,  either  with  simultaneous  or 
secondary  putrefactive  infection,  and  that  gangrene  is  a  symj)tom 
rather  than  a  disease. 

(b)  Symptoms. — There  is  irregular,  usually  moderate,  fever,  with 
prostration,  rapid  pulse,  and  loss  of  flesh.  Infrequently  the  general 
symptoms  may  be  slight. 

The  physical  signs  are  those  of  cavity,  provided  the  latter  is  suffi- 
ciently large  and  so  situated  as  to  be  accessible  to  the  usual  methods 
of  determining  its  presence.  If  the  cavities  are  small  and  deep- 
seated  ihey  will  elude  recognition,  and  only  the  signs  of  the  bronchi- 
tis, which  always  coexists,  can  be  detected. 

The  characteristic  symptoms  are  the  intensely  fetid  odour  of  the 
breath  and  the  character  of  the  sputum.  The  expectorated  material 
is  usually  abundant,  and  when  allowed  to  stand  separates  into  three 
layers,  the  uppermost  consisting  of  a  thick,  grayish  froth ;  the  mid- 
dle, of  a  watery,  occasionally  greenish  or  brownish,  fluid ;  and  the 
undermost  of  a  heavy  greenish-brown  sediment  containing  fragments 
of  lung  tissue,  abundant  elastic  fibres,  pus,  blood  pigment,  fatty  crys- 
tals, granular  matter,  bacteria,  and  leptothrix.  Eed  cells  are  often 
present,  not  infrequently  in  macroscopic  quantities.  Dittrich's  plugs 
(page  836)  are  not  found.  Profuse  haemoptysis  may  occur  from  ero- 
sion of  a  large  vessel ;  the  pleura  may  be  perforated,  causing  emphy- 
sema or  pyopneumothorax ;  and  cerebral  abscess  may  be  a  conse- 
quence, as  in  bronchiectasis. 

(c)  Diagnosis. — The  distinguishing  symptom  is  the  horrible  odour 
of  the  breath,  which  may  permeate  the  air  of  a  large  ward.  It  is  more 
intense  than  that  of  putrid  bronchitis  or  abscess,  and  this  fact,  to- 
gether with  an  examination  of  the  sputum,  will  aid  in  separating  gan- 
grene from  either  of  the  affections  just  mentioned.  Xevertheless 
considerable  difficulty  may  be  experienced  in  the  differential  diagnosis. 

{d)  Prognosis. — In  the  majority  of  cases  death  results.  If  the 
gangrene  is  strictly  circumscribed,  recovery  may  occur  through  en- 
capsulation, with  discharge  of  the  broken-down  tissues  by  way  of 
the  bronchi.  In  accessible  localized  cavities,  whose  situation  can  be 
accurately  determined,  surgical  interference  has  been  successful. 

XIV.  "Nevr  Growths  in  the  Lungs. — The  most  common 
forms  are  carcinoma  and  sarcoma ;  rarely  primary  and  unilateral, 
usually  secondary  and  bilateral.    The  primary  forms  occur  with  equal 


DISEASES  OP  THE  LUNGS  855 

frequency  in  each  sex ;  the  secondary  involvements  are  more  common 
in  women.  The  secondary  neoplasms  may  originate  by  contiguity 
from  disease  of  the  mammary  gland  (most  common),  pleura,  medias- 
tinum, or  esophagus ;  or  by  metastasis  from  carcinoma  of  the  liver, 
uterus,  or  rectum,  or  an  osteo-sarcoma.  The  associated  lesions  are 
pleurisy,  either  carcinomatous  or  sero-fibrinous,  with,  perhaps,  a 
hemorrhagic  effusion ;  and  enlargement  of  the  tracheal,  bronchial, 
cervical,  and,  rarely,  the  inguinal,  lymph  glands. 

(a)  Symptoms. — The  disease  may  be  quite  latent  so  far  as  pulmo- 
nary symptoms  are  concerned.  Indeed,  in  any  case,  the  symptom* 
are  variable,  depending  upon  the  size,  localization,  multiplicity,  and 
other  characters  of  the  growths.  There  may  be  at  first  simply  the 
evidences  of  a  bronchitis.  Ultimately  there  is  cough,  with  the  so- 
called  prune-juice  or  currant-jelly,  rarely  grass-green,  sputum,  due  to 
an  admixture  of  blood  or  altered  blood  pigment;  pain,  depending 
largely  on  the  degree  to  which  the  pleura  is  involved ;  and  dyspncea, 
which  may  be  paroxysmal  and  caused  by  pressure  on  the  trachea. 
The  breath  and  sputum  may  be  offensive  because  of  putrefactive 
infection  of  necrotic  areas  (gangrene). 

Certain  pressure  symptoms  will  be  present  according  to  the  size 
and  site  of  the  growth.  Thus  there  may  be  dysphagia,  from  pressure 
on  the  esophagus;  dyspnoea,  from  pressure  on  the  trachea  or  large 
bronchi ;  hoarseness  and  aphonia,  from  pressure  on  the  recurrent 
laryngeal  nerve  and  consequent  vocal-cord  paralyses ;  distention  of 
the  veins,  cyanosis,  and  oedema  of  the  face,  neck,  and  one  or  both  of 
the  upper  extremities,  from  pressure  on  the  intrathoracic  venous 
trunks ;  and  displacement  of  the  apex  beat,  the  heart  having  been 
dislocated.  Fever  is  occasionally  present,  cachexia  develops,  and  pro- 
fuse haemoptysis  has  been  noted.  The  physical  signs  are  variable, 
depending  partly  on  the  growth,  but  largely  on  the  presence  or  ab- 
sence of  pleural  effusion.  The  affected  side  may  be  enlarged  and 
immobile  if  the  tumour  is  large,  although  the  bulging  is  more  com- 
monly due  to  fluid.  The  superficial  veins  of  the  chest  may  be  dis- 
tended, and  the  face,  neck,  and  upper  extremities  cedematous.  There 
is  dulness  or  flatness,  the  vocal  fremitus  is  diminished  or  absent, 
pleural  friction  sounds  are  frequent,  and  the  breath  sounds  are  usu- 
ally weakened.  Less  commonly  there  is  bronchial  breathing.  The 
cervical  or  axillary  glands  may  be  found  enlarged  and  hard. 

{h)  Diagnosis. — Primary  growths  are  difficult  to  diagnose,  and  a 
positive  decision  must  often  be  withheld  until  somewhat  distinctive 
symptoms  are  manifest,  viz.,  the  progressive  cachexia,  the  peculiar 
sputum,  the  pressure  symptoms,  the  glandular  enlargements,  and 
the  finding  of  unilateral,  irregular,  and  indefinite  physical  signs. 


856  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

In  secondary  growths,  the  occurrence  of  such  pulmonary  symp- 
toms as  have  been  described,  in  conjunction  with  the  presence  of 
malignant  disease  elsewhere,  or  a  history  of  the  previous  removal 
of  a  carcinomatous  or  sarcomatous  growth,  should  enable  a  diagnosis. 

If  the  pleura  is  involved,  an  examination  of  the  aspirated  fluid 
(page  651)  may  reveal  characteristic  cells. 

(c)  Prognosis. — The  disease  ends  fatally  after  an  average  dura- 
tion of  from  6  to  8  months,  with  extremes  of  6  weeks  and  2  years. 


V.  DISEASES  OF  THE   PLEURA 

I.  Pleurisy  in  General. — Inflammation  of  the  pleura  is 
doubtless,  for  the  most  part,  a  symptom  of  a  condition  rather  than  a 
separate  disease.  In  the  majority  of  cases  it  is  excited  by  micro- 
organisms or  their  products  ;  less  frequently  by  an  intoxication  such 
as  that  of  nephritis  or  gout ;  cold,  exposure,  and  injury  simply  pre- 
dispose. Pleurisy  may  be  acute  or  chronic  ;  and,  according  to  patho- 
logical character,  fibrinous,  sero-fibrinous,  purulent,  or  hemorrhagic. 
One  of  these  may  shift  into  another,  or  terminate  in  a  chronic  form, 
I)ut  in  a  considerable  number  of  cases  the  original  character  of  the 
inflammation  persists  without  change — e.  g,,  a  sero-fibrinous  pleurisy 
remains  sero-fibrinous. 

No  one  micro-organism  is  found  in  acute  pleurisy.  Thus  the 
^Bacillus  tuberculosis  is  responsible  for  many  cases,  either  primary  or 
secondary,  although  the  germs  occur  in  such  scanty  numbers  that 
they  are  rarely  detected  except  by  the  injection  of  large  quantities 
of  the  exudate  into  guinea-pigs.  In  the  pleurisy  associated  with 
lobar  pneumonia  the  pneumococcus  is  found,  although  the  germ  may 
be  present  without  pneumonia  ;  and  in  that  occurring  with  broncho- 
pneumonia and  some  cases  of  lobar  pneumonia  the  streptococcus  is 
the  active  agent.  In  purulent  pleurisy  the  pneumococcus  or  strep- 
tococcus may  be  discovered.  Occasionally  noted  are  the  Staphi/lo- 
coccus,  Bacillus  colt  communis,  Friedliinder's  bacillus,  typhoid  bacillus, 
diphtheria  bacillus,  gonococcus,  proteus,  and  the  bacillus  of  anthrax. 
The  three  principal  bacteriological  forms  of  pleurisy  are  the  tuhercu- 
lous,  pnetimococcic,  and  streptococcic. 

II.  Acute  Fibrinous  Pleurisy.  —  Causes. — Dry  or  plastic 
pleurisy  (without  fluid  exudate)  may  perhaps  occur  as  a  result  of 
cold,  but  much  more  commonly  it  is  secondary,  especially  to  lobar 
pneumonia,  less  frequently  to  pulmonary  abscess,  gangrene,  carci- 
noma, or  infarctions ;  or  to  pyaemia,  rheumatic  fever,  chronic  ne- 
phritis, or  chronic  alcoholism  ;  or  originate  by  extension  from  peri- 
carditis, peritonitis,  or  hepatitis.     It  has  a  special  relation  to  tuber- 


DISEASES  OP  THE  PLEURA  857 

culosis,  occurring  sometimes  as  a  primary  infection,  more  commonly 
as  a  secondary  event  to  a  pulmonary  tuberculous  focus. 

Symptoins. — There  are  stitch  pains  in  the  side,  usually  in  the 
neighbourhood  of  the  nipple,  increased  by  movement  and  especially 
by  inspiration,  and  accompanied  by  a  dry  and  painful  cough.  Both 
cough  and  respiration  are  restrained,  and  the  patient  bends  toward 
the  affected  side  in  order  to  minimize  the  pain.  For  the  same  rea- 
son the  breathing  is  hurried,  shallow,  jerking,  and  mainly  abdominal 
in  type.  Fever  is  usually  present,  but  seldom  exceeds  101°,  and  in 
mild  cases  may  hardly  rise  above  the  normal. 

Physical  examination  reveals  deficient  expansion  on  the  affected 
side,  with  rubbing,  grazing,  or  crepitating  friction  sounds.  Unless 
the  amount  of  fibrin  is  considerable  there  will  be  no  change  in  the 
vocal  fremitus  or  the  percussion  note. 

Diagnosis  and  Prognosis. — The  severe  pain  of  pleurodynia  and 
intercostal  neuralgia  may  closely  simulate  a  'dry  pleurisy,  but  the 
absence  of  fever  and  friction  sounds  in  the  former  two  renders  the 
discrimination  easy.  Eecovery  is  usual  after  a  duration  of  from  a  few 
days  to  2  or  3  weeks,  but  repeated  attacks  lead  to  extensive  adhesions 
and  thickening  of  the  pleura.  The  possibility  of  its  occurrence,  either 
at  the  base  or  the  apex  of  the  lung,  as  a  symptom  of  tuberculosis, 
should  be  borne  in  mind. 

III.  Sero-fLbrinous  Pleurisy. — May  be  the  second  stage  of  a 
dry  pleurisy,  but  there  is  often  a  serous  exudate  from  the  first. 

Causes. — These  are  essentially  the  same  as  for  II  preceding.  The 
proportion  of  cases  due  to  tuberculous  infection  is  variously  esti- 
mated at  from  one  third  to  three  fourths,  usually  secondary  to  pul- 
monary tuberculosis,  occasionally  to  tuberculous  peritonitis.  Other 
cases  arise  in  connection  with  rheumatic  fever,  lobar  or  broncho- 
pneumonia, typhoid  fever,  pericarditis,  carcinoma  or  cirrhosis  of  the 
liver,  and  chronic  nephritis.  Exposure  to  cold  and  damp,  or  injuries 
of  the  chest,  quickly  predispose. 

Symptoms.— As  a  rule  the  onset  is  gradual.  There  is  pain  in  the 
side,  usually  referred  to  the  nipple  or  axilla,  less  commonly  (when  the 
diaphragmatic  pleura  is  involved)  to  the  abdomen  or  the  lower  part 
of  the  back.  It  is  sharp  and  catching,  and  aggravated  by  coughing, 
deep  breathing,  or  other  movements.  When  effusion  occurs  and  the 
inflamed  surfaces  are  separated  the  pain  lessens  or  disappears.  There 
is  dyspnoea,  due  at  first  to  the  pain,  later,  unless  the  effusion  has  oc- 
curred very  slowly,  to  pressure  of  fluid  upon  the  lung.  Large,  slowly 
formed  effusions,  as  in  latent  pleurisy,  may  be  unattended  by  dyspnoea 
except  on  exertion.  In  severe  cases  orthopnoea  and  cyanosis  may  be 
manifest.     The  patient  is  apt  to  lie  upon  the  affected  side.     Cough, 


858  DIAGNOSIS,   DIRECT   AND  DIFFERENTIAL 

usually  short  and  dry,  or  with  a  slight,  occasionally  blood-streaked 
expectoration,  is  an  early  symptom.  There  is  fever,  which  at  the 
onset  may  be  102°  to  103°,  often  falling  in  a  day  or  two  to  101°  or  even 
less,  and  usually  disappearing,  always  by  lysis,  in  from  1  to  3  or  more 
weeks.  The  affected  side  may  be  1  or  2  degrees  warmer  than  the 
other.  The  pulse  is  frequent,  and  in  large  effusions  may  present 
abnormalities  in  rhythm  and  size.  Except  during  the  absorption  of 
the  fluid,  when  it  may  increase  to  80  or  more  ounces,  the  total  daily 
output  of  urine  is  diminished.  The  bowels  are  usually  constipated. 
Nausea  and  vomiting  are  infrequent  initial  symptoms. 

The  physical  signs  are  important,  and  vary  with  the  three  stages 
of  the  disease :  the  dry  stage,  the  stage  of  effusion,  and  the  stage  of 
resorption.  The  signs  of  the  first  stage  are  those  of  acute  fibrinous 
pleurisy  (see  II  preceding) ;  of  the  second  as  follows  : 

Inspection  and  Palpation. — The  affected  side  expands  imperfectly, 
and  if  the  effusion  is  large  there  is  an  increase  in  its  size  with  oblit- 
eration or  bulging  of  the  intercostal  spaces.  (Edema  of  the  chest 
walls  and  fluctuation  are  very  seldom  manifest.  Depending  upon 
the  quantity  of  the  effusion  the  apex  beat  is  displaced  to  a  varying 
extent :  in  right-side  exudates,  to  or  beyond  the  left  mammillary  line 
in  the  4th  or  5th  interspace,  or  even  into  the  axilla;  in  left-side 
exudates  it  may  lie  behind  the  sternum  and  be  imperceptible,  or  be 
carried  to  or  to  the  outside  of  the  right  mammillary  line  in  the  3d 
and  4th  interspaces.  It  should  be  remembered  that  the  liver  or  the 
spleen  may  be  pushed  downward  by  the  effusion,  and  the  displace- 
ment may  simulate  enlargement  of  these  organs.  The  vocal  fremitus 
is  diminished  or  absent  according  to  the  amount  of  the  effusion — a 
most  valuable  sign — although  it  may  persist  with  large  exudates  if 
there  are  conducting  bands  of  adhesion  between  lung  and  chest  wall, 
is  present  in  infants  especially  while  crying,  and  is  less  reliable  in 
women  than  in  men.  Mensuration. — In  large  effusions,  after  making 
due  allowance  for  the  normally  larger  size  of  the  right  chest,  the  af- 
fected side  is  found  upon  measurement  to  exceed  the  other  by  ^  to  1| 
inches,  especially  at  the  end  of  expiration. 

Percussion. — There  is  impaired  resonance,  passing  into  dulness  or 
absolute  flatness  as  the  effusion  increases.  This  is  usually  first  per- 
ceived posteriorly.  If,  by  gentle  percussion,  the  upper  limit  of  the 
dulness  is  determined,  it  is  found  to  be  at  a  higher  level  posteriorly 
than  in  front.  With  a  moderate  effusion,  the  patient  sitting  upright, 
the  line  of  dulness  has  the  "  S  "  curve.  This  line,  beginning  rather 
low  down  in  the  back,  passes  upward  from  the  spine  and  curves 
obliquely  across  the  back  to  the  axillary  region,  whence  it  descends 
anteriorly  to  the  sternum.     Movable  dulness — a  change  in  the  posi- 


DISEASES  OF  THE  PLEURA  859 

tion  of  the  line  of  dulness  obtained  by  marking  it  in  the  mammillary 
line  while  erect,  and  then  while  lying  down — is  an  unmistakable  sign 
of  fluid,  but  can  not  be  demonstrated  in  very  large  or  encysted 
effusions.  The  dulness  or  flatness  of  fluid  has  a  peculiar  resistant 
quality  readily  recognised  by  practice.  Skoda's  resonance,  a  tym- 
panitic percussion  note,  which  may  be  elicited  under  the  clavicles 
and  above  the  level  of  the  fluid  posteriorly,  is  very  suggestive  of 
effusion.  With  large  effusions  cracked-pot  resonance  and  the  tracheal 
tone  may  be  obtained.  On  the  right  side  the  dulness  is  continuous 
with  that  of  the  liver ;  on  the  left  side,  in  the  mammillary  line,  it 
may  extend  downward  and  abolish  the  tympanitic  resonance  of 
Traube's  semilunar  space. 

AVith  reference  to  the  amount  of  fluid.,  it  may  be  clinically  useful 
to  consider  as  a  slight  effusion  one  which  causes  distinct  dulness  only 
at  the  base  posteriorly ;  a  moderate  one,  dulness  rising  to  the  4th  rib 
anteriorly ;  a  large  one,  dulness  up  to  the  2d  rib ;  and  a  copious 
effusion,  dulness  to  the  clavicle,  perhaps  passing  beyond  the  sternum 
to  the  opposite  side. 

Auscultation. — Commonly  the  breath  sounds  over  the  fluid  are 
weak  or  absent,  but  not  infrequently  in  large  effusions  there  is  dis- 
tinct but  distant  bronchial  breathing.  At  and  above  the  level  of  the 
fluid  the  breathing  is  broncho-vesicular  or  even  bronchial.  The  vocal 
resonance  is  usually  annulled  over  the  body  of  the  effusion,  but  there 
may  be  bronchophony.  At  the  upper  line  of  the  fluid  there  is  often 
a  peculiar  quavering,  hesitating  quality  of  the  voice  sounds,  or  the 
bleating  sounds  of  egophony  may  be  present.  In  children  the  voice 
and  breath  sounds  may  have  a  metallic  or  amphoric  quality,  which, 
with  the  loud  rales  sometimes  heard,  will  strongly  but  incorrectly 
suggest  the  presence  of  a  cavity.  The  ready  transmission  of  the 
whispered  voice  (Baccelli's  sign)  is  indicative  of  a  serous  rather  than 
a  purulent  exudate.  If  the  portion  of  the  pleura  which  overlies  the 
heart  is  inflamed  there  may  be  a  pleuro-pericardial  friction  sound. 

Varieties.— (1)  Latent  Pleurisy.— In  a  certain  proportion  of  cases 
the  onset  of  the  disease  is  insidious,  with  little  or  no  pain,  a  sub- 
febrile  temperature,  and  dyspnoea,  slight,  and  manifested  only  on 
exertion.  The  patient  is  conscious  simply  of  an  indefinite  malaise; 
but  on  examination  a  copious  effusion  may  be  found,  which  has  oc- 
curred so  gradually  that  the  intrathoracic  organs  have  been  able  to 
adjust  themselves  to  the  changed  conditions  without  notable  distress. 

(2)  Diaphragmatic  Pleurisy .—V\evir\i\%,  usually  dry,  sometimes 
serous,  and  limited  to  the  diaphragmatic  pleura,  may  occur  alone,  or 
be  a  part  of  a  general  pleurisy.  The  pain  is  sharp  and  severe,  and 
is  felt  in  the  epigastrium,  especially  in  a  line  from  the  end  of  the  10th 


860  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

rib  to  the  ensiform  cartilage.  It  is  aggravated  by  pressure  upon  the 
insertion  of  the  diaphragm  at  the  10th  rib,  and  by  breathing  or  swal- 
lowing. The  abdominal  muscles  are  fixed,  and  the  respiration  is  of 
the  thoracic  type,  sometimes  with  severe  dyspnoea  and,  occasionally, 
anginal  attacks,  vomiting,  and  severe  cough.  There  may  be  fever, 
perhaps  of  high  degree.  An  entire  absence  of  physical  signs  with 
the  presence  of  severe  subjective  symptoms  is  characteristic  of  this 
variety  of  pleurisy.     Rarely  the  inflammation  is  purulent. 

(3)  Interlobar  Pleurisy. — In  all  cases  of  acute  pleurisy  the  serous 
surfaces  lying  between  the  lobes  are  inflamed,  and  not  very  uncom- 
monly they  become  adherent,  thus  inclosing  fluid,  either  serous  or 
purulent,  between  the  apposed  portions  of  the  lung.  This  takes 
place  most  frequently  close  to  the  root  of  the  right  lung,  between 
the  upper  and  middle  lobes.  Such  a  collection,  usually  small  in 
amount,  may  perforate  a  bronchus  with  resulting  purulent  sputum, 
an  event  which,  as  the  other  symptoms  are  quite  indefinite  and  the 
history  of  a  previous  pleurisy  is  sometimes  absent,  may  be  the  first 
suggestive  evidence  of  the  condition.  The  diagnosis  is  extremely 
difficult,  and  may  require  a  number  of  exploratory  punctures. 

(4)  Encysted  Pleurisy. — The  effusion,  sometimes  serous,  more 
commonly  purulent,  is  encapsulated  by  the  formation  of  limiting 
adhesions  between  the  pleural  surfaces.  The  loculi  or  sacs  may  be 
present  in  any  part  of  the  chest,  often  in  that  part  of  the  pleura 
between  the  midaxillary  line  and  the  spine,  or  between  the  base  of 
the  lung  and  the  diaphragm.  With  a  pleuritic  history  suggestively 
circumscribed  dull  areas  may  be,  but  are  seldom,  encountered.  Usu- 
ally the  diagnosis  is  beset  with  difficulties,  and  is  made  by  an  assidu- 
ous use  of  the  aspirating  needle  in  suspected  cases  presenting  indefi- 
nite pleuritic  symptoms  and  signs. 

(5)  Tuherculoiis  Pleurisy. — See  page  731. 

Diagnosis. — In  the  majority  of  cases  there  is  little  difficulty  in 
making  a  correct  diagnosis  from  the  symptoms,  particularly  the 
physical  signs.     The  following  conditions  may  cause  uncertainty : 

(1)  Pneumonia. — The  bronchial  or  amphoric  respiration  and  bron- 
chophony which  may  be  present  in  some  cases  of  pleurisy,  especially 
in  children,  may  be  very  perplexing,  and  a  pneumococcus  pleurisy 
at  the  time  of  onset  may  closely  simulate  a  lobar  pneumonia.  In 
the  latter  disease  there  is  an  initial  rigour,  the  fever  is  higher,  the 
prostration  more  decided,  the  dyspnoea  of  greater  intensity,  and  there 
is  rusty  sputum.  Labial  herpes  is  suggestive,  and  the  unilateral 
flush  on  the  cheek  is  not  seen,  as  a  rule,  in  pleurisy.  Moreover,  in 
pneumonia  the  dulness  is  less  resistant,  the  vocal  fremitus  and  vocal 
resonance  are  increased,  not  diminished  or  absent ;  there  is  no  dis- 


DISEASES  OP  THE  PLEUEA  861 

placement  of  heart,  spleen,  or  liver,  and  the  intercostal  spaces  do  not 
bulge.  Finally,  the  crucial  and  safe  test  of  exploratory  puncture  is 
decisive,  and  should  always  be  employed  in  a  doubtful  case.  It 
should,  of  course,  be  remembered  that  pneumonia  and  a  pleuritic 
effusion  may  coexist  (pleuro-pneumonia). 

(2)  Hydrothorax.— The  majority  of  the  physical  signs  are  iden- 
tical with  those  of  pleurisy,  but  the  absence  of  fever,  pain,  and  fric- 
tion sounds,  together  with  the  history  of  disease  of  the  heart  or  kid- 
ney in  hydrothorax,  usually  enables  a  ready  differentiation. 

(3)  Pericardial  Effusion. — This,  if  extremely  copious,  may  closely 
simulate  a  left-side  pleural  effusion.  But  in  pericardial  effusion 
there  is  pulmonary  resonance  at  the  base,  tympanitic  or  dull  tympa- 
nitic resonance  in  the  axilla  and  around  the  border  of  the  distended 
sac,  and  the  heart  is  not  displaced  to  the  right  of  the  sternum. 
Moreover,  the  dyspnoea  is  extreme  in  comparison  with  the  apparent 
amount  of  effusion,  the  pulse  is  small  and  paradoxical  (page  373),  and 
there  is  often  a  history  of  antecedent  rheumatic  fever. 

(4)  Intrathoracic  Grotvths. — Carcinoma  of  the  lung  or  pleura,  or 
hydatid  cysts  of  the  pleura,  may  cause  dulness,  absent  or  weak  breath 
sounds,  and  displacement  of  the  apex  beat,  thus  closely  simulating  a 
pleural  effusion.  But  the  dulness  is  more  circumscribed  and  lies 
most  commonly  in  the  middle  or  upper  part  of  the  chest,  while  the 
vocal  fremitus  and  resonance  are  often  preserved,  thus  resembling 
consolidation  rather  than  fluid.  The  history,  too,  is  apt  to  differ 
from  that  of  a  pleurisy.  It  is  to  be  remembered,  however,  that 
pleural  effusion  is  a  common  concomitant  of  such  growths  (page 
854),  and,  if  present,  a  differential  diagnosis  is  extremely  difficult  or 
impossible  until  pressure  symptoms  become  manifest. 

(5)  Hepatic  Abscess  or  Cyst. — This,  when  of  sufficient  size  and 
suitably  located,  may  push  the  diaphragm  high  up  and  cause  dulness 
and  weak  or  absent  respiration  at  the  right  base,  thus  simulating  a 
pleural  effusion.  The  upper  line  of  dulness  in  such  cases  is  immov- 
able and  often  curved,  convexity  upward,  and  a  friction  sound  is 
audible  over  the  dull  area,  which  would  not  be  the  case  if  the  pleural 
surfaces  were  separated  by  fluid. 

Course  and  Prognosis. — In  non-tuberculous  cases  the  fever  lasts 
from  1  to  3  weeks,  according  to  the  severity  of  the  attack,  but  the 
non-febrile  stage  is  extremely  variable.  Small  effusions  may  disap- 
pear very  rapidly,  but  the  resorption  of  large  effusions  may  require 
many  weeks  or  several  months  if  not  aspirated.  In  tuberculous  pleu- 
risy the  resorptive  process  is  apt  to  be  slow.  If  a  sero-fibrinous  pleu- 
risy becomes  purulent  the  fever  persists.  As  the  effusion  is  resorbed 
the  physical  signs  gradually  shift  back  to  the  normal,  and  rubbing, 


862  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

creaking,  or  crepitating  friction  sounds  become  audible  when  the 
previously  separated  pleural  surfaces  are  again  in  contact.  Dulness 
and  weak  breath  sounds  may  persist  at  the  base  for  a  few  or  many 
months.  The  j^t'ognosis  is  usually  good,  and  even  in  tuberculous 
cases  complete  recovery  may  take  place.  In  rare  instances  sudden 
death  may  occur,  due  possibly  to  oedema  of  the  opposite  lung,  cardiac 
degeneration,  or  embolism  or  thrombosis  of  the  pulmonary  artery  or 
of  the  heart  itself. 

IV.  Purulent  Pleurisy. — («)  Causes. — Empyema  is  a  rare 
sequence  of  acute  sero-fibrinous  pleurisy,  except  in  children,  in  whom 
effusion,  if  not  purulent  at  the  onset,  may  rapidly  become  so.  It  is 
common  as  a  secondary  lesion  in  infections,  especially  scarlet  fever, 
pneumonia,  pulmonary  tuberculosis,  or  pyaemia,  rarely  in  measles, 
pertussis,  and  typhoid  fever.  Finally,  it  may  follow  perforation  of  a 
tuberculous  or  gangrenous  cavity  or  a  subphrenic  abscess  into  the 
pleura,  carcinoma  of  the  lung  or  esophagus,  fracture  of  a  rib,  or  a 
penetrating  wound  of  the  chest. 

(i)  Symptoms.  —  The  onset  may  be  sudden  and.  severe,  with 
cough,  dyspnoea,  and  pain  in  the  side,  subsequently  becoming  less 
marked.  More  commonly  it  comes  on  insidiously,  as  a  secondary 
event,  and  the  thoracic  symptoms  are  mild  or  even  lacking.  Fever  is 
always  present,  usually  irregular  and  intermittent,  and  often  accom- 
panied by  chills  and  sweats.  There  is  always  a  leucocytosis,  often  of 
high  grade ;  and  the  urine  may  contain  indican  and  albumoses,  find- 
ings indicative  of  a  purulent  rather  than  a  serous  effusion. 

The  physical  signs  are  identical  with  those  of  sero-fibrinous  pleu- 
risy (page  858),  except  for  certain  suggestive  modifications.  In  empy- 
ema there  may  be  distention  of  the  veins  and  oedema  of  the  chest 
wall,  signs  which  are  extremely  rare  in  serous  effusions.  The 
enlargement  of  the  affected  side  is  much  greater,  and  bulging  of  the 
interspaces  much  more  common,  especially  in  children,  and  in  them 
the  breath  sounds  over  the  exudate  may  be  of  a  distinctly  bronchial 
character.  The  whispered  voice  is  not  as  a  rule  transmitted  through 
a  purulent  effusion  (Baccelli's  sign).  In  neglected  cases  a  fluctuat- 
ing, reddened  pouting  or  protrusion  may  be  noted,  indicating  an 
imminent  external  discharge  {empyema  necessitatis),  or  a  fistulous 
opening  may  already  be  present.  This  takes  place  most  commonly 
in  front,  at  the  5th  interspace,  but  may  occur  in  the  3d,  4th,  or  5th 
space,  or  posteriorly,  at  the  angle  of  the  scapula.  There  may  be 
multiple  openings.  The  displacement  of  the  liver  and  heart  is 
greater  in  empyema  than  with  the  same  amount  of  serous  effusion. 
In  certain  cases  of  empyema,  but  occurring  with  extreme  rarity  in 
serous  exudates,  there  is  a  distinct  pulsation,  synchronous  with  the 


DISEASES  OF  THE  PLEURA  863 

heart's  action,  over  the  exudate.  It  may  be  felt  or  seen  in  2  or 
3  interspaces,  or  over  the  front  and  side  of  the  chest,  very  seldom 
posteriorly ;  or  the  protruding  tumour  of  an  empyema  necessitatis 
may  pulsate.  The  effusion  of  a  pulsating  pleurisy  is  usually  large, 
with  rare  exceptions  upon  the  left  side,  and  the  heart  action  is 
strong  and  forcible. 

(c)  Course  and  Prognosis. — Very  seldom  the  purulent  fluid  is 
absorbed,  with  resultant  great  thickening  of  the  pleura  and  retrac- 
tion of  the  chest  wall.  Perforation  of  the  chest  wall  is  common, 
and  in  rare  cases  a  communication  may  be  established  with  the 
stomach,  esophagus,  peritoneum,  or  pericardium.  The  pus  may 
enter  a  bronchial  tube  either  by  way  of  a  perforation,  or  by  percola- 
tion through  the  spongy  lung  tissue  when  its  protecting  pleural  cov- 
ering has  become  necrotic.  The  pus  has  been  known  to  pass  down 
along  the  spine  to  the  iliac  fossae  and  point  at  the  usual  situations  of 
a  lumbar  or  psoas  abscess. 

The  progyiosis  depends  somewhat  on  the  nature  of  the  primary 
disease.  A  pneumococcus  empyema  has  a  favourable  outlook  ;  tuber- 
culous and  streptococcic  empyemas  are  less  promising.  Drainage 
by  way  of  a  perforated  bronchus  is,  in  a  considerable  number  of 
instances,  followed  by  recovery ;  so  also  with  perforation  of  the 
chest  wall.  Much  depends  on  an  early  diagnosis  and  prompt  surgical 
treatment.  That  no  case,  however  desperate,  should  be  deprived 
of  operation  is  an  axiom  the  truth  of  which  has  been  repeatedly 
verified.  The  prognosis  is  rather  better  in  children  than  in  adults, 
but  judging  from  personal  experience  the  percentage  of  recoveries, 
taking  all  cases  together,  should  be  large. 

{(l)  Diagnosis. — The  discrimination  between  sero-fibrinous  pleu- 
risy and  empyema  depends  upon  exploratory  puncture.  A  failure  to 
discover  micro-organisms  in  a  creamy  pus  is  suggestive  of  the  tuber- 
culous nature  of  the  inflammation.  A  pulsating  pleurisy  may  be 
differentiated  from  an  aneurism  by  the  pleuritic  history,  the  absence 
of  bruit  and  diastolic  shock,  and  the  location  of  the  swelling  farther 
to  the  left  than  is  usual  in  aneurism. 

Y.  Hemorrhagic  Pleurisy.— A  bloody  exudate  may  be  due  to 
tuberculosis  or  carcinoma  involving  the  pleura ;  hepatic  cirrhosis  or 
chronic  nephritis ;  the  severer  types  of  the  acute  infections  when 
complicated  by  pleurisy;  accidental  wounds  of  the  lung  during 
aspiration;  and  occasionally,  in  otherwise  healthy  persons,  to  un- 
known causes.  Pure  blood  in  the  pleural  cavity  {hcBmothorax)  may 
be  due  to  penetrating  wounds  of  the  chest ;  the  rupture  of  an  aneu- 
rism ;  or  the  pressure  of  a  tumour  on  the  thoracic  veins. 

VI.  Chronic  Pleurisy.— Two  varieties  are  recognised : 


864  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Chronic  Pleurisy  with  Effusion. — This  is  usually  a  sequence  of 
acute  sero-fibrinous  pleurisy ;  less  commonly  the  condition  may  be 
found  without  a  history  of  a  definite  time  of  onset.  The  physical 
signs  are  identical  with  those  of  acute  pleurisy  with  effusion.  Atten- 
tion may  be  drawn  to  the  condition  only  by  slight  dyspnoea  upon 
exertion  and  a  subfebrile  evening  rise  of  temperature.  The  effusion 
may  remain  for  months  or  years  without  diminution  in  amount  or 
change  in  character.  If,  as  may  occur,  especially  in  children,  it  be- 
comes purulent,  the  symptoms  of  empyema  supervene. 

Chronic  Dry  Pleurisy. — Adhesive  pleurisy  may  be  a  sequel  of  acute 
or  chronic  pleurisy  with  a  serous  or  purulent  effusion,  the  fluid  exu- 
date having  been  resorbed  or  discharged ;  or  it  may  be  primary  and 
dry  from  the  beginning,  and  perhaps  of  tuberculous  origin.  Bron- 
chiectases may  develop.  A  primitive  dry  pleurisy  may  originate  a 
chronic  interstitial  pneumonia,  and  is  sometimes  associated  with  adhe- 
sive (proliferative)  peritonitis  and  pericarditis. 

The  subjective  symptoms  are  slight.  There  may  be  occasional 
stitch  pains  and  dragging  sensations  in  the  affected  side,  but  the  gen- 
eral health  is  often  unimpaired  for  years. 

The  physical  signs  in  the  milder  degrees  of  chronic  adhesive  pleu- 
ris-y  comprise  slight  retraction  of  the  affected  side,  with  impaired 
expansion,  moderate  dulness,  and  weakened  breath  sounds.  In  the 
severer  cases,  especially  those  which  follow  empyema  necessitatis, 
there  is  marked  shrinking  of  the  affected  side,  the  spine  is  curved, 
the  shoulder  sags,  and  the  expansion  is  poor  or  absent.  The  heart 
may  be  drawn  to  the  right  or  left  by  the  retraction  of  the  fibrous 
tissue.  The  vocal  fremitus  is  diminished  or  absent,  and  there  is 
moderate  or  well-marked  dulness,  with  a  weak  respiratory  murmur 
and  occasional  friction  sounds,  over  the  lower  half  of  the  side  in- 
volved. In  rare  instances  there  may  be  unilateral  fiushing  or  sweat- 
ing of  the  face  or  dilatation  of  the  pupil,  probably  due  to  an  in- 
volvement, in  the  indurative  process,  of  the  first  thoracic  ganglion  at 
the  apex  of  the  pleural  cavity. 

VII.  Hydrothorax. — A  non-inflammatory  pleural  effusion  is 
usually  a  part  of  a  general  dropsy  due  to  cardiac  disease,  in  which  it 
is  as  a  rule  unilateral  and  on  the  right  side  ;  to  renal  disease,  in  which 
the  hydrothorax  is  almost  always  bilateral ;  and,  also  usually  bilateral, 
to  poverty  or  disease  of  the  blood,  as  in  pernicious  anaemia,  leucgemia, 
scurvy,  malaria,  s^'philis,  carcinoma,  and  severe  chronic  diarrhoea  or 
dysentery.  The  symptoms,  aside  from  those  due  to  the  causative 
affection,  are  dyspnoea,  cyanosis,  orthopnoea,  and  pseudo-asthmatic 
paroxysms,  their  severity  depending  on  the  amount  of  the  fluid. 
The  physical  signs  are  mainly  those  of  pleuritic  effusion  (page  858). 


DISEASES  OF  THE  PLEUKA  865 

VIII.  PneTimothorax. — Air  alone  is  rarely  present  in  the  pleu- 
ral cavity,  the  latter  almost  always  containing  serum  (sero-  or  hydro- 
pneumothorax),  or,  much  more  commonly,  pus  (pyopneumothorax) 
in  addition  to  its  gaseous  content. 

Causes. — The  most  common  cause  is  a  perforation  of  the  lung 
due  to  the  rupture  of  a  tuberculous  cavity  or  cheesy  focus  (90  per 
cent  of  all  cases),  or  of  cavities  due  to  inhalation  pneumonia,  ab- 
scess, gangrene,  bronchiectasis,  suppurating  bronchial  glands,  hem- 
orrhagic infarctions,  or  hydatid  cysts.  It  may  be  caused  by  perfo- 
ration of  the  lung  by  an  empyema,  or  perforation  of  the  pleural  cavity 
by  an  air-containing  subphrenic  abscess  or  abscess  or  carcinoma  of 
the  esophagus.  The  growth  of  the  gas  bacillus  in  a  pleural  exudate 
is  a  rare  cause ;  so  also  is  the  rupture  of  normal  or  emphysematous 
air  vesicles,  especially  though  not  solely  as  the  result  of  violent 
coughing  or  muscular  exertion  in  lifting  or  straining.  Penetrating 
wounds  of  the  chest,  including  as  a  rarity  exploratory  puncture,  may 
be  responsible.  It  is  most  frequent  in  adult  males,  and  most  com- 
mon on  the  left  side  (2  to  1). 

Symptoms. — Earely  the  onset  may  be  gradual  and  without  urgent 
symptoms.  Usually  there  are  sudden  and  severe  pain  in  the  side,  in- 
tense dyspnoea,  often  with  cyanosis,  and  the  pulse  is  frequent  and 
weak.  In  the  gravest  cases,  when  the  perforation  is  large  and  runs 
obliquely  so  that  it  has  a  valvular  action,  the  pleural  cavity  becomes 
tensely  distended  with  air,  the  lung  is  totally  compressed,  and  symp- 
toms of  collapse— syncope,  sweating,  subnormal  temperature,  and 
thready  pulse — ensue,  perhaps  soon  followed  by  death. 

The  physical  signs  are  characteristic,  depending  upon  the  simul- 
taneous presence  of  air  and  fluid  in  the  pleural  cavity,  for  in  the 
large  majority  of  instances  pleurisy  with  effusion,  seldom  serous,  usu- 
ally purulent,  succeeds  upon  the  perforation.  The  affected  side  is 
markedly  distended  and  immobile.  The  vocal  fremitus  is  diminished 
or  absent.  The  percussion  sounds  are  variable,  depending  partly 
upon  the  size  and  shape  of  the  air-containing  cavity,  largely  upon  the 
degree  of  tension  of  the  contained  air  and  the  presence  or  absence  of 
an  effusion.  Over  the  fluid  at  the  base  there  is  dulness  or  flatness. 
Over  the  air  there  is  usually  a  tympanitic  note,  often  with  a  some- 
what amphoric  quality ;  or  there  may  be  hyperresonance ;  or  dull 
tympany  (Skodaic  resonance) ;  or,  when  the  tension  is  extreme,  actual 
dulness— a  fact  to  be  remembered.  Wintrich's  change  of  sound 
(page  406)  or  cracked-pot  resonance  may  be  elicited  when  there  is  a 
free  communication  between  a  bronchus  and  the  pleural  cavity.  The 
transition  from  the  upper  limit  of  fluid  dulness  to  the  tympanitic 
area  is  abrupt,  and  movable  dulness  is  more  easily  detected  than  in 


866  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

simple  pleural  effusions.  The  voice  sounds  are  ringing  and  amphoric. 
The  heart,  liver,  and  spleen  are  displaced  to  a  greater  extent  than  in 
serous  pleurisy,  and  in  left  pneumothorax  the  cardiac  dulness  may- 
disappear.  Usually  the  respiratory  murmur  is  diminished  or  absent, 
but  there  may  be  distinct,  but  distant  and  generally  weak,  amphoric 
respiration.  Einging  rales  may  be  heard,  also  metallic  tinkling  upon 
coughing  or  deep  inspiration.  The  succussion  sound  and  the  coin 
sound  are  extremely  characteristic  phenomena. 

DiflFerential  Diagnosis. — The  history  and  the  physical  signs  are  so 
distinctive  that  a  mistake  in  diagnosis  is  not  common. 

An  extremely  large  pulmonary  cavity  may  afford  a  tympanitic 
percussion  note  and  ringing  or  amphoric  rales,  but  the  succussion 
sound  and,  except  in  rare  instances,  the  coin  sound  are  absent.  More- 
over, the  heart,  liver,  and  spleen  are  not  dislocated,  vocal  fremitus  is 
usually  increased,  and  there  is  depression  rather  than  bulging  of  the 
interspaces.  A  differentiation  of  pneumothorax  from  the  rare  suh- 
phrenic  pyopneumotliorax  (page  823)  may  be  required. 

A  distended  stomach,  by  giving  rise  to  tympanitic  percussion  over 
the  left  thorax,  with  succussion  sounds  and  metallic  tinkling,  may 
simulate  a  left  pneumothorax,  but  the  thorax  itself  is  not  distended, 
and  a  careful  physical  examination,  together  with  the  history,  will 
usually  prevent  confusion. 

Because  of  the  occasional  occurrence  of  a  dull  percussion  note 
over  a  pneumothorax  a  diagnosis  of  pleurisy  icith  effusion  may  be 
made ;  or,  on  the  other  hand,  an  unusually  sonorous  percussion  sound 
in  emphysema  may  suggest  pneumothorax ;  but  in  both  instances 
the  succussion  sounds,  metallic  tinkling,  and  coin  sounds  are  absent. 

Diaphragmatic  hernia,  a  very  rare  condition,  which  is  usually 
due  to  violent  exertion  or  a  crushing  injury,  but  is  occasionally  con- 
genital, may  exactly  simulate  pneumothorax,  the  air-containing 
stomach  and  intestines  lying  within  the  pleural  sac.  A  history  of 
severe  traumatism,  the  presence  of  cooing  or  mumbling  sounds  (nor- 
mal to  the  abdomen)  over  the  chest,  and  perhaps  the  abrupt  dis- 
appearance of  the  thoracic  symptoms  consequent  upon  a  sudden 
return  of  the  protruding  viscera  to  below  the  diaphragm,  may  sug- 
gest the  correct  diagnosis. 

Prognosis. — In  the  cases  due  to  tuberculosis,  gangrene,  or  abscess 
of  the  lung,  death  usually  takes  place  within  a  few  weeks.  Sub- 
sequent to  empyema  the  prognosis  is  more  favourable,  and  the  cases 
occurring  in  previously  healthy  individuals  frequently  recover.  The 
mortality  in  all  cases  is  about  70  per  cent  (West). 

IX.  New  Growths  of  the  Pleura. — These  almost  always 
arise  by  extension  from  carcinoma  of  the  lung,  less  commonly  by 


DISEASES  OP  THE  PLEURA  AND  MEDIASTINUM  867 

metastasis  from  the  lung  or  mammary  gland.  Primary  malignant 
disease  of  the  pleura  (endothelioma)  is  of  rare  occurrence. 

The  symptoms  and  signs  of  secondary  disease  of  the  pleura  are 
those  of  carcinoma  of  the  lung  (page  854)  plus  the  evidences  of  a 
chronic  pleurisy,  with  or  without  effusion.  The  previous  occurrence 
of  malignant  disease  of  the  breast,  and  the  finding  of  many  mitotic 
cells  in  the  aspirated  fluid  suggest  the  nature  of  the  pleuritic  disease. 
Primary  carcinoma  of  the  pleura  affords  simply  the  evidences  of 
chronic  pleurisy,  with  or  without  effusion.  Irregular  slight  fever 
with  occasional  subnormal  falls  may  be  present ;  there  is  pain,  rather 
greater  than  that  of  pleurisy ;  and  cachexia  may  develop.  The  diag- 
nosis is  rarely  made  during  life,  beyond  a  suspicion. 

X.  Diseases  of  the  Mediastinum. — Under  this  heading  are 
comprised  tumours^  abscess,,  and   enlarged  glands. 

(I)  Mediastinal  Tumours. — The  most  common  of  these  are 
sarcoma,  carcinoma,  and  lymphoma.  The  principal  points  of  ori- 
gin are  the  lungs  and  pleura,  the  lymph  glands,  and  the  remains 
of  the  thymus  gland.  Males  between  30  and  40  years  of  age  are 
most  commonly  affected. 

Symptoms. — The  symptoms  are  due  to  intrathoracic  pressure,  and 
the  disease  is  latent  until  the  growth  is  of  suflBcient  size  to  encroach 
upon  the  surrounding  structures. 

Dyspnoea  is  constant,  apt  to  occur  early  in  the  disease,  and  is 
usually  due  to  pressure  on  the  recurrent  laryngeal  nerves  or  the 
trachea,  less  commonly  to  displacement  of  the  heart  or  great  vessels, 
or  the  presence  of  a  large  pleural  effusion.  Occasionally  the  dyspnoea 
may  be  paroxysmal.  A  brazen  cough,  often  violent  and  paroxysmal, 
and  due  to  pressure  upon  the  recurrent  laryngeal  nerves  ("  aneuris- 
mal  cough  "),  usually  accompanies  the  dyspncea ;  a  husky  or  hoarse 
voice,  or  aphonia,  also  may  be  manifest.  The  pulse  may  be  either 
abnormally  slow  or  rapid,  owing  to  pressure  or  irritation  of  the  pneu- 
mogastric  or  sympathetic  nerves ;  and,  rarely,  sympathetic  involve- 
ment may  cause  unequal  pupils  or  localised  flushings.  There  are 
often  evidences  of  pressure  upon  the  vessels  (or  thrombosis),  most 
commonly  the  superior  vena  cava  and  its  tributaries.  The  visible 
veins  of  the  head,  neck,  upper  chest,  and  upper  extremities  become 
distended,  the  parts  may  be  cold,  cyanotic,  and  cedematous,  and  the 
fingers  may  be  clubbed.  There  may  be  bulging  of  the  sternum  or  a 
protruding,  perhaps  pulsating,  swelling  over  or  at  one  side  of  the 
sternum,  due  to  involvement  and  erosion  of  the  bone,  particularly  if 
the  growth  be  a  lymphoma.  The  cervical  glands  may  be  enlarged. 
There  may  be  unilateral  retraction  of  the  chest,  and  the  apex 
beat  may  be   thrust  away  from   its  normal   position.     There   are 


868  DIAGNOSIS,   DIRECT  AXD  DIFFERENTIAL 

dulness  and  diminished  or  absent  vocal  fremitus  over  the  areas  at 
which  the  growth  is  in  contact  with  the  chest  wall ;  and  over 
the  same  areas  the  breath  sounds  are  absent  or  weak,  rarely 
bronchial,  the  vocal  resonance  is  usually  lacking,  and  the  sounds 
of  the  heart  are  not  transmitted.  There  may  be  a  systolic  bruit 
over  a  protrusion.  In  many  cases  the  signs  of  pleural  effusion  are 
superadded. 

The  site  of  the  growth  may  be  suggested  by  a  certain  grouping  of 
symptoms  and  signs,  as  follows  : 

Anterior  Mediastinum. — The  physical  signs  of  pressure  are  prom- 
inent :  mainly  venous  distention,  oedema,  voice  changes,  dyspnoea,  or 
pupillary  inequalities,  with  enlarged  cervical  glands  and  bulging 
and  erosion  of  the  sternum.  The  growth  may  be  palpable  in  the 
episternal  notch.     It  commonly  originates  in  the  thymus  gland. 

Middle  and  Posterior  Mediastinum. — The  physical  signs  are  slight 
as  compared  to  the  symptoms,  of  which  the  most  important  are  early 
and  persistent  dyspnoea,  brazen  paroxysmal  cough,  dysphagia,  occa- 
sional fever,  and  frequent  cachexia.  There  may  be  oedema  of  the  up- 
per abdominal  wall  from  pressure  on  the  azygos  veins.  The  growth 
here  usually  originates  in  the  lymph  glands. 

Pleura  and  Lung. — If  the  growth  starts  in  the  lung  or  pleura  the 
pressure  symptoms  are,  at  first  certainly,  slight,  and  the  clinical  pic- 
ture is  that  of  a  pleurisy,  with  pain,  cough,  and  effusion.  The  pain 
increases,  the  cervical  glands  may  enlarge,  the  cough  persists,  and 
there  may  be  a  bloody  mucoid  expectoration.  The  patient  rapidly 
becomes  anaemic,  thin,  and  cachectic. 

Differential  Diagnosis. — Mediastinal  tumour  is  to  be  separated 
from  pleurisy  tvith  effusion  by  the  fact  that  in  the  latter  the  physical 
signs  are  limited  to  the  lower  rather  than  the  upper  half  of  the  chest, 
there  is  fever,  and  the  onset  is  as  a  rule  more  acute ;  from  pericardi- 
tis with  effusion,  by  the  pyriform  rather  than  irregular  dulness,  the 
finding  of  the  apex  beat  in,  rather  than  outside  of,  the  area  of  dul- 
ness, and  the  usual  presence  of  fever,  in  pericarditis. 

Most  commonly,  the  differential  diagnosis  wavers  between  a  me- 
diastinal growth  and  thoracic  aneurism — a  problem  often  difficult, 
and  not  seldom  impossible,  of  solution.  Both  conditions  give  rise  to 
pressure  symptoms  which  may  be  identical.  The  diastolic  shock, 
ringing  aortic  second  sound,  tracheal  tugging,  and,  if  an  external 
swelling  is  present,  expansile  pulsation,  of  aneurism  are  absent  in 
mediastinal  tumours.  In  the  latter  pain  is  less  severe,  and  cachexia 
and  enlargement  of  the  cervical  and  axillary  glands  are  much  more 
common.  Furthermore,  aneurisms  usually,  mediastinal  tumours 
rarely,  have  a  duration  of  more  than  18  months. 


DISEASES  OF  THE  MEDIASTINUM  869 

(II)  Mediastinal  Abscess. — A  rare  condition,  which  may  be 
4iciite,  usually  due  to  injury,  less  commonly  to  infectious  diseases, 
especially  erysipelas,  smallpox,  measles,  and  rheumatism ;  or  chronic^ 
generally  of  tuberculous  origin ;  and  is  most  frequently  seated  in  the 
anterior  mediastinum.     The  majority  occur  in  males. 

Symptoms. — In  acute  abscess  there  is  sharp,  often  throbbing,  sub- 
sternal pain,  with  fever,  perhaps  also  with  chills,  profuse  sweats, 
and  prostration.  If  the  abscess  is  of  suflBcient  size  there  may  be 
cough  and  dyspnoea  from  pressure.  If,  as  may  happen,  the  abscess 
points  at  an  intercostal  space,  or  erodes  and  perforates  the  sternum, 
a  fluctuating  and  pulsating  swelling  may  appear,  or  it  may  become 
palpable  in  the  episternal  notch.  Previous  to  the  appearance  of  a 
swelling,  dulness  upon  percussion  over  the  seat  of  the  abscess  may  be 
the  only  physical  sign.  The  pus  may  discharge  into  the  trachea  or 
esophagus  after  perforation,  and  in  rare  instances  has  made  its  way 
into  the  abdomen.  A  chronic  abscess  may  afford  signs  similar  to 
those  of  mediastinal  growths. 

Differential  Diagnosis. — A  fluctuating  and  pulsating  abscess  may 
be  differentiated  from  aneurism  by  the  absence  of  diastolic  shock, 
expansile  jjulsation,  and  murmur ;  and  in  the  acute  abscess  by  a  his- 
tory of  injury  and  the  presence  of  chill,  fever,  and  sweat.  Explora- 
tory puncture  with  a  fine  needle  is  allowable.  An  acute  abscess  is 
separated  from  a  mediastinal  growth  by  the  febrile  symptoms ;  a 
chronic  abscess,  by  puncture.  In  many  abscesses,  especially  the 
chronic  form,  spontaneous  cure  occurs  by  inspissation  of  the  pus. 

(III)  Mediastinal  Lymphadenitis. — Inflammation  of  the  me- 
diastinal lymph  glands  may  be  simple  or  suppurative. 

Simple. — The  glands  are  much  swollen  in  influenza,  pertussis, 
measles,  tuberculosis,  and  broncho-pneumonia;  and,  to  a  lesser  degree, 
in  all  inflammatory  affections  of  the  lungs  and  bronchi.  Whether 
enlargement  of  these  glands  can  be  determined  by  the  presence  of 
dulness  over  the  upper  sternum,  or  over  the  upper  part  of  the  inter- 
scapular region  and  the  dorsal  vertebrae  as  far  down  as  the  fourth 
(GuEXEAu  DE  Mussy),  is  opeu  to  question. 

Suppurative. — Suppuration  of  the  mediastinal  glands  is  most 
commonly  tuberculous,  but  may  follow  the  preceding.  There  are 
no  physical  signs,  but  the  pus  may  discharge,  after  perforation,  by 
way  of  a  bronchus  or  the  esophagus,  or,  as  in  a  reported  case,  per- 
forate the  aorta.  This  condition  is  to  be  remembered  as  a  possible 
explanation  of  a  single  profuse  expectoration  of  pus  during  the 
course  of  pulmonary  tuberculosis,  as  in  a  case  under  my  care. 


57 


870  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

SECTION     IV 
DISEASES   OF  THE   CIECULATOEY  SYSTEM 

{See  also  Section  XXXI,  Part  J,  pages  308  to  382) 

I.  DISEASES  OF  THE   PERICARDIUM 

I.  Pericarditis  in  General. — Inflammation  of  the  pericar- 
dium occurs  as  a  result  of  irritation  from  materials  contained  in  the 
blood,  or  by  extension  of  an  inflammatory  process  from  neighbouring 
structures,  or  in  consequence  of  injury. 

From  30  to  70  per  cent  of  the  cases  of  pericarditis  are  caused  by 
the  toxine  of  rheumatic  fever  or  acute  tonsilitis.  Less  commonly  it 
is  due  to  pyaemia  and  scarlet  fever ;  still  more  rarely  to  smallpox, 
influenza,  diphtheria,  and  measles ;  and  may  be  of  tuberculous  origin. 
It  is  also  associated  with  gout ;  nephritis,  especially  the  chronic 
interstitial  form ;  scurvy,  purpura  haemorrhagica,  and  diabetes.  By 
extension  it  may  complicate  pleuro-pneumonia,  especially  in  children 
and  topers  ;  pleurisy,  particularly  if  tuberculous  ;  mediastinal  tumour 
or  abscess ;  ulcerative  endocarditis,  and  cardiac  valvular  disease,  espe- 
cially at  the  aortic  orifice ;  disease  of  the  vertebrae,  ribs,  and  sternum ; 
disease  of  the  bronchial  glands  and  the  esophagus ;  ruptured  aortic 
aneurism ;  and  even  result,  by  perforation  into  the  pericardium,  from 
disease  of  the  abdominal  organs.  The  following  varieties  of  peri- 
carditis are  recognised :  plastic  or  fibrinous,  sero-fibri)ious,  supptira- 
tive,  hemorrhagic,  and  adhesive.  One  of  these  forms  may  shift  into 
another.  Different  micro-organisms  have  been  found  in  the  exudate, 
although  attempts  to  discover  them  are  not  always  successful.  The 
Staphylococcus,  Streptococcus,  Pneumococcus,  Bacillus  coli,  and  tuber- 
cle bacilli  have  been  encountered. 

II.  Acute  Plastic  Pericarditis. — Symptoms. — This,  the  most 
common  variety,  is  usually  secondary  to  some  existing  disease.  In 
the  majority  of  cases  special  subjective  symptoms  are  lacking  and 
only  a  routine  examination  of  the  heart  enables  its  recognition. 
In  other  instances  there  may  be  vague  sternal  discomfort  or  con- 
striction, or  actual  pain,  usually  slight,  exceptionally  severe  and 
anginose  in  type.  It  is  felt  over  the  pericardium,  occasionally 
extending  to  the  left  arm ;  or  at  the  ensif orm  cartilage  and  over  the 
upper  abdomen.  It  is  seldom  increased  by  pressure.  There  may  be 
dyspnoea,  palpitation,  and  perhaps  a  weak  and  irregular  pulse.  Fever, 
rarely  exceeding  102°  to  102.5°,  is  present.  The  physical  signs  are 
friction  fremitus,  not  always  present  and  usually  felt  over  the  lower 


DISEASES  OF  TEE   PERICARDIUM  871 

praecordial  area,  and  pericardial  friction  sounds.  These  sounds, 
superficial  and  intensified  by  pressure,  usually  double,  rarely  single 
or  triple,  are  synchronous  with,  but  last  longer  than,  the  first  and 
second  sounds  of  the  heart.  The  usual  points  of  maximum  audi- 
bility, which  often  change  with  position,  are  in  the  fourth  and  fifth 
interspaces  and  the  neighbouring  parts  of  the  sternum,  or  over  the 
aortic  area ;  less  frequently  at  the  apex  or  along  the  whole  length 
of  the  sternum.  As  a  rule,  their  audibility  is  limited  to  small  areas ; 
and  they  vary  from  time  to  time  in  position  and  character.  The 
quality  of  the  sound  is  described  as  grating,  rubbing,  whizzing,  or 
creaking.     There  may  be  a  pleuro-pericardial  friction  sound. 

Diagnosis.— The  pericardial  friction  sounds  are  so  distinctive 
that  mistakes  are  not  common.  The  to-and-fro  friction  sound  may 
suggest  aortic  incompetency,  but  the  superficial  character  of  the 
pericardial  rub,  its  variability,  increased  intensity  upon  pressure,  and 
the  lack  of  ef  act  correspondence  with  the  events  of  the  cardiac  cycle, 
together  with  the  absence  of  cardiac  hypertrophy  and  "  shot "  pulse, 
will  separate  it  from  the  valvular  lesion.  Very  seldom  there  is  a  fine 
systolic  crepitation  at  the  base  or  the  apex,  due  perhaps  to  abnormal 
dryness  or  calcareous  changes  of  the  pericardium  without  inflam- 
mation. 

Course  and  Prognosis. — Plastic  pericarditis  is  never  fatal,  but 
often  constitutes  the  first  stage  of  the  sero-fibrinous  form ;  or  may 
cause  (especially  tuberculous)  extensive  thickening  and  adhesion. 

III.  Sero-fibrinous  Pericarditis.  —  This  occurs  most  fre- 
quently as  a  sequel  of  plastic  pericarditis  in  connection  with  acute 
rheumatic  fever,  sometimes  preceding  the  articular  symptoms,  more 
rarely  appearing  without  antecedent  joint  inflammations ;  also  with 
nephritis,  pulmonary  tuberculosis,  and  septicaemic  conditions. 

Symptoms. — In  many  cases,  usually  those  secondary  to  some 
already  existing  disease,  the  onset  is  insidious,  with  an  entire  absence 
of  subjective  symptoms.  In  other,  especially  primary,  cases  there  is 
praecordial  pain,  discomfort,  or  distress,  aggravated  by  pressure  over 
the  lower  sternum.  As  effusion  occurs,  dyspnoea,  left-side  decubitus, 
even  orthopnoea,  become  manifest.  The  face  is  cyanotic  and  anxious, 
the  breathing  is  laboured,  often  irregular,  the  pulse  small  and  perhaps 
paradoxical.  Aphonia,  irritative  cough,  dyspliagia,  and  distention  of 
the  veins  of  the  neck  may  result  from  the  pressure  of  a  large  effusion. 
There  is  fever,  usually  irregular,  and  varying  from  101°  to  10-3°.  In 
the  graver  cases  there  may  be  constant  restlessness  and  persistent 
insomnia,  followed  by  delirium,  stupor,  and  coma.  The  condition 
may  be  such  as  to  resemble  delirium  tremens,  or  the  patient  may 
exhibit  great  mental  depression. 


872  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

The  2^^iysical  signs,  after  effusion  has  taken  place,  are  numerous 
and  important.  There  is  prsecordial  bulging  in  children,  even  with 
a  moderate  exudate ;  and  in  adults,  if  the  effusion  is  copious,  the 
anterior  and  lateral  portions  of  the  chest  are  enlarged,  the  intercostal 
spaces  are  prominent,  the  nipple  is  elevated,  and  there  may  be  cedema 
of  the  walls.  The  left  lobe  of  the  liver  may  be  depressed  by  the 
weight  of  the  fluid,  and  in  consequence  the  epigastric  region  become 
distinctly  prominent.  The  apex  beat  and  the  thrust  of  the  heart 
become  less  and  less  palpable  and  may  finally  disappear  as  the  effu- 
sion increases — an  important  sign.  Eriction  fremitus  and  friction 
sounds  may  persist  at  the  base,  rarely  at  the  apex,  and  are  most  read- 
ily elicited  when  sitting  upright,  but  are  ordinarily  not  heard  over 
the  body  of  the  heart  in  any  but  slight  effusions.  Percussion  shows 
a  much  increased  triangular  area  of  dulness,  within  which  a  feeble 
apex  beat  is  felt.  Dulness  in  the  fifth  interspace  to  the  right  of  the 
sternum  is  present  even  with  slight  effusions ;  and  in  Targe  effusions 
there  may  be  a  limited  area  of  slight  or  marked  dulness  in  the  left 
infrascapular  region.  The  lung  having  been  forced  back  and  com- 
pressed, there  may  be  dull  tympany,  with  weak  or  bronchial  breath- 
ing in  the  axilla  to  the  left  of  the  triangular  area  of  dulness.  The 
heart  sounds  at  the  apex  are  muffled,  faint  and  distant ;  at  the  base 
the  second  sounds,  especially  the  pulmonary,  may  be  clear  and  accen- 
tuated.    There  may  be  a  systolic  endocardial  murmur. 

Course  and  Prognosis. — The  acuteness  and  rapidity  of  the  disease 
are  variable.  The  effusion  may  reach  its  height  within  2  or  3  days 
and  the  process  of  resorption  then  begin ;  or  it  may  require  several 
weeks  of  gradual  increase  to  attain  the  maximum,  as  in  the  so-called 
subacute  and  chronic  cases.  Eheumatic  effusions  may  disappear  in 
2  or  3  weeks  after  absorption  has  begun.  In  large  and  fatal  effusions 
death  occurs  by  asthenia  at  the  end  of  2  or  3  weeks ;  or,  in  severe 
cases  attended  by  delirium  and  extreme  restlessness,  in  a  week  or  10 
days.  In  moderate  sero-fibrinous  effusions  recovery  is  the  rule,  with 
resulting  adhesion  between  the  pericardial  surfaces. 

DilFerential  Diagnosis. — The  insidious  onset  of  the  disease  leads 
to  many  diagnostic  errors  of  omission,  and  unless  the  case  has  been 
watched  from  the  beginning,  it  may  be  difficult  and  at  times  impos- 
sible, especially  if  the  chest  walls  are  unusually  thick,  to  distinguish 
between  a  copious  pericardial  effusion  and  a  dilated  heart,  possibly 
also  a  pleural  exudate.  As  a  rule,  with  proper  opportunities  for 
observation  from  an  early  period,  the  diagnosis  is  readily  made. 
The  differential  points  are  as  follows : 

(1)  Pleurisy  witli  Effusion. — See  page  861. 

(2)  Dilatation  of  the  Heart. — In  this,  as  compared  with  pericar- 


DISEASES  OP  THE  PERICARDIUM  873 

dial  effusion,  the  apex  beat  is  visible,  diffused,  and  wavy,  and  the 
shock  or  impulse  of  the  heart  is  more  clearly  palpable;  the  area 
of  dulness  is  not  so  distinctly  triangular,  it  does  not  vary  with 
change  of  position,  and,  although  it  may  be  quite  as  extensive  as 
that  of  an  effusion,  the  impulse  of  the  heart  will  be  visible  or  pal- 
pable over  its  entire  extent.  Only  in  rare  instances  is  the  dilatation 
so  great  as  to  compress  the  lung  and  cause  a  dull  tympanicity  in  the 
axillary  region.  Instead  of  its  distant  muffled  character  in  pericar- 
dial effusion,  the  first  sound,  although  short  and  weak,  is  distinctly 
and  clearly  heard.  Friction  sounds  and  fremitus  are  absent.  More- 
over, there  is  usually  no  pain  or  fever,  and  commonly  there  is  a  his- 
tory of  chronic  cardiac  disease. 

IV.  Purulent  Pericarditis. — Causes. — May  follow  a  serous 
pericarditis,  or  may  be  purulent  from  the  outset,  particularly  when 
due  to  tuberculosis,  sepsis,  or  the  acute  infections. 

Symptoms.,  Diagnosis^  and  Progtiosis. — The  physical  signs  are 
identical  with  those  of  a  serous  pericarditis ;  so  also  are  the  symp- 
toms, except  that  there  may  be  recurring  chills,  an  irregular  or 
suppurative  type  of  fever,  and  a  greater  degree  of  prostration. 
The  only  positive  evidence  of  empyema  of  the  pericardium  is  ob- 
tained by  exploratory  puncture,  but  the  special  symptoms  men- 
tioned, together  with  the  presence  of  an  antecedent  affection  which 
is  capable  of  causing  it,  may  lead  to  a  correct  conjecture  as  to 
the  purulent  nature  of  the  effusion.  The  |)rognosis  is  unfavoura- 
ble. The  pus  may  discharge  into  the  pleura,  esophagus,  stomach, 
or  bronchi. 

V.  Hemorrhagic  Pericarditis.— The  effusion  of  tuberculous 
or  cancerous  pericarditis,  whether  serous  or  purulent,  is  especially 
apt  to  be  hemorrhagic,  so  also  with  the  effusion  occurring  in  those 
who  are  old,  debilitated,  or  the  subjects  of  scurvy,  purpura,  etc. 

VI.  Chronic  Adhesive  Pericarditis. —  Varieties.— \js\xq\\j  a 
sequel  of  the  acute  forms.  If  there  is  simply  adhesion  between  the 
visceral  and  parietal  layers  of  the  pericardium,  there  are,  as  a  rule, 
no  recognisable  symptoms  indicative  of  the  condition.  But  if,  in 
addition,  the  chronic  inflammatory  process  extends  to  the  medias- 
tinal and  pleural  tissues  external  to  the  parietal  layer  of  the  peri- 
cardium, and  the  latter  in  consequence  becomes  adherent  to  the 
pleura  and  the  chest  walls  (indurative  mediastino-pericarditis),  ex- 
treme cardiac  hypertrophy  and  dilatation  may  result,  especially  in 
persons  under  30  years  of  age.  In  some  cases,  especially  in  children, 
there  may  be  an  associated  proliferative  peritonitis,  involving  par- 
ticularly the  peritoneal  covering  of  the  liver  and  spleen. 

Symptoms.— The  condition  is  often  latent  and  discovered  only 


874  DIAGNOSIS,   DIRECT  AXD   DIFFERENTIAL 

at  autopsy.     In  other  cases  the  symptoms  are  those  of  cardiac  hyper- 
trophy and  dilatation  and  sequent  myocardial  failure. 

The  physical  signs.,  when  present,  are  as  follows  :  Inspection  may 
show  a  marked  bulging  of  the  pericardium,  and  the  wavy  cardiac 
impulse  may  be  visible  over  a  large  area.  There  is  systolic  retrac- 
tion of  the  apex,  and  if  the  heart  is  extensively  adherent  to  the  dia- 
phragm a  systolic  tug  over  the  left  7th  and  8th  ribs  anteriorly,  and 
the  left  11th  and  12th  ribs  posteriorly,  may  be  seen.  For  a  similar 
reason  the  diaphragm  may  not  be  able  to  descend  during  inspiration, 
and  the  usual  epigastric  respiratory  movement  is  lacking.  There 
may  be  diastolic  collapse  of  the  jugular  veins  (Friedreich's  sign),  but 
this  is  of  little  value.  The  apex  beat  may  not  change  position  when 
the  patient  is  turned  upon  his  left  side,  the  adhesions  preventing. 
There  may  be  a  diastolic  shock,  a  sudden  rebound  of  the  heart  walls 
during  diastole,  after  having  been  drawn  together  during  systole 
against  the  resistance  of  the  adhesions.  The  pulsus  paradoxus 
may  be  present.  The  area  of  cardiac  dulness  is  much  increased, 
and  its  outlines  above  and  to  the  left  may  not  be  changed  by 
deep  inspiration,  the  pleuro  -  pericardial  adhesions  preventing  the 
normal  intrusion  of  the  lung  between  the  heart  and  the  chest 
wall.  Murmurs  are  not  necessarily  present,  but  they  may  be  heard 
as  evidence  of  pre-existing  valvular  disease,  or  are  due  to  relative 
InsuflBciencies  at  the  mitral,  tricuspid,  and  pulmonary  openings. 
Earely  there  is  a  distinct  presystolic  murmur.  Dry  or  crackling 
rales  (mediastinal  friction  sounds)  may  be  heard  occasionally  along 
the  sternum. 

VII.  Hydropericardium. — A  non-inflammatory  effusion  (dropsy 
of  the  pericardium)  is  usually  a  part  of  the  general  dropsy  of  renal 
or  cardiac  disease,  and  may  be  associated  with  hydrothorax ;  rarely 
it  occurs  alone,  especially  in  scarlatinous  nephritis.  It  may  also  be 
caused  by  the  pressure  of  an  aneurism  or  mediastinal  growth,  or 
by  thrombosis  of  the  cardiac  veins.  The  physical  signs  are  those  of 
pericarditis  with  effusion,  excepting  the  friction  sounds,  pain,  and 
other  evidences  of  inflammation.  Dyspnoea  is  practically  the  only 
symptom,  and  the  condition  is  often  unrecognised. 

VIII.  Haemopericardiuin. — Pure  blood  in  the  pericardium 
occurs  as  a  consequence  of  the  rupture  of  an  aortic  aneurism,  aneu- 
rism of  the  coronary  arteries,  and  rupture  of  the  heart ;  or  from  pene- 
trating wounds  of  the  heart.  If  due  to  the  bursting  of  an  aneurism, 
death  occurs  rapidly  from  mechanical  interference  with  the  action  of 
the  heart.  In  wound  or  rupture  of  the  heart  the  blood  may  escape 
slowly  and  life  be  prolonged  for  hours  or  days  with  dyspnoea,  signs  of 
effusion,  and  steady  failure  of  the  heart  muscle. 


DISEASES  OF  THE  PERICARDIUM  AND  HEART  875 

IX.  Pnexunopericardiuin. — Air  in  the  pericardium  is  usually 
caused  by  a  penetrating  wound.  Less  commonly  it  is  due  to  a  per- 
foration from  the  lungs,  especially  of  a  tuberculous  cavity,  or  an 
empyema,  or  ulcerative  or  malignant  disease  of  the  esophagus  or 
stomach ;  and  in  some  cases  to  the  growth  of  the  gas  bacillus  in  an 
existing  pericardial  effusion.  The  pericardium  always  becomes  in- 
flamed as  a  result  of  a  perforation,  and  effusion,  usually  purulent, 
results.  The  symptoms  are  substantially  those  of  pericarditis  with 
effusion.  The  physical  signs,  when  gas  and  fluid  coexist  in  large 
amount,  are :  An  area  of  dulness  over  the  fluid  and  of  marked  tym- 
panicity  over  the  gas,  the  dull  area  changing  its  site  and  shape  to  a 
notable  degree  with  a  change  of  posture.  The  apex  beat  may  be 
feeble  or  absent,  and  the  heart  sounds  weak  and  distant.  Friction 
sounds  may  be  heard,  together  with  the  curious  and  characteristic 
splashing  or  "  water-wheel "  sounds  (page  363). 

II.    DISEASES   OF   THE    HEART 

I.  Acute  Endocarditis. — Acute  inflammation  of  the  lining 
membrane  of  the  heart  is  usually  confined  to  the  valves,  is  almost  in- 
variably a  secondary  process,  and  in  many,  if  not  all,  cases  is  caused 
by  micro-organisms,  cold  and  exposure  predisposing.  The  most 
common  organisms  are  the  streptococcus,  staphylococcus,  pneumo- 
coccus,  and  gonococcus;  less  frequently  the  diphtheria  bacillus. 
Bacillus  typhosus.  Bacillus  coli,  influenza  bacillus,  and  others. 

Clinically  two  forms  are  recognised,  simple  endocarditis  and  malig- 
nant or  ulcerative  endocarditis,  although  the  pathological  process  is 
practically  the  same  in  both  and  the  differences  are  mainly  in  severity 
.and  malignancy. 

(I)  Simple  (Benign)  Acute  Endocarditis.— C«ws6-s.— Most  fre- 
quently associated  with  acute  rheumatic  fever,  tonsilitis,  chorea, 
pneumonia,  scarlet  fever,  and  phthisis ;  less  commonly  with  small- 
pox, chicken-pox,  typhoid  fever,  measles,  erysipelas,  and  diphtheria. 
Occurs  as  an  intercurrent  or  terminal  event  in  the  subjects  of  carci- 
noma, nephritis,  gout,  and  diabetes;  or  during  a  chronic  endocarditis. 

Symptoms.— Except  in  a  small  minority  of  cases  the  disease  is 
latent,  and  there  are  no  symptoms  pointing  to  the  heart.  There  may 
be  fever,  or  an  increase  in  that  which  may  be  already  present  as  a  part 
of  the  causative  disease,  with  palpitation  and  increased  frequency, 
possiblv  also  irregularity,  of  the  pulse.  Praecordial  pain  and  dyspnoea 
are  of^  rare  occurrence.  The  physical  signs,  unfortunately,  are 
extremely  unreliable.  Unless  there  is  hypertrophy  or  dilatation 
-due  to  pre-existing  valvular  disease,  or  dilatation  caused  by  an  asso- 


876  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

ciated  acute  myocarditis,  inspection,  palpation,  and  percussion  will 
reveal  nothing  abnormal.  Auscultation  usually  discovers  a  soft,, 
blowing,  systolic  murmur,  heard  most  commonly  over  the  mitral 
area,  less  frequently  over  the  aortic  cartilage,  and  not  transmitted 
to  any  great  distance.  K  the  heart  has  been  watched  from  the 
beginning  there  may  have  been  a  roughening  or  murmurish  pro- 
longation of  the  first  sound,  slowly  evolving  into  a  murmur. 

Diagnosis. — The  presence  of  one  of  the  causative  diseases  is  of 
great  importance  in  making  a  probable  diagnosis.  A  soft  blowing 
murmur  may  be  present  in  many  acute  febrile  diseases  without  endo- 
cardial inflammation,  but  it  is  more  likely  to  indicate  endocarditis  if 
it  is  heard  only  or  most  distinctly  over  the  mitral  area ;  less  likely  if 
over  the  aortic  area;  and  least  likely  if  over  the  pulmonary  area. 
The  most  reliable  physical  sign,  in  conjunction  with  the  history,  is 
the  observed  development  of  a  roughened,  murmurish  first  sound  into 
a  well-marked  systolic  mitral  murmur.  It  is  hardly  possible  to  rec- 
ognise attacks  of  simple  endocarditis  recurring  in  a  case  of  chronic 
valvular  disease,  as  the  physical  signs  of  the  latter  are  practically 
unaltered  by  the  supervention  of  an  acute  benign  valvulitis. 

Prognosis. — Favourable  as  to  life,  but  unfavourable  as  to  the  sub- 
sequent occurrence  of  chronic  valvular  defects. 

(II)  Malignant  (Ulcerative)  Endocarditis. — Causes. — Earely  pri- 
mary ;  in  the  great  majority  secondary  to  a  pre-existing  disease, 
especially  to  pneumonia ;  less  frequently  to  septicaemia,  erysipelas,, 
puerperal  fever,  and  gonorrhoea ;  least  commonly  to  acute  rheu- 
matic fever,  typhoid  fever,  scarlet  fever,  smallpox,  diphtheria,  and 
tuberculosis.  Chronic  valvular  disease  strongly  predisposes.  It  is 
to  be  borne  in  mind  that  a  benign  endocarditis  may  become  malig- 
nant, and  that  there  are  many  grades  of  severity  between  the  ex- 
tremes. 

Symptoms  and  Clinical  Varieties. — The  manner  of  invasion  and 
the  symptoms  of  ulcerative  endocarditis  are  so  variable  that  it  is 
best  to  consider  first  the  general  symptom^,  which  are  present  in  the 
majority  of  cases,  and,  second,  the  clinical  forms  of  the  disease. 

If,  as  usual,  it  is  a  condition  secondary  to  one  of  the  causative 
diseases  previously  enumerated,  there  may  be  simply  an  increase  in 
the  height  of  the  fever  or  a  change  in  its  type.  Ordinarily,  however, 
there  are  chills,  high  and  irregular  fever  followed  by  sweats,  some- 
times very  profuse,  with  delirium,  and  progressive  weakness  and 
emaciation.  These  symptoms  are  also  present  in  the  rare  primary 
form  of  the  disease  occurring  without  a  recognisable  antecedent 
cause.  The  fever  is  not  invariably  irregular  and  remittent,  but  may 
be  of  the  continued  type.     In  some  cases  delirium  may  be  followed. 


DISEASES  OF  THE   HEART  87T 

by  stupor  or  coma.  There  may  be  praecordial  oppression  and  dyspnoea. 
Jaundice  and  a  diffuse  roseolous  or  papular  erythema  may  be  present. 

Certain  phenomena,  of  much  diagnostic  value,  are  due  to  the 
lodgment  of  septic  particles  or  vegetations  which  are  detached  from 
the  inflamed  endocardium  and  swept  to  various  parts  or  organs  of 
the  body.  Thus  there  may  be  embolism  of  the  spleen  with  localized 
peritonitis,  pain,  and  enlargement  of  the  organ ;  of  the  kidney,  with 
pain  and  haematuria ;  of  the  liver,  with  pain  and  perihepatitis ;  of 
the  cerebrum,  with  hemiplegia ;  of  the  retina,  with  dimness  of  vision ;. 
of  the  stomach  and  intestines,  with  vomiting  and  diarrhoea  (not 
necessarily  of  embolic  origin) ;  of  the  skin  and  subcutaneous  tissues,, 
with  ecchymoses  or  petechial  spots ;  parotid  abscess ;  or  abscess  or 
gangrene  in  any  part  of  the  body.  In  right-side  endocarditis  there 
may  be  pulmonary  infarcts  with  resulting  pneumonia,  pleurisy, 
abscess,  or  gangrene.  Pericarditis  and  acute  suppurative  meningitis 
have  been  noted.     Leucocytosis  is  always  present. 

The  cardiac  physical  signs  may  be  absolutely  lacking.  Commonly 
there  are  one  or  more  systolic  murmurs  of  variable  intensity  either 
at  apex  or  base.  The  signs  of  an  associated  pericarditis,  pleurisy,  or 
pneumonia  may  be  discovered.  If,  as  frequently  happens,  the  endo- 
carditis has  supervened  upon  chronic  valvular  disease,  the  physical 
signs  of  the  existing  valvular  defects,  with  their  resultant  hyper- 
trophy or  dilatation,  will  be  present. 

Four  clinical  varieties  or  groups  are  recognised,  the  cardiac^  septic 
or  pi/(Bmic,  typhoid,  and  cerebral. 

(1)  Cardiac  Type. — This  group  embraces  those  cases  in  which  an 
acute  malignant  endocarditis  occurs  in  the  course  of  chronic  valvular 
disease.  The  onset  is  often  abrupt,  initiated  by  a  chill,  and  followed 
by  high  fever,  which  may  be  regularly  or  irregularly  remittent  or  in- 
termittent, with  or  without  recurring  chills.  Many  of  the  symptoms 
of  the  pyemic  or  typhoid  forms— see  (2)  and  (3)  following— may  be 
present.  The  already  existing  murmurs  may  remain  unchanged  in 
character,  or  may  become  more  intense  and  of  a  more  blowing  qual- 
ity. These  cases  may  be  acute  and  fatal,  or  chronic,  lasting  from  sev- 
eral months  to  a  year  or  even  longer ;  and  in  exceptional  instances 
recovery  may  take  place  after  a  varying  period.  The  latter  can  not 
properly  be  classed  as  malignant,  but  are  examples  of  a  severe  al- 
though benign  endocarditis. 

(2)  Septic  or  Pytemic  Type.— The  symptoms  are  those  of  a  pyaemia 
(page  697),  and  the  attack  usually  occurs  in  connection  with  suppu- 
rating wounds,  acute  necrosis,  or  puerperal  infection.  It  may  be  an 
initial  or  a  secondary  event  in  the  pyaemic  process,  and  indeed  is 
an  arterial  pyaemia.     The  cardiac  symptoms  may  be  overshadowed 


378  DIAGNOSIS,   DIRECT  AND   DIFFERP:XTIAL 

"by  the  general  symptoms  unless  the  occurrence  of  suggestive  embolic 
phenomena  attracts  attention  to  the  heart.  This  type  may  ensue  in 
the  course  of  chronic  heart  disease  without  a  recognisable  focus  of 
infection.  It  is  attended  with  rigours,  high  fever,  and  sweats,  and 
may  closely  resemble  quotidian  or  tertian  malarial  fever.  The  dura- 
tion varies  from  a  few  weeks  to  3  or  4  months. 

(3)  Typhoid  Type. — This  closely  simulates  typhoid  fever.  There 
may  be  early  prostration,  irregular  fever,  delirium,  drowsiness,  or 
coma,  with  diarrhoea,  abdominal  tenderness  and  distention,  dry  brown 
tongue,  parotitis,  and  a  cutaneous  rash,  sometimes  petechial.  Cardiac 
signs  and  symptoms  may  be  absent,  and  when  present  their  signifi- 
cance may  be  quite  unappreciated. 

(4)  Cerebral  Type. — A  small  proportion  of  cases  resemble  an 
acute  cerebro-spinal  (page  672)  or  cerebral  meningitis  with  either 
acute  delirium  or  coma  as  the  principal  symptom. 

Duration  and  Prognosis. — Usual  duration  from  5  to  6  weeks, 
■except  the  cases  supervening  upon  chronic  cardiac  disease,  which 
may  be  protracted  for  several  months.  Occasionally  death  occurs 
within  a  few  days.  If  the  clinical  term  "  malignant "  is  taken  at  its 
iull  value  the  prognosis  is  invariably  fatal,  the  few  cases  which 
recover  belonging  in  strictness  to  the  benign  form. 

Differential  Diagnosis. — If  the  disease  supervenes  upon  chronic 
valvular  disease,  and  there  are  chills,  irregular  fever,  sweats  and 
embolic  phenomena,  the  diagnosis  is  usually  not  difl&cult.  The 
immediately  previous  occurrence  of  one  of  the  causative  diseases 
or  conditions,  e.  g.,  pneumonia  or  sepsis,  is  of  much  value.  In  the 
absence  of  chronic  cardiac  disease  or  other  suggestive  antecedent  ail- 
ment, or  of  present  cardiac  or  embolic  symptoms,  the  larger  number 
of  cases  are  to  be  separated  from  intermittent  malarial  fever  (see 
page  709),  or,  more  commonly,  typhoid  fever  (see  page  667).  In  a 
certain  proportion  of  cases  a  differential  diagnosis  is  impossible. 

II.  Chronic  Endocarditis. — An  overgrowth  of  fibrous  tissue, 
affecting  mainly  the  valves  of  the  heart,  which  by  subsequent  con- 
traction causes  deformation  of  the  valve  segments. 

Causes. — It  may  be,  and  usually  is,  a  sequel  of  acute  endocarditis, 
of  rheumatic  origin  in  the  majority  of  cases ;  or  may  be  primary  and 
begin  insidiously.  Its  course  in  either  case  is  essentially  chronic  and 
progressive.  The  causes  of  the  first  are  the  same  as  those  of  acute 
endocarditis  in  general  (page  875) ;  of  the  second,  alcoholism,  gout, 
plumbism,  syphilis,  diabetes,  and  long-continued  heavy  muscular 
exertion.  Arteriosclerosis,  atheroma,  and  chronic  interstitial  ne- 
phritis are  often  associated  with  the  second  group,  sometimes  as 
cause,  sometimes  as  effect,  and  have  the  same  etiology. 


DISEASES  OP  THE  HEART  879 

Symptoms. — Clinically  chronic  endocarditis  manifests  itself  as 
chronic  valvular  disease,  and  its  symptoms  are  those  of  various  dis- 
turbances and  ultimate  failure  of  the  circulation.  About  one  half 
of  the  cases  follow  rheumatic  endocarditis.  If  the  valve  segments 
are  thickened,  curled,  and  retracted  they  fail  to  close,  and  incompe- 
tency with  regurgitation  results ;  if  the  edges  of  the  segments  become 
adherent,  stenosis,  with  obstruction  to  the  blood  current,  ensues. 
A  diseased  valve  segment  may  rupture. 

III.  Chronic  Valvular  Disease.— See  also  pages  312  to  318. 

(I)  Aortic  Incompetency. —  Causes. — Occurs  mainly  in  men  of  mid- 
dle age,  and  is  due  most  commonly  to  prolonged  and  severe  muscu- 
lar exertion,  alcohol,  gout,  syphilis,  or  lead,  all  of  which  may  initiate 
slowly  progressive  deforming  changes  in  the  valve ;  less  frequently 
to  rheumatic  endocarditis,  rarely  to  rupture.  Occasionally  it  is  rela- 
tive, the  aortic  ring  enlarging,  either  in  consequence  of  aortic  scle- 
rosis and  dilatation  or  aortic  aneurism,  to  an  extent  which  prevents 
apposition  of  the  segments,  even  though  normal.  Sclerosis  of  the 
aorta,  often  with  atheroma  and  calcification  which  may  involve  the 
coronary  arteries,  is  a  frequent  associated  lesion. 

Symptoms. — In  this  lesion  the  left  ventricle  tends  to  be  over- 
distended,  and  dilatation  precedes  hypertrophy.  So  long  as  the 
compensation  is  efficient  there  may  be  no  cardiac  symptoms ;  but  in 
a  certain  proportion  of  cases,  even  though  compensation  is  main- 
tained, there  may  be  dull  praecordial  aching  and  oppression,  or  more 
frequently  a  sharper  pain  which  radiates  into  the  neck  and  the  arms, 
the  left  shoulder  and  arm  in  particular.  Paroxysms  of  true  angina 
pectoris  may  occur.  Dyspnoea,  praecordial  distress,  and  palpitation 
■often  result  from  slight  exertion,  and  vertigo,  faintness,  flashes  of 
light  before  the  eyes,  tinnitus  aurium,  and  a  throbbing  headache  may 
be  manifest,  especially  if  the  patient  gets  up  quickly  from  a  recum- 
bent posture.  Occasionally  there  is  redness  and  a  feeling  of  heat  in 
the  skin,  followed  by  copious  sweating. 

When  the  heart  begins  to  fail  dyspnoea,  sometimes  orthopnoea, 
rarely  with  cyanosis,  appears,  especially  at  night.  General  anasarca 
is  not  of  frequent  occurrence,  except  when  mitral  incompetency  co- 
exists, but  oedema  of  the  lower  extremities  may  be  an  early  symptom, 
and  is  favoured  by  the  marked  anaemia  which  is  commonly  associated 
with  aortic  incompetency.  Cough,  pulmonary  congestion  or  oedema, 
and  perhaps  hemoptysis,  may  be  present.  Restless  sleep  and  fre- 
<iuent  distressing  dreams  are  very  common.  Mental  symptoms,  such 
as  irritability,  depression,  or  peevishness,  are  often  present,  and  mel- 
ancholia or  other  forms  of  insanity,  perhaps  with  suicidal  propensi- 
ties, will  appear  in  a  small  number  of  cases.     In  the  later  stages  of 


880  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

the  disease  prostration  becomes  evident,  and  there  may  be  recurrent 
endocarditis  with  moderate  irregular  fever  and  embolic  phenomena. 

Physical  Signs. — The  praecordium  may  bulge,  especially  in  chil- 
dren, and  there  is  a  large  area  of  visible  impulse.  The  carotids  and 
other  accessible  arteries  (brachial,  femoral,  etc.)  are  seen  to  pulsate 
violently,  and  there  is  epigastric  throbbing.  The  capillary  pulse  is 
readily  perceived,  and  in  some  instances  the  veins  of  the  hands  and 
feet  may  pulsate.  The  impulse  of  the  heart,  unless  dilatation  pre- 
dominates over  hypertrophy,  is  strong  and  heaving,  and  a  diastolic 
thrill  is  occasionally  felt.  The  apex  beat  is  palpable  in  the  6th  or 
7th  interspace  outside  of  the  mammillary  line.  The  pulse  has  the 
water-hammer  character,  "  Corrigan's  pulse."  The  area  of  cardiac 
dulness  is  greatly  increased,  extending  mainly  downward  and  to  the 
left  unless  marked  dilatation  is  present. 

Upon  auscultation  a  diastolic  murmur  is  heard  over  the  aortic 
area  (Fig.  101,  page  356),  soft,  blowing,  rarely  harsh,  and  often  almost 
inaudible.  With  it  is  frequently  associated  an  aortic  systolic  mur- 
mur, generally  due  to  roughening  of  the  segments,  and  not  indicative 
of  aortic  stenosis.  If  the  incompetency  is  marked  the  aortic  second 
sound  will  be  replaced  by  the  diastolic  murmur.  At  the  apex  a  sys- 
tolic mitral  murmur  is  often  heard,  due  to  actual  or  relative  mitral 
insufficiency,  less  commonly  a  presystolic  mitral  murmur  (Flint's). 
Double  murmurs  may  at  times  be  heard  in  the  carotid,  subclavian, 
and  femoral  arteries,  and  a  short  systolic  flapping  sound  (not  mur- 
mur) is  common  in  the  same  and  even  smaller  arteries. 

Diagnosis. — This  is  usually  easy.  A  diastolic  murmur,  even 
though  faint,  over  the  aortic  area,  the  throbbing  arteries,  the  peculiar 
pulse,  and  the  hypertrophy  of  the  left  ventricle,  constitute  a  reliable 
combination  of  signs.  The  tremendous  pulsation  of  the  innominate 
and  right  carotid  arteries  has  led  to  a  mistaken  diagnosis  of  thoracic 
aneurism  {q.  v.),  and  indeed  there  may  be  a  certain  degree  of  dilata- 
tion of  the  first  portion  of  the  aorta,  with  some  increase  of  dulness, 
in  connection  with  aortic  incompetency. 

Prognosis. — Ultimately  unfavourable,  although  good  compensa- 
tion may  be  maintained  for  years.  Sudden  death  occurs  in  a  larger 
proportion  of  cases  than  with  any  other  valvular  defect. 

(II)  Aortic  Stenosis. — Xarrowing  of  the  aortic  orifice  without  a 
certain  degree  of  valvular  incompetency  is  of  rare  occurrence,  and 
indeed  is  much  less  frequently  met  with  than  the  latter. 

Causes. — Occurs  mainly  in  old  men,  and  is  usually  due  to  slow 
sclerotic,  atheromatous,  and  calcareous  changes,  often  constituting  a 
part  of  a  general  arteriosclerosis  and  involving  the  coronary  arteries. 
Infrequently  it  is  a  result  of  rheumatic  and  other  forms  of  endo- 


DISEASES  OP  THE  HEART  881 

carditis ;  may  be  congenital ;  and  occasionally  the  orifice  is  of  nor- 
mal size,  but  opens  into  a  dilated  aorta — relative  stenosis. 

Symptoms. — So  long  as  the  hypertrophy  compensates  for  the 
obstruction  the  disease  is  latent.  The  earliest  symptoms  of  beginning 
muscular  failure  are  vertigo  and  faintness,  due  to  cerebral  anaemia, 
with  praecordial  oppression  or  anginal  pain  and  palpitation  after 
exertion.  In  the  later  stages  the  mitral  and  subsequently  the  tri- 
cuspid valves  may  become  relatively  insufficient  because  of  cardiac 
dilatation,  with  the  usual  indirect  evidences  of  general  venous  stasis 
(page  316).  Embolic  phenomena  and  Cheyne-Stokes  respiration  may 
become  manifest. 

Physical  Signs. — The  apex  beat  is  carried  to  the  left  and  down- 
ward, and,  unless  hypertrophic  emphysema  coexists,  is  strong  and 
forcible.  A  systolic  thrill,  often  of  marked  intensity,  is  apt  to  be 
felt  over  the  aortic  area.  The  area  of  heart  dulness  is  increased, 
provided  the  oftentimes  associated  emphysema  does  not  mask  it. 
The  aortic  second  sound  is  usually  weak,  and  a  systolic  murmur 
(described  at  page  355)  is  heard  over  the  aortic  area,  frequently  asso- 
ciated with  the  diastolic  murmur  of  aortic  incompetency;  and  if 
relative  mitral  insufficiency  has  been  established  there  will  be  a  blow- 
ing systolic  murmur  at  the  apex.  The  rather  characteristic  pulsus 
tardus  (pages  377,  378)  is  present. 

Diagnosis. — An  aortic  systolic  murmur  is  in  the  majority  of 
■cases  not  due  to  stenosis,  but  if  it  is  harsh,  rough,  or  musical,  and 
associated  with  thrill,  cardiac  hypertrophy,  and  pulsus  tardus  in  an 
elderly  person,  a  diagnosis  of  this  lesion  is  permissible. 

(Ill)  Mitral  Incompetency. — May  be  due  to  deformation  of  the 
valve  segments  or  shortening  of  the  chordae  tendineae ;  or  to  dilata- 
tion of  the  ventricle  with  relative  incompetency.  It  constitutes  at 
least  one  half  of  all  cases  of  valvular  disease.  As  consequences  of 
this  defect,  first  the  left  auricle,  then  the  left  ventricle,  finally  the 
right  ventricle  and  auricle  become  dilated  and  hypertrophied. 

Causes. — The  organic  defects  are  usually  due  to  rheumatic  or 
other  form  of  endocarditis,  or  constitute  a  part  of  a  general  arterio- 
sclerosis;  while  relative  incompetency  results  from  left  ventricular 
dilatation  due  to  aortic  stenosis  or  incompetency,  or  succeeds  the 
hypertrophy  of  chronic  nephritis  or  arteriosclerosis,  or  the  muscular 
weakness  of  severe  anaemia  or  protracted  febrile  diseases. 

Sijmptoms.—^\i\\e  compensation  is  perfect  there  are  no  sub- 
jective evidences  of  cardiac  disease.  If  good,  though  not  perfect, 
there  is  moderate  dyspnoea  on  exertion,  the  face  may  have  a  slightly 
-cyanotic  tint,  and  the  venous  radicles  of  the  cheeks  are  plainly 
visible.     Clubbing  of  the  fingers  is  common  in  cases  of  long  dura- 


882  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

tion,  especially  in  children.  There  may  he  cardiac  palpitation. 
There  is  a  marked  tendency  to  attacks  of  bronchitis  and  the  slighter 
grades  of  gastro-intestinal  disturbances.  Undue  muscular  exertion 
may  produce  severe,  but  at  this  stage  usually  temporary,  pulmonary 
congestion,  oedema,  or  haemoptysis.  When  compensation  is  broken 
and  dilatation  exceeds  hypertrophy,  the  pulse  becomes  extremely 
irregular,  there  is  palpitation,  dyspnoea,  or  orthopncea ;  cough,  some- 
times with  frothy,  bloody  sputum ;  cyanosis  and  slight  jaundice. 
There  are  evidences  of  gastro-intestinal  catarrh  (nausea,  diarrhcea), 
hemorrhoids,  and  enlargement  of  the  liver  and  spleen.  There  is 
cedema,  beginning  in  the  feet  and  extending  upward,  often  with 
ascites  and  hydrothorax.  The  urine  is  scanty,  high  coloured,  and 
contains  albumin  and  often  casts.  All  of  these  symptoms  are  evi- 
dences of  general  venous  congestion  (Fig.  79,  page  317).  Starting 
during  sleep  is  a  common  and  most  grievous  occurrence. 

Physical  Signs. — In  children  the  praecordium  may  be  prominent. 
The  apex  beat  lies  to  the  left  and  below,  according  to  the  degree  of 
hypertrophy,  and  the  area  of  visible  and  palpable  pulsation  is  greatly 
increased.  If  compensation  is  still  good  the  impulse  is  the  heaving 
and  forcible  stroke  of  hypertrophy;  if  broken,  the  weak,  wavy,^ 
diffuse  pulsation  of  a  dilated  heart.  Occasionally  there  is  a  systolic 
thrill  at  the  apex.  There  may  be  epigastric  pulsation  due  to  right 
ventricular  hypertrophy  and  dilatation ;  as  well  as  pulsating  jugulars 
and  pulsating  liver,  significant  of  tricuspid  insufficiency.  The  j)uls& 
is  small  and  compressible,  and  when  the  heart  fails  is  absolutely 
arrhythmic.  There  may  be  contractions  of  the  heart  which  are  not 
represented  at  the  wrist  (ineffectual  systole).  The  area  of  cardiac 
dulness  is  increased,  both  to  left  and  right,  because  both  left  and. 
right  ventricles  are  dilated  and  hypertrophied.  A  blowing  or  musical 
systolic  murmur,  either  accompanying  or  replacing  the  first  sound,  is. 
heard  at  the  apex,  transmitted  to  the  left,  and  heard  posteriorly  at 
the  angle  of  the  scapula  (Fig.  99,  page  354).  Although  its  maximum 
intensity  is  usually  at  the  apex,  it  may  be  loudest  or  heard  only  at 
the  base  of  the  heart  or  along  the  left  sternal  edge.  Occasionally 
it  is  perceptible  when  the  patient  is  lying  down,  and  disappears  if  he 
stands  up.  The  second  sound  is  generally  very  distinctly  audible  at 
the  apex ;  and  the  second  pulmonary  sound  is  accentuated  over  the 
pulmonary  area.  If  there  is  associated  tricuspid  incompetence  there 
is  a  systolic  murmur  in  its  area. 

Diagnosis. — The  characteristic  physical  signs  are  a  systolic  mur- 
mur transmitted  to  the  left  and  heard  posteriorly ;  accentuation  of 
the  pulmonary  second  sound,  and  evidence  of  both  right-  and  left- 
heapt  hypertrophy. 


DISEASES  OF  THE  HEART  883 

The  foregoing  combination  of  physical  signs  is  essential  for  a 
diagnosis,  as  a  systolic  mitral  murmur  occurs  in  various  conditions 
unconnected  with  organic  mitral  valvular  defects  or  relative  incom- 
petency (page  353).  Whether  the  insufficiency  is  due  to  deforma- 
tion of  the  valve,  or  is  relative,  can  not  always  be  determined.  If 
it  occurs  in  the  subjects  of  chronic  nephritis,  general  arteriosclerosis, 
or  aortic  lesions,  all  of  which  cause  hypertrophy  and  dilatation  of  the 
left  ventricle,  the  mitral  incompetence  is  probably  relative. 

Prognosis. — Life  may  be  prolonged  for  many  years  if  compensa- 
tion is  maintained.  There  are  apt  to  be  repeated  breaks  of  com- 
pensation, each  becoming  more  severe,  ending  with  general  anasarca, 
cardiac  dilatation,  and  death,  rarely  sudden,  usually  from  progressive 
weakness  of  the  heart  muscle.  Xot  infrequently  permanent  arrhyth- 
mia follows  the  first  rupture  of  compensation. 

(IV)  Mitral  Stenosis. — Causes. — Narrowing  of  the  mitral  orifice 
is  usually  due  to  endocarditis,  generally  rheumatic;  occasionally,  per- 
haps, to  the  strain  of  whooping  cough ;  is  more  frequent  in  females 
and  in  young  rather  than  elderly  persons.  The  most  frequent  form 
of  constriction  is  the  buttonhole  opening,  less  commonly  it  is  funnel- 
shaped.  As  a  result  of  the  narrowing  the  left  ventricle  remains  of 
normal  size,  or  becomes  smaller,  unless  mitral  incompetency  coexists ; 
while  the  left  auricle  and  subsequently  the  right  ventricle  and  auricle 
become  hypertrophied  and  ultimately  dilated,  with  sequent  tricuspid 
insufficiency  and  systemic  venous  congestion. 

Symptoms. — Except  for  a  varying  degree  of  dyspnoea  and  palpi- 
tation following  unusual  muscular  exertion,  there  may  be  an  entire 
absence  of  symptoms  so  long  as  compensation  is  good.  There  is  a 
liability  to  attacks  of  recurrent  endocarditis,  and  the  resulting  vegeta- 
tions may  become  detached  and  swept  away,  thus  causing  embolic 
phenomena,  especially  asphasia  or  aphasic  hemiplegia.  Paralysis  of 
the  left  vocal  cord,  due  to  the  pressure  of  the  hypertrophied  left 
auricle  and  simulating  one  of  the  effects  of  aortic  aneurism,  has  been 
noted.  Anaemia  and  left  intercostal  neuralgia  are  very  common. 
When  compensation  is  failing  the  resulting  symptoms  are  practically 
those  of  mitral  incompetency.  There  are  more  or  less  constant  dysp- 
noea, frequent  and  arrhythmic  pulse,  cough,  bronchitis,  and  conges- 
tion or  oedema  of  the  lungs,  with  cyanosis,  blood-stained  expectora- 
tion, or  occasionally  haemoptysis.  These  symptoms  are  especially  apt 
to  occur  after  severe  muscular  exertion,  and  there  may  be  frequent 
recurrences.  (Edema  of  the  lower  extremities  and  general  anasarca 
are  not  common  unless  tricuspid  insufficiency  coexists.  Late  in  the 
disease  ascites  may  occur,  especially  in  children,  and  is  associated 
with  great  swelling  of  the  liver.    An  enlarged,  perhaps  pulsating. 


584  DIAGNOSIS,  DIRECT  AND  DIFFERENTIAL 

liver,  due  to  passive  congestion,  is  very  frequent  in  mitral  stenosis 
when  the  right  heart  fails.  Elevations  of  temperature,  symptomatic 
of  recurrent  endocarditis,  are  not  uncommon. 

Physical  Signs. — Owing  to  hypertrophy  of  the  right  ventricle  the 
lower  sternum  and  5th  and  6th  left  cartilages  may  be  prominent, 
particularly  in  children,  and  the  main  impulse  of  the  heart  is  usually 
visible  over  the  same  area.  Pulsation  may  often  be  seen  in  the  2d, 
3d,  and  4th  interspaces  to  the  left,  rarely  also  to  the  right,  of  the 
sternum,  if  the  chest  walls  are  not  too  thick ;  and  pulsation  of  the 
epigastrium,  due  to  the  hypertrophied  right  ventricle,  is  common.  The 
■apex  beat,  unless  mitral  incompetency  or  other  cause  of  left  ventricu- 
lar hypertrophy  coexists,  may  remain  in  its  normal  position  or  be 
displaced  somewhat  to  the  left,  rarely  to  the  outside  of  the  mammil- 
lary  line,  depending  upon  the  degree  of  right  ventricular  enlarge- 
ment. The  strongest  impulse  is  usually  felt  over  the  lower  sternum 
and  5th  and  6th  left  interspaces,  perhaps  also  in  the  ith,  3d,  and  2d 
spaces.  The  impulse  in  the  left  2d  space  is  ascribed  either  to  the 
hypertrophied  left  auricle  or  to  the  increased  tension  in  the  conus 
-arteriosus  and  pulmonary  artery,  both  views  having  supporters.  In 
the  bulk  of  the  cases  there  is  the  characteristic  rough,  purring  thrill, 
best  felt  within  the  nipple  line  in  the  3d  or  4th,  sometimes  the  5th, 
interspaces.  It  is  diastolic,  beginning  just  after  the  second  sound, 
«nds  abruptly  with  the  apex  impulse,  and  is  most  marked  during  ex- 
piration. It  is  pathognomonic  of  mitral  stenosis,  and  when  found  per- 
mits a  diagnosis  by  palpation  alone.  The  area  of  cardiac  dulness  is 
increased  to  the  right,  as  well  as  upward  along  the  left  sternal  mar- 
gin to  the  2d  rib ;  but  not  to  the  left  and  downward  unless  left 
ventricular  hypertrophy  coexists  as  a  result  of  mitral  regurgitation. 
Internal  to  and  a  little  above  the  apex  beat  is  a  presystolic  murmur, 
variously  described  as  rough,  rolling,  blubbering,  churning,  vibratory, 
purring,  or  hesitating,  whose  audibility  is  usually  limited  to  a  two- 
inch  circle,  but  at  times  may  be  very  widely  heard  (Fig.  97,  page 
352).  It  is  variable,  appearing  and  disappearing  in  accordance  with 
the  strength  of  the  auricular  systole  ;  may  occupy  the  whole  or  the 
middle  or  the  latter  part  of  the  diastolic  period  (Fig.  98,  page  353) ; 
and  may  be  heard  only  after  exertion.  The  first  sound,  in  which  this 
murmur  abruptly  terminates,  is  short,  sharp,  and  snapping ;  the  pul- 
monary second  sound  is  loudly  accentuated  and  heard  over  a  wide  area, 
and  the  aortic  second  sound  is  relatively  and  actually  weak.  There 
may  be  reduplication  of  the  second  sound.  The  murmurs  of  mitral 
-and  tricuspid  incompetency,  the  latter  often  a  secondary  result,  may 
be  heard.  The  pulse,  with  marked  stenosis,  is  notably  small,  and 
when  the  heart  fails  becomes  irregular  like  that  of  incompetency. 


DISEASES  OP  THE  HEART  885 

When  compensation  is  broken  the  thrill  and  the  murmur  may 
disappear,  the  snap  of  the  first  sound  remaining.  Xot  infrequently 
the  sounds  are  reduplicated,  the  impulse  is  diffuse  and  weak,  and 
there  may  be  systolic  jugular  pulsation  and  pulsating  liver,  from  tri- 
cuspid insuflBciency.  If  the  strength  of  the  left  auricle  and  right 
ventricle  is  restored,  the  murmur  reappears. 

Diagnosis. — The  signs  which  justify  a  diagnosis  of  mitral  stenosis 
are  :  a  presystolic  thrill  and  murmur  with  the  characters  described ; 
evidence  of  right-heart  hypertrophy,  the  left  heart  remaining  of 
normal  size  ;  and  an  accentuated  pulmonary  second  sound.  If  aortic 
regurgitation,  or  aortic  stenosis  and  adherent  pericardium  are  found 
to  exist,  the  presence  of  a  presystolic  mitral  murmur  is  not  positive 
evidence  of  mitral  stenosis  (see  (2),  page  353). 

Prognosis. — Ultimately  unfavourable,  although  with  proper  care 
many  years  may  elapse  before  death  occurs  by  gradual  failure  of 
compensation,  perhaps  after  repeated  temporary  breaks. 

(V)  Tricuspid  Incompetency. — Causes. — Karely  this  is  primary, 
ihe  valve  segments  becoming  deformed  as  a  result  of  right-heart 
endocarditis  during  foetal  life  or  in  early  childhood ;  as  a  rule  it  is 
relative  and  secondary  to  left  heart,  especially  mitral,  valvular  dis- 
ease, or  to  interstitial  pneumonia  and  emphysema. 

Symptoms. — The  symptoms  are  largely  dependent  upon  the  causa- 
tive valvular  or  pulmonary  disease,  and  are  for  the  most  part  the 
evidences  of  stasis  in  the  lungs  and  systemic  veins. 

Physical  Signs. — The  characteristic  and  indubitable  signs  of  tri- 
cuspid regurgitation  are  :  systolic  pulsation  in  the  jugulars,  especially 
the  right ;  swollen  and  pulsating  liver ;  and  the  presence  of  a  soft, 
low  systolic  murmur  over  the  lower  sternum  ((*),  page  357).  The 
pulmonary  second  sound  is  accentuated,  the  cardiac  dulness  is  in- 
creased to  the  right,  and  there  is  epigastric  pulsation. 

(VI)  Tricuspid  Stenosis.— This  may  be  either  congenital,  and 
combined  with  other  defects  of  development,  or  acquired,  occur- 
ring as  a  secondary  result  to  left-heart  lesions.  It  is  most  com- 
monly associated  with  mitral  stenosis  (both  largely  due  to  rheumatic 
endocarditis),  less  frequently  with  aortic  incompetency,  and  is  very 
rare  as  a  primary  and  isolated  condition.  It  occurs  in  females  rather 
than  males  (5  to  1).  The  symptoms  are  those  of  the  associated  valvu- 
lar defects.  Facial  cyanosis  and  extreme  anasarca  are  terminal  evi- 
dences. 

Physical  Signs.— There  may  be  a  presystolic  thrill  over  the  tricus- 
pid area  ;  the  area  of  cardiac  dulness  is  enlarged  to  the  right,  and 
a   presystolic  murmur  may  be  heard   {{a),  page  357).     A  positive 
diagnosis  is  rarely  practicable,  unless  it  is  an  isolated  lesion,  because 
58 


886  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

of  the  difficulty  of  separating  the  usually  co-existent  mitral  presys- 
tolic from  a  tricuspid  presystolic  murmur. 

(VII)  Pulmonary  Incompetence.— (See  (b),  page  359).  A  differen- 
tial diagnosis  from  aortic  incompetency  is  rarely  possible,  although 
the  absence  of  Corrigan's  pulse  and  the  non-discovery  of  left  ventricu- 
lar dilatation  and  hypertrophy  will  tend  to  exclude  the  latter. 

(VIII)  Pulmonary  Stenosis. — This  is  usually  congenital.  There 
is  apt  to  be  cyanosis  and  systemic  venous  engorgement. 

The  physical  signs,  when  present,  are  the  evidences  of  right  ven- 
tricular hypertrophy  and  the  presence  of  a  systolic  thrill  and  mur- 
mur in  the  pulmonary  area.  The  murmur  is  of  a  rough  or  harsh 
quality,  usually  strictly  localized  and  apparently  superficial,  and,  of 
course,  is  not  transmitted  into  the  arteries  of  the  neck,  a  differential 
point  between  it  and  the  similar  murmur  of  aortic  stenosis.  The 
pulmonary  second  sound  is  weak  and  may  be  accompanied  or  re- 
placed by  the  diastolic  murmur  of  associated  incompetency. 

A  diagnosis  of  pulmonary  stenosis  must  be  made  with  great  re- 
serve because  of  the  very  frequent  occurrence  of  pulmonary  systolic 
murmurs,  usually  of  anaemic  origin  (see  (a),  page  358). 

(IX)  Combined  Valvular  Defects. — The  statistics  regarding  the 
relative  frequency  of  certain  combinations  of  valvular  defects  are 
variable.  In  general  aortic  and  mitral  lesions  most  commonly  co- 
exist, then  mitral  and  tricuspid,  finally  aortic,  mitral,  and  tricuspids 
The  particular  combinations  in  the  usual  order  of  frequency  are  : 

1.  Aortic  incompetency  and  stenosis  and  mitral  incompetency. 

2.  Mitral  stenosis  and  incompetency. 

3.  Aortic  stenosis  and  mitral  stenosis. 

4.  Mitral  stenosis  and  aortic  incompetency. 

With  reference  to  combined  murmurs,  see  page  359. 

IV.  Hypertrophy  of  the  Heart.— Increased  thickness  of 
the  muscular  walls  of  the  heart — hypertrophy — may  exist  without 
dilatation  of  the  chambers  {simple  hypertrophy) ;  more  commonly 
the  hypertrophy  is  associated  with  dilatation  {eccentric  hypertrophy). 
So-called  concentric  hypertrophy — thickened  walls  with  lessened  size 
of  the  cavities — is  a  post-mortem  contraction  event. 

Causes. — The  hypertrophy  may  affect  one  cavity,  one  side,  or  the 
whole  of  the  heart. 

(1)  Left  Ventricular  Hypertrophy. — Maybe  due  to  aortic  stenosis, 
aortic  and  mitral  incompetency,  which  increase  the  intraventricular 
pressure ;  pericardial  adhesions  and  fibrous  myocarditis,  which  inter- 
fere with  the  contraction  of  the  heart  muscle  and  increase  its  work ; 
general  arteriosclerosis  and  the  presence  of  irritating  substances  in 
the  blood  in  gout,  chronic  nephritis,  lead-poisoning,  and  syphilis,  alL 


DISEASES  OF  THE  HEART  887 

of  which,  either  by  producing  organic  narrowing  or  by  causing  pro- 
longed contraction  of  the  arterioles,  heighten  the  arterial  pressure 
and  create  an  obstruction  to  the  work  of  the  left  ventricle  ;  congeni- 
tal narrowing  of  the  aorta,  aneurism  of  the  same  vessel,  or  stenosia 
caused  by  external  pressure  upon  it;  persistent  overaction  of  the 
muscle  as  in  the  tachycardia  of  exophthalmic  goitre,  the  tea,  coffee, 
and  alcohol  habits,  or  long-continued  neurotic  palpitation ;  and 
habitual  excessive  eating  and  drinking,  especially  the  drinking  of 
enormous  quantities  of  beer.  Prolonged  and  severe  muscular  work 
is  an  additional  and  sometimes  important  factor. 

Many  of  these  causes  operate  to  produce  varying  degrees  of  simul- 
taneous right  ventricular  hypertrophy. 

(2)  Right  Ventricular  Hypertrophy. — May  be  due  to  mitral  steno- 
sis and  mitral  incompetency ;  and  emphysema,  chronic  interstitial 
pneumonia,  or  extensive  pleural  adhesions,  all  of  which  raise  the 
pressure  and  increase  the  resistance  in  the  pulmonary  circuit.  Valv- 
ular lesions  on  the  right  side,  especially  pulmonary  stenosis,  will 
also  cause  hypertrophy  of  the  right  ventricle. 

(3)  Auricular  Hypertrophy. — This  is  always  conjoined  with  dilata- 
tion, and  when  affecting  the  left  auricle  occurs  in  mitral  incompe- 
tency or  mitral  stenosis,  especially  the  latter ;  when  affecting  the 
right  auricle,  it  is  found  in  all  conditions  which  raise  the  pulmonary 
blood  pressure  (see  (2)  preceding) ;  and  in  tricuspid  or  pulmonary 
incompetence  or  stenosis. 

Symptoms. — As  a  rule  the  condition— almost  invariably  conserva- 
tive— is  subjectively  latent  until  the  hypertrophied  muscle  can  no 
longer  respond  to  the  demands  upon  it  and  ruptured  compensation 
becomes  manifest.  The  earlier  symptoms  of  well-marked  hypertro- 
phy, especially  of  the  left  ventricle,  consist  of  an  indefinite  sense  of 
prsecordial  discomfort  or  fulness,  most  marked  when  lying  upon  the 
left  side.  The  sensation  is  seldom  that  of  pain,  and  palpitation  or  a 
consciousness  of  the  overaction  of  the  heart  is  usually  not  perceived 
except  when  the  patient  is  neurasthenic  or  addicted  to  the  overuse 
of  tobacco.  There  may  be  a  sense  of  fulness  or  throbbing  in  the 
head,  headache,  flushing  of  the  face,  carotid  throbbing,  vertigo,  tin- 
nitus aurium,  flashes  of  light,  exophthalmos,  and  epistaxis.  General 
arteriosclerosis  is  a  frequent  concomitant  event,  either  as  cause  or 
result  of  the  hypertrophy,  and  broncho-pulmonary  or  cerebral  hemor- 
rhage, due  to  rupture  of  the  sclerotic  smaller  vessels  by  the  increased 
force  of  the  heart,  may  occur. 

(1)  Physical  Signs  of  Left  Ventricular  Hypertrophy.— The  praecor- 
dium  may  be  prominent,  especially  in  children,  and  an  extensive 
impulse  is  visible.      On  palpation  the  impulse  is  characteristically 


DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

slow,  heaving,  and  forcible  (nnless  a  notable  degree  of  dilatation  co- 
exists, when  it  is  rather  more  sudden),  and  the  apex  beat  is  dis- 
placed downward,  perhaps  to  the  7th  or  8th  interspace,  and  to  the 
left  even  as  much  as  3  inches  outside  of  the  mammillary  line.  But  in 
the  more  common  degrees  of  hypertrophy  the  apex  lies  in  the  6th 
space,  in  or  a  little  outside  of  the  mammillary  line.  The  percussion 
dulness  is  increased  downward,  to  the  left,  and  vertically  (Fig.  88,  p. 
336).  In  simple  hypertrophy  without  valvular  lesions  there  are  no 
murmurs,  but  the  first  sound  is  loud,  prolonged,  and  booming,  often 
with  a  clicking  or  murmurish  quality;  if  dilatation  coexists  it  is 
shorter  and  sharper.  Aortic  closure  is  accentuated  and  clear  or  ring- 
ing, and  the  second  sound  often  reduplicated,  especially  in  the  hyper- 
trophy of  chronic  nephritis ;  if  the  ventricle  is  also  dilated,  or  the 
heart  action  weak,  the  second  sound  is  less  clear  and  intense.  If 
the  hypertrophy  is  due  to  valvular  defects  there  will  be  the  physical 
signs  of  the  special  lesions  present.  If  the  hypertrophy  is  unaccom- 
panied by  dilatation,  the  pulse  is  large,  strong,  regular,  of  increased 
tension,  and  often  not  more  frequent  than  normal ;  if  with  dilata- 
tion, it  is  softer  and  as  a  rule  of  greater  frequency. 

(2)  Symptoms  and  Physical  Signs  of  Right  Ventricular  Hypertro- 
phy.— There  are  no  symptoms  while  compensation  is  maintained, 
except  moderate  dyspncea  following  unusual  muscular  exertion ;  or 
praecordial  discomfort,  cough,  and  dyspncea,  when  the  hypertrophy 
is  a  sequence  of  emphysema  or  chronic  interstitial  pneumonia.  In 
course  of  time,  when  dilatation  and  relative  tricuspid  incompetency 
occur,  there  will  be  persistent  dyspnoea,  bronchitis,  pulmonary  con- 
gestion or  oedema,  cyanosis,  haemoptysis,  and  evidence  of  systemic 
venous  stasis.  The  physical  signs  are  (perhaps)  an  unusual  promi- 
nence of  the  lower  sternum  and  the  6th  and  7th  left  cartilages,  with 
a  visible  somewhat  diffuse  impulse  over  the  same  area,  often  also  in 
the  epigastrium.  Unless  the  chest  walls  are  thick,  pulsation  is  fre- 
quently present  in  the  3d  and  4th  interspaces  to  the  right  of  the 
sternum,  particularly  if  there  is  much  dilatation.  The  apex  beat  is 
carried  to  the  left,  usually  with  but  slight  downward  displacement, 
and  is  diffuse,  lacking  the  well-defined  thrust  of  left  ventricular 
hypertrophy.  The  cardiac  dulness  is  increased  mainly  to  the  right, 
perhaps  an  inch  or  more  beyond  the  sternal  margin.  The  first  sound 
over  the  tricuspid  area  is  louder  than  usual,  and  on  account  of 
the  increased  tension  in  the  pulmonary  artery  the  pulmonary  second 
sound  is  accentuated,  and  reduplication  of  the  second  sound  may 
occur.  The  radial  pulse  is  of  small  volume,  and  if  dilatation  is  pres- 
ent may  be  frequent  and  arrhythmic. 

(3)  Signs  of  Auricular  Hypertrophy. — The  physical  signs  of  hy- 


DISEASES  OP  THE  HEART  ggg 

pertrophy,  always  combined  with  dilatation,  of  the  left  auricle,  are 
few  and  indefinite.  There  may  be  dulness  to  the  left  of  the  sternum 
in  the  3d  or  2d  interspaces,  with  a  presystolic  impulse  or  wave 
in  the  2d  space.  The  presence  of  left  auricular  enlargement  may 
always  be  inferred  if  the  presystolic  murmur  of  mitral  stenosis  is 
heard,  or  if  mitral  incompetency  exists. 

Hypertrophy,  never  without  dilatation,  of  the  right  auricle,  is 
secondary  to  incompetency  or  stenosis  of  the  tricuspid  valve  with 
associated  right  ventricular  hypertrophy  and  dilatation.  There  is 
dulness  in  the  3d  and  4th  interspaces  to  the  right  of*  the  sternum, 
often  with  a  presystolic  wavy  pulsation  in  the  same  area,  systolic 
Jugular  pulsation,  and  evidences  of  general  venous  engorgement. 

Differential  Diagnosis. — Chronic  interstitial  pneumonia,  phthisis 
with  fibrosis  and  retraction,  and  chronic  dry  pleurisy  (all  on  the  left 
side)  may,  by  uncovering  the  heart,  give  rise  to  an  extensive  area  of 
pulsation,  which  is  at  times  mistaken  for  hypertrophy.  The  less 
forcible  and  less  heaving  impact,  together  with  the  evidences  of  pul- 
monary disease,  will  enable  a  differentiation;  so  also  with  the  unusu- 
ally marked  impulse  often  found  in  deformities  of  the  chest. 

The  increased  area  of  dulness  caused  by  aneurism,  pericardial 
effusion,  and  mediastinal  growths,  may  simulate  that  of  hypertrophy, 
but  a  careful  consideration  of  the  physical  signs  Mill  usually  suffice  to 
exclude  these  conditions.  Displacement  of  the  apex  beat  by  extra- 
cardial  lesions  can  generally  be  discriminated  by  the  absence  of  a 
forcible,  heaving  impulse  or  of  an  increased,  although  shifted,  area 
of  dulness.  Hypertrophy  may  be  quite  overlooked  or  impossible  of 
recognition  in  hypertrophic  emphysema. 

V.  Dilatation  of  the  Heart. — The  walls  of  a  dilated  heart 
are  either  thicker  or  thinner  than  normal,  while  the  size  of  the  cavi- 
ties is  increased  out  of  proportion  to  the  thickness  of  their  walls. 
If  the  heart  walls  are  thick  and  their  muscular  power  ample  to  sus- 
tain the  circulation,  a  considerable  increase  in  the  size  of  the  cham- 
bers may  exist,  which  is  properly  termed  eccentric  hypertrophy 
(page  886)  rather  than  dilatation. 

Causes. — Dilatation  depends  upon  two  general  causes:  (1)  in- 
creased endocardial  pressure,  and  (2)  weakness  of  the  heart  walls. 

The  causes  of  increased  pressure  are  practically  the  same  as  those 
of  hypertrophy  (page  886).  Whether  dilatation  or  hypertrophy  will 
result  from  the  greater  tension  depends  in  part  upon  the  suddenness 
and  severity  of  the  strain.  Dilatation  is  more  apt  to  result  from  an 
abrupt  and  intense  increase  of  pressure ;  hypertrophy  from  slighter 
but  persistent  strain.  If  the  heart  walls  are  weakened  from  myo- 
cardial inflammation  or  degeneration,  or  other  cause,  they  will  yield 


890  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

to  a  normal,  much  more  readily  to  an  abnormally  high,  degree  of 
endocardial  pressure.  Thus  in  valvular  lesions  with  a  constant  but 
moderate  increase  of  pressure,  progressive  hypertrophy  takes  place 
until  the  musculature  depreciates,  when  dilatation  will  occur.  On 
the  other  hand,  severe  and  unaccustomed  muscular  exertion  will 
cause  acute  dilatation,  especially  of  the  right  ventricle,  followed  for 
weeks,  months,  or  years  by  dyspncea  and  other  symptoms  of  heart 
strain  upon  exercise.  So  also  there  may  be  acute  dilatation  in  the 
myocarditis  and  parenchymatous  or  other  degenerations  or  nutritive 
disturbances  of  the  heart  muscle  associated  with  scarlet  fever,  ery- 
sipelas, typhus  and  typhoid  fevers,  rheumatic  fever,  acute  endocar- 
ditis or  pericarditis,  the  anaemias,  and  leucaemia.  Slow  dilatation 
occurs  in  the  more  chronic  degenerative  and  sclerotic  processes,  often 
induced  by  diet,  mode  of  life,  and  especially  the  excessive  use  of  alco- 
hol combined  with  persistent  overexertion  (irritable  heart).  Some 
cases,  either  acute  or  chronic,  occur  without  recognisable  cause. 

Symptoms. — When  dilatation  takes  place  slowly  the  symptoms  are 
those  previously  described  as  characteristic  of  gradual  failure  of  com- 
pensation in  valvular  lesions  (page  315).  Acute  dilatation  occurring 
in  fevers  or  in  chronic  hypertrophy  is  indicated  by  dyspnoea,  palpita- 
tion, sometimes  praecordial  oppression  or  pain,  a  weak  and  frequent 
pulse,  and  the  evidences  of  systemic  venous  stasis. 

Physical  Signs. — A  distinct  apex  beat  is  often  absent,  or  if  present 
is  weak.  Usually  the  impulse  is  widely  diffused,  wavy,  and  undulat- 
ing; and  though  plainly  visible  can  not,  in  many  cases,  be  felt  by  the 
palpating  hand,  a  sign  of  much  value.  Unless  emphysema  is 
present  the  area  of  cardiac  dulness  is  increased  vertically  and  trans- 
versely. The  first  sound  is  short  and  flapping,  often  resembling  the 
second  sound,  which  is  also  weakened.  Embryocardia  and  the  gallop 
rhythm  are  common.  The  presence  of  murmurs  due  to  valvular 
disease  may  mask  the  characters  of  the  sounds ;  but  a  murmur, 
especially  that  of  mitral  stenosis,  may  disappear  as  the  heart  weakens. 
A  well-marked  apical  systolic  murmur,  due  to  relative  mitral  incom- 
petency, may,  however,  make  its  appearance,  subsequently  vanishing 
if  the  dilatation  is  overcome.  The  pulse  is  of  small  volume,  weak, 
frequent,  and  often  extremely  arrhythmic. 

The  signs  just  described  relate  mainly  to  left  ventricular  dilata- 
tion. Those  which  may  enable  a  diagnosis  of  predominating  right 
ventricular  dilatation  are  the  location  of  the  chief  impulse  below 
or  to  the  right  of  the  ensiform  appendix,  with  little  or  no  impulse 
in  the  usual  place  of  the  apex  beat,  an  undulating  pulsation  close  to 
the  left  sternal  margin  in  the  4th.  5th,  and  6th  interspaces,  and  an 
excessive  increase  of  the  cardiac  dulness  to  the  risrht  of  the  sternum. 


DISEASES  OF  THE  HEART  891 

A  pulsation  in  the  3d  interspace  to  the  right  of  the  sternum,  systolic 
if  there  is  tricuspid  regurgitation,  is  indicative  of  right  auricular 
dilatation.  Pulsation,  either  systolic  or  pre-systolic,  in  the  2d  space 
to  the  left  of  the  sternum,  may  be  manifest,  and  if  pre-systolic,  has 
been  afl&rmed  and  denied  as  an  evidence  of  left  auricular  dilatation. 

Differential  Diagnosis. — Dilatation  requires  to  be  distinguished 
from  hypertrophy  and  from  large  pericardial  effusions. 

(1)  Cardiac  Hyiiertrophy. — A  slow,  strong,  heaving  impulse,  a  dis- 
tinct although  large  and  rounded  apex  beat,  lying  downward  and  to 
the  left,  and  the  presence  of  a  dull,  prolonged,  and  loud  first  sound, 
with  an  accentuated  second  sound,  are  usually  sufl&cient  to  announce 
hypertrophy  rather  than  dilatation. 

(2)  Pericardial  Effusion. — See  page  872. 

VI.  Fatty  Heart. — Two  varieties  are  recognised :  fatty  degen- 
eration of  the  muscular  fibres,  and  fatty  infiltration  or  overgrowth, 
an  increase  of  the  normal  subpericardial  fat. 

(I)  Fatty  Degeneration. — Occurs  in  connection  with  carcinoma, 
phthisis,  prolonged  infectious  fevers,  severe  acute  or  chronic  anae- 
mias, phosphorus  poisoning,  disease  of  the  coronary  arteries,  peri- 
carditis, old  age,  and  cardiac  hypertrophies  in  general.  In  all  these 
instances  there  is  defective  nutrition  of  the  heart  muscle. 

The  symptoms  and  signs,  so  long  as  dilatation  does  not  occur,  are 
negative;  and  when  present  are  practically  those  of  dilatation,  either 
acute  after  severe  muscular  exertion  or  chronic  and  slow  in  their 
onset.  There  may  be  syncopal  or  anginal  attacks,  or  seizures  of 
cardiac  asthma,  especially  in  the  early  morning  hours ;  and  periods 
of  bradycardia,  pseudo-apoplectic  attacks,  Cheyue-Stokes  breathing, 
and  delusional  or  maniacal  mental  states.  Dyspnoea,  palpitation,  and 
a  small  and  irregular  pulse  are  common,  the  heart  sounds  may  be 
weak  with  a  galloping  rhythm,  and  the  apical  systolic  murmur  of  dila- 
tation may  develop.  None  of  these  signs  and  symptoms  are  distinc- 
tive, as  they  occur  also  in  chronic  myocarditis,  and  a  diagnosis  of 
fatty  degeneration  is  rarely  more  than  probable. 

(II)  Fatty  Infiltration.— This  is  almost  always  a  part  of  general 
obesity,  affecting  men  rather  than  women,  and  occurring  usually  be- 
tween 40  and  70  years  of  age.  No  symptoms  are  present  until  dila- 
tation occurs,  after  which  there  maybe  bronchitis,  vertigo,  and  pseudo- 
apoplectic  and  syncopal  attacks,  with  feeble  pulse  and  heart  sounds. 

The  diagnosis  depends  upon  the  presence  of  obesity,  plus  the  evi- 
dences of  cardiac  weakness. 

YII.  Myocarditis. — Two  varieties  :  acute  and  chronic. 

(I)  Acute  Myocarditis.— (1)  Acute  circumscribed  myocarditis  or 
abscess  of  the  heart  occurs  in  pyaemia,  diphtheria,  typhoid  fever. 


892  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

malignant  endocarditis,  and  other  septic  conditions.  The  condition 
can  not  be  diagnosed,  beyond  a  suspicion,  during  life. 

(2)  Acute  diffuse  myocarditis,  of  which  parenchymatous  degenera- 
tion or  cloudy  swelling  forms  a  goodly  part,  is  met  with  mainly  as 
a  result  of  the  infectious  fevers  such  as  smallpox,  typhus  and  typhoid 
fevers,  diphtheria,  scarlet  fever,  and  acute  rheumatic  fever;  or  in 
connection  with  acute  endocarditis  or  pericarditis.  The  si/nqjtotns 
are  simply  those  of  marked  cardiac  weakness  and  do  not  point  to  the 
cause  of  the  feebleness.  There  is  usually  a  small,  feeble,  frequent, 
and  often  irregular  pulse,  perhaps  with  palpitation  of  the  heart  and 
a  tendency  to  syncope.  The  jil^ysical  signs  are  practically  those  of 
cardiac  dilatation,  which  in  varying  degrees  is  such  a  common  and 
immediate  sequence  of  the  myocardial  inflammation. 

(II)  Chronic  (or  Fibrous)  Myocarditis. — Causes. — The  fibroid 
heart  may  succeed  acute  myocarditis,  but  in  the  majority  of  instances 
it  is  secondary  to  lesions  of  the  coronary  arteries,  especially  obliterat- 
ing arteritis,  less  commonly  thrombosis  or  embolism  (white  or  anaemic 
infarcts) ;  or  to  interference  with  the  coronary  circulation  as  in  valv- 
ular disease  of  the  heart ;  or  is  associated  with  hypertrophy ;  and 
also  occurs,  affecting  the  superficial  layers  of  the  muscle,  as  a  result 
of  chronic  endocarditis  or  pericarditis.  The  remoter  causes  are  gout, 
alcohol,  lead-poisoning,  syphilis,  rheumatism,  chronic  nephritis,  and 
diabetes,  i.  e.,  the  usual  agencies  which  cause  arteriosclerosis. 

Symptoms. — The  condition  may  be  quite  latent.  Angina  pectoris 
and  a  weak,  irregular,  often  slow  pulse  (50  to  30),  are  somewhat 
characteristic  ;  and  when  the  sclerosed  heart  is  slowly  failing  and  dilat- 
ing, dyspnoea,  cardiac  asthma,  palpitation,  precordial  constriction,  and 
evidences  of  general  venous  stasis  appear.  There  may  be  recurring, 
sometimes  fatal,  pseudo-apoplectic  seizures,  which  may  be  preceded 
by  occasional  vertigo  and  syncopal  attacks ;  or  true  apoplexy  may 
terminate  life  or  cause  a  hemiplegia.  Chronic  mania  or  other  form 
of  psychosis  may  develop. 

Physical  Signs. — The  signs  are  practically  those  of  a  dilated 
heart,  often  with  a  systolic  murmur  at  the  apex  (relative  mitral  in- 
competency) and  a  galloping  rhythm. 

Diagnosis. — As  Osier  well  says  :  "  For  practical  purposes  we  may 
group  the  cases  of  myocardial  disease  as  follows  : 

"(1)  Those  in  which  sudden  death  occurs  with  or  without  previ- 
ous indications  of  heart  trouble.  Sclerosis  of  the  coronary  arteries 
exists,  in  some  instances  with  recent  thrombus  and  white  infarcts,  in 
others  extensive  fibroid  disease,  in  others  again,  fatty  degeneration. 
Many  patients  never  complain  of  cardiac  distress,  but  enjoy  unusual 
vigour  of  mind  and  body. 


DISEASES  OF  THE  HEART 


893 


"  (2)  Cases  in  which  there  are  cardiac  arrhythmia,  shortness  of 
breath  on  exertion,  attacks  of  cardiac  asthma,  sometimes  anginal 
attacks,  collapse  symptoms  with  sweats  and  extremely  slow  pulse, 
and  occasionally  marked  mental  symptoms.  These  are  the  cases  in 
which  the  condition  may  be  strongly  suspected,  and,  in  some  instances, 
diagnosed.  It  is  rarely  possible  to  make  a  distinction  between  the 
fatty  and  fibroid  heart. 

"  (3)  Cases  in  which  there  are  cardiac  insufficiency  and  symptoms 
of  dilatation  of  the  heart.  Dropsy  is  often  present,  and  with  a  loud 
murmur  at  the  apex  it  may  be  difficult,  unless  the  case  has  been 
seen  from  the  outset,  to  determine  whether  or  not  a  valvular  lesion 
is  present." 

VIII.  Aneurism  of  the  Heart. — The  aneurism  may  involve 
either  the  valves  of  the  heart  or  its  walls.  The  former  results 
from  acute  endocarditis,  which  softens  or  erodes  one  or  more  cusps, 
causing  thinning  and  bulging  or  actual  perforation  of  the  segment, 
in  the  latter  case  with  consequent  incomptency.  Aneurism  of  the 
wall  usually  affects  the  apical  portion  of  the  left  ventricle,  and  is 
caused  most  commonly  by  chronic  myocarditis,  less  frequently  by 
acute  endocarditis,  pericarditis,  or  gumma.  In  well-marked  cases 
the  thinned  portion  of  the  wall  projects  sufficiently  to  constitute  a 
rounded  tumour  which  may  equal  the  heart  itself  in  size.  The  heart 
may  rupture.  The  physical  signs  are  not  in  the  least  distinctive. 
There  may  be  a  visible  pulsating  swelling  in  the  region  of  the  apex, 
occasionally  with  pressure  perforation  of  the  chest  wall ;  but  as  the 
condition  is  rare  and  the  physical  signs  are  practically  those  of  car- 
diac hypertrophy  or  dilatation,  a  positive  or  even  a  probable  diagno- 
sis during  life  is  exceedingly  infrequent. 

IX.  Rupture  of  the  Heart. — Eare,  and  usually  takes  place 
in  the  anterior  wall  of  the  left  ventricle,  most  commonly  as  a  result 
of  fatty  or  fibroid  degeneration,  less  frequently  gumma,  abscess,  or 
acute  coronary  embolic  softening.  The  usual  immediate  cause  is 
overexertion.  In  most  cases  this  accident  is  immediately  fatal.  If 
life  is  prolonged,  as  it  may  be  for  several  hours  or  even  days,  there 
will  be  intense  praecordial  pain  and  oppression,  with  the  symptoms 
of  internal  hemorrhage  (page  150).  The  physical  signs  of  pericar- 
dial eifusion  rapidly  develop. 

X.  Cardiac  Neuroses.  —  These  are  palpitation,  tachycardia 
(page  369),  bradycardia  (page  371),  arrhythmia  (page  372),  and 
angina  pectoris. 

(I)  Palpitation.— This  is  an  overstrong  and  usually  too  frequent 
action  of  the  heart,  either  regular  or  irregular,  of  which  the  patient 
is  uncomfortably  conscious.     The  presence  of  the  subjective  sensa- 


894  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

tion,  not  simply  an  overrapid  heart  action,  constitutes  the  cardinal 
characteristic  of  this  neurosis.  There  is  often  an  underlying  abnor^ 
mal  excitability  of  the  nervous  system. 

Causes. — Occurs  more  commonly  in  women  than  in  men,  espc 
daily  at  puberty,  the  menstrual  period,  or  the  menopause.  Frequent 
causes  are  anaemia,  hysteria,  neurasthenia,  dyspepsia,  worry,  anxiety. 
or  strong  emotions ;  overuse  of  tea,  coffee,  tobacco,  and  alcohol ;  less 
frequently  the  acute  fevers ;  conjoined  illness,  excitement  and  unac- 
customed physical  exertion  (irritable  heart  of  soldiers) ;  and  occa- 
sionally organic  valvular  or  myocardial  disease. 

Symptoms. — The  condition  is  usually  paroxysmal,  not  often  con- 
tinuous or,  if  so,  is  attended  with  exacerbations.  In  the  milder  cases 
there  is  simply  a  consciousness  of  sinking  or  fluttering  of  the 
heart ;  in  the  more  marked  instances  the  heart  throbs  or  beats  vio- 
lently, usually  with  increased  rapidity  (110  to  160),  often  irregularly, 
and  there  is  mental  anxiety  with  sensations  of  dyspnoea  and  oppres- 
sion, or  even  nausea  and  praecordial  pain.  The  peripheral  arteries 
may  pulsate  strongly.  The  face  and  skin  may  be  flushed.  A  copious 
amount  of  clear  pale  urine  may  be  voided  after  the  attack.  A  par- 
oxysm usually  terminates  within  an  hour,  but  may  continue  for 
hours  or  days.  In  the  majority  of  cases  examination  of  the  heart 
affords  negative  results.  There  may  be  a  more  widely  diffused  and 
forcible  impulse  than  normal,  with  clear,  sharp,  or  accentuated  heart 
sounds.  Murmurs  due  to  ansemia  or  the  rapid  action  of  the  heart 
may  be  heard,  especially  in  the  pulmonary  area,  seldom  at  the  apex. 
Ordinarily  murmurs  are  absent. 

Diagnosis. — The  presence  of  a  subjective  consciousness  of  the 
heart  beat  is  essential  to  the  diagnosis.  Eapid  heart  action,  not  per- 
ceptible to  the  patient,  is  tachycardia,  not  palpitation.  Examination 
of  the  heart  during  the  intervals  of  the  attacks  will  separate  the 
cases  of  purely  nervous  palpitation  from  those  which  are  symptom- 
atic of  anaemia  or  chronic  valvular  lesions.  The  prognosis  is  good 
as  to  life,  but  if  the  attacks  are  frequent  and  prolonged  for  years 
hypertrophy  of  the  heart  may  ensue. 

(II)  Angina  Pectoris. — A  symptom,  not  a  disease. 

Causes. — "With  very  rare  exceptions  stenocardia  or  breast  pang 
is  associated  with  arteriosclerosis,  which  may  be  general  or  local,  but 
in  either  case  affects  the  aorta,  at  its  origin,  and  the  coronary  arteries. 
The  latter  may  be  narrowed  at  their  roots,  or  their  main  divisions  be 
the  seat  of  an  obliterating  endocarditis.  Myocardial  changes  usually 
coexist.  It  occurs  most  frequently  in  aortic  insufficiency  and  adhe- 
rent pericardium,  much  less  commonly  with  mitral  lesions.  The 
exciting  causes  of  an  attack  are  muscular  exertion,  strong  mental 


DISEASES  OF  THE  HEART  895 

emotion,  gastric  distention  or  disturbance,  and  exposure  to  cold. 
The  attacks,  in  the  great  majority  of  cases,  affect  men,  usually  over 
40  years  of  age. 

Symptoms. — The  attack  begins  suddenly,  with  pain,  usually  intense 
and  excruciating,  in  the  region  of  the  heart.  The  pain  radiates  into 
the  neck,  the  left  shoulder,  and  down  the  arm  to  the  fingers,  some- 
times to  the  right  arm  and  down  the  body.  There  is  also  a  sense 
of  cardiac  constriction,  often  with  coldness  and  numbness  of  the 
praecordium  and  the  fingers.  The  face  is  pale  or  ashy  gray  and  be- 
trays a  feeling  of  intense  anxiety.  The  face  and  body  are  often  cov- 
ered with  large  drops  of  cold  perspiration.  A  sense  of  impending 
death  is  a  usual  and  characteristic  symptom.  There  may  or  may 
not  be  dyspnoea,  sometimes  associated  with  wheezing  or  asthmatic 
breathing.  The  arterial  tension  is  usually  increased,  and  while  the 
action  of  the  heart  may  be  arrhythmic,  it  is  often  regular  and  normal. 
The  patient  may  be  restless,  but  more  commonly  holds  himself  quiet 
and  passive  in  fearful  expectation  of  what  may  happen. 

The  attack  lasts  from  a  few  seconds  to  two  minutes,  and  often 
terminates  with  eructations,  nausea  and  vomiting,  or  the  voiding  of 
a  large  quantity  of  clear  pale  urine. 

Variations  and  Course. — There  is  much  variation  in  the  severity 
of  the  ailment  in  different  persons  and  in  the  same  person  at  differ- 
ent times.  The  milder  cases  present  praecordial  oppression  and  dis- 
comfort, with  slight  cardiac  pain  radiating  to  the  neck  and  arm  ;  and 
there  are  all  grades  between  this  and  the  severe  seizures  previously 
described.  Death  may  occur  in  the  first  attack ;  or  there  may  be 
frequent  paroxysms  for  a  number  of  successive  days ;  or  the  seizures 
may  be  few  and  spread  over  many  years. 

Differential  Diagnosis.— An  attack  of  severe  cardiac  pain  hav- 
ing the  characteristics  previously  noted  is  probably  a  true  angina, 
but  if  in  addition  there  are  evidences  of  arteriosclerosis  or  aortic 
Talvular  lesions,  and  the  seizure  occurs  in  men  over  40  years  of 
age,  it  is  without  a  doubt  true  angina  pectoris.  A  positive  diag- 
nosis can  not  be  made  in  the  slighter  painful  manifestations  unless 
arterial  and  valvular  lesions  are  recognisable.  Confusion  may  arise 
in  connection  with  the  following  conditions : 

(1)  Locomotor  Ataxia.— The  girdle  sensation  and  sharp  neuralgic 
pains  of  locomotor  ataxia  if  seated  in  the  thorax,  and  especially  if 
associated  with  arteriosclerosis,  may  bear  a  rather  close  resemblance 
to  the  milder  forms  of  true  angina,  but  the  presence  of  the  Argyll- 
Eobertson  pupil  and  disorders  of  co- ordination,  with  the  absent 
patellar  reflexes,  will  declare  for  the  former.  Moreover,  the  attacks 
in  this  case  are  often  independent  of  exertion  or  other  exciting  cause. 


896  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

(2)  Gastralgia. — See  page  774. 

(3)  Pseudo-angina. — Three  varieties  of  false  angina^  not  associated 
with  organic  changes,  have  been  described.  Neurotic  Form. — Seen  in 
hysterical  or  neurasthenic  women  or  in  neurasthenic  men,  often  with 
coexisting  dyspepsia.  The  attacks  usually  occur  at  night  with  parox- 
ysmal substernal  pain,  palpitation,  and  a  sense  of  cardiac  fulness  or 
distention.  This  condition  may  be  also  a  sequel  of  influenza.  Vaso- 
motor Angina  (Nothnagel). — Consists  of  a  primary  coldness,  numb- 
ness, or  stiffness  of  the  extremities,  and  pallor  of  the  face  (vasomotor 
spasm)  followed  by  syncopal  sensations  and  severe  praecordial  pain. 
Toxic  Angina. — Due  to  the  overuse  of  tea,  coffee,  and  tobacco.  In 
addition  to  the  ordinary  palpitation  and  irregularity  of  heart  action 
which  may  be  caused  by  these  forms  of  poisoning,  there  may  be  car- 
diac pain  of  such  severity  that  it  is  properly  termed  a  pseudo-angina. 
It  is  sometimes  associated  with  coldness  of  the  extremities,  faintness, 
and  weak  pulse. 

It  is  not  always  easy  to  differentiate  between  true  and  false  an- 
gina, especially  in  women,  and  some  serious  mistakes  have  been 
made.  The  importance  of  the  history,  and  in  particular  of  a  search- 
ing and  careful  physical  examination,  must  be  strongly  emphasized. 
The  following  table  (Huchard,  quoted  by  Osler)  is  of  much  service : 

TRUE   ANGINA  PSEUDO-AXGINA 

Most  common  between  the  ages  of  40  At  every  age,  even  6  years. 
and  50  years. 

Most    common    in    men.      Attacks  Most  common   in    women.     Attacks 

brought  on  by  exertion.  spontaneous. 

Attacks    rarely    periodical    or    noc-  Often  periodical  and  nocturnal, 
turnal. 

Not  associated  with  other  symptoms.  Associated  with  nervous  symptoms. 

Vasomotor    form     rare.     Agonizing  Vasomotor  form  common.     Pain  less 

pain  and  sensation  of  compression  by  a  severe :  sensation  of  distention, 
vice. 

Pain  of   short  duration.     Attitude:  Pain  lasts  1  or  2  houi's.     Agitation 

silence,  immobility,  and  activity. 

Lesions :  sclerosis  of  coronary  artery.  Neuralgia  of  nerves  and  cardioplexus. 

Prognosis  grave,  often  fatal.  Never  fatal. 

Arterial  medication.  Antineuralgic  medication. 

Prognosis. — In  true  angina  always  grave ;  in  pseudo-angina 
always  favourable.  The  accuracy  of  the  prognosis  in  a  given  case  de- 
pends upon  the  correctness  of  the  diagnosis.  It  must  not  be  for- 
gotten that  sudden  death  occurs  in  many  cases  of  angina  at  other 
times  than  during  a  paroxysm. 

XI.  Congenital  Anomalies  of  the  Heart.— («)  Causes  and 
Varieties. — These  anomalies  result  from  an  arrest  of  development,  or 


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DISEASES  OF  THE  HEART  897 

foetal  endocarditis,  or  both.     With  reference  to  the  frequency  of  the 
drfferent  lesions  and  their  association,  Holt's  tables  are  as  follows  : 

The  Frequency  of  the  Different  Lesiom  in  2J^  Autopsies  upon  Cases  of  Congenital 

Cardiac  Anomaly 

Defect  ia  the  ventricular  septum 149  cases;  only  lesion  in  5  cases. 

Defect  in  the  auricular  septum  or  patent  foramen 

ovale J26  " 

Pulmonic  stenosis  or  atresia 108  " 

Patent  ductus  arteriosus 68  " 

Abnoi-malities  in  the  origin  of  the  great  vessels. .     45  « 

Pulmonic  insufficiency 17  « 

Tricuspid  insufficiency g  « 

Tricuspid  stenosis  or  atresia 3  " 

Mitral  insufficiency 1  « 

Mitral  stenosis  or  atresia 6  " 

Aortic  insufficiency 1  « 

Aortic  stenosis  or  atresia 6  " 

Transposition  of  the  heart 2  " 

Ectocardia 1  « 

The  most  Frequent  Associated  Lesions 
Pulmonic  stenosis,  with  defect  in  the  ventricular 

septum 92  cases ;  only  lesion  in  20  cases. 

Pulmonic  stenosis,  with  defect  in  the  auricular 

septum 52  "  "  "    8    " 

Defects  in  both  septa 82  "  "  "  17    « 

Pulmonic  stenosis  and  defects  in  both  septa 36  "  "  "  21    " 

(b)  Symptoms. — The  most  distinctive  symptom  is  cyanosis,  which 
has  been  noted  in  about  90  per  cent  of  all  cases.  It  may  be  slight 
and  manifest  only  after  exertion  ;  or  limited  to  the  small  extremities ; 
or  the  entire  surface  may  be  continuously  leaden  and  livid,  the  morbus 
cmruleus  or  "  blue  disease."  In  the  great  majority  of  cases  this 
symptom  makes  its  appearance  within  the  first  week  or,  at  least,  the 
first  month  of  life ;  in  rare  cases  this  and  other  symptoms  may  not 
show  themselves  for  periods  varying  from  1  to  16  years  after  birth. 
A  cool  skin,  cough,  dyspnoea  on  exertion,  and  extreme  clubbing  of 
the  fingers  and  toes  are  frequent  symptoms ;  less  commonly  oedema, 
dropsy  of  cavities,  and  bleeding  from  the  nose  or  lungs. 

(c)  Diagnosis. — The  cardinal  physical  signs  of  congenital  cardiac 
disease  in  children  are  cyanosis,  murmurs,  and  right  ventricular 
hypertrophy — a  combination  which  permits  a  diagnosis  of  a  congenital 
lesion.  The  murmur  in  two  thirds  of  the  cases  is  systolic,  usually 
loud  and  rough,  and  most  intense  over  the  pulmonary  area.  The 
right  ventricle  is  hypertrophied  because,  under  foetal  conditions,  the 
bulk  of  the  work  falls  upon  it,  and  practically  all  malformations 
involve  a  continuance  of  the  prenatal  task. 


898  DIAGNOSIS,   DIRECT  AND    DIFFERENTIAL 

To  determine  the  exact  lesion  or  defect  which  is  present  is  al- 
ways extremely  difficult,  and  in  the  majority  of  cases  the  diagnosis 
of  its  precise  nature  must  be  conjectural.  Two  sets  of  conclu- 
sions are  appended  :  (A)  Holt's,  and  (B)  Hochsinger's,  abstracted  by 
Osier. 

(A)  "  A  Systolic  Murmur  at  the  Base,  ivith  Cyanosis. — This  is  the 
most  common  combination  met  with  and  was  present  in  about  one 
third  of  all  the  cases.  In  over  80  per  cent  of  the  cases  with  these 
symptoms,  pulmonic  stenosis  was  found.  The  remainder  were  com- 
plicated cases  of  quite  a  wide  variety.  Pulmonic  stenosis  was  usu- 
ally associated  with  a  defect  in  one  of  the  cardiac  septa,  or  a  patent 
ductus  arteriosus. 

"  A  Systolic  Murmur  without  Cyanosis. — In  the  cases  followed  to 
autopsy  this  was  not  a  frequent  combination,  being  noted  but  6 
times,  and  usually  dependent  upon  a  defect  in  the  ventricular  sep- 
tum without  pulmonic  stenosis,  or  upon  tricuspid  regurgitation. 
Judging  from  my  own  clinical  experience,  a  systolic  murmur  with- 
out cyanosis  is  more  common  than  is  indicated  by  these  figures. 

"  A  Systolic  Murmur  at  the  Apex  with  Cyanosis. — Of  the  6  cases 
with  this  combination,  all  were  examples  of  complex  malformation, 
the  most  frequent  lesions  being  a  defect  in  the  auricular  septum, 
transposition  of  the  great  vessels,  and  patent  ductus  arteriosus. 

^^  Cyanosis  tvithout  murmurs  was  noted  14  times.  It  indicates 
either  pulmonic  atresia  or  the  transposition  or  irregular  origin  of  the 
great  vessels. 

"  Diastolic  murmurs  were  heard  in  2  cases,  and  depended  upon 
pulmonic  insufficiency. 

"  A  presystolic  murmur  was  noted  in  a  single  case.  It  was  local- 
ized at  the  right  base,  and  the  only  lesion  was  a  patent  foramen 
ovale. 

"  Absence  of  both  cyanosis  and  murmurs  was  recorded  in  5  cases. 
The  lesions  found  were,  atresia  of  the  aorta,  both  arteries  arising 
from  the  right  ventricle,  or  defective  septa. 

"  It  will  be  seen  that  about  the  only  cases  in  which  a  fairly  posi- 
tive diagnosis  can  be  made  is  pulmonic  stenosis  with  a  deficient  ven- 
tricular septum.  Enlargement  of  the  right  heart,  being  common  to 
nearly  all  the  varieties,  is  of  no  diagnostic  value. 

^^  Diagnosis  of  Congenital  from  Acquired  Disease. — Congenital  dis- 
ease may  be  suspected  if  the  patient  is  under  2  years  of  age  ;  if  there 
is  no  history  of  previous  rheumatism ;  if  the  murmur  is  atypical  in 
its  location,  character,  or  transmission ;  if  there  is  a  very  loud  mur- 
mur at  the  base ;  if  there  is  cyanosis ;  and  if  there  is  evidence  of 
enlargement  of  the  right  heart. 


DISEASES  OP  THE  HEART  899 

^^  Diagnosis  of  Congenital  from  Ancemic  Murmurs. — This  is  often 
a  more  difficult  matter  than  to  decide  between  congenital  and  ac- 
quired disease.  From  a  murmur  alone  one  should  be  very  cautious 
in  making  a  diagnosis  of  cardiac  malformation  in  a  very  anaemic 
infant.  Anaemic  murmurs  are  systolic,  basic,  unaccompanied  by  en- 
largement of  the  heart ;  usually  heard  in  the  carotids,  often  in  the 
subclavian  arteries,  but  are  seldom  so  loud  as  those  due  to  malforma- 
tions. In  some  cases  it  may  be  necessary  to  watch  the  effect  of 
treatment  or  the  course  of  the  disease  before  deciding  the  question." 

(B)  "  (1)  In  childhood,  loud,  rough,  musical  heart  murmurs,  with 
normal  or  only  slight  increase  in  the  heart  dulness,  occur  only  in  con- 
genital heart  disease.  The  acquired  endocardial  defects  with  loud 
heart  murmurs  in  young  children  are  almost  always  associated  with 
great  increase  in  the  heart  dulness.  In  the  transposition  of  the 
large  arterial  trunks  there  may  be  no  cyanosis,  no  heart  murmur,  and 
an  absence  of  hypertrophy. 

"  (2)  In  young  children  heart  murmurs  with  great  increase  in  the 
cardiac  dulness  and  feeble  apex  beat  suggest  congenital  changes. 
The  increased  dulness  is  chiefly  of  the  right  heart,  whereas  the  left 
is  only  slightly  altered.  On  the  other  hand,  in  the  acquired  endo- 
carditis in  children,  the  left  heart  is  chiefly  affected  and  the  apex 
beat  is  visible  ;  the  dilatation  of  the  right  heart  comes  late  and  does 
not  materially  change  the  increased  strength  of  the  apex  beat. 

"  (3)  The  entire  absence  of  murmurs  at  the  apex,  with  their  evi- 
dent presence  in  the  region  of  the  auricles  and  over  the  pulmonary 
orifice,  is  always  an  important  element  in  differential  diagnosis,  and 
points  rather  to  septum  defect  or  pulmonary  stenosis  than  to  endo- 
carditis. 

"  (4)  An  abnormally  weak  second  pulmonic  sound  associated  with 
a  distinct  systolic  murmur  is  a  symptom  which  in  early  childhood  is 
only  to  be  explained  by  the  assumption  of  a  congenital  pulmonary  ste- 
nosis, and  possesoes  therefore  an  importance  from  a  point  of  differen- 
tial diagnosis  which  is  not  to  be  underestimated. 

"  (5)  Absence  of  a  palpable  thrill,  despite  loud  murmurs  which 
are  heard  over  the  whole  praecordial  region,  is  rare  except  with  con- 
genital defects  in  the  septum,  and  it  speaks  therefore  against  an 
acquired  cardiac  affection. 

"  (6)  Loud,  especially  vibratory,  systolic  murmurs,  with  the  point 
of  maximum  intensity  over  the  upper  third  of  the  sternum,  asso- 
ciated with  a  lack  of  marked  symptoms  of  hypertrophy  of  the  left 
ventricle,  are  very  important  for  the  diagnosis  of  a  persistence  of  the 
ductus  Botalli,  and  can  not  be  explained  by  the  assumption  of  an 
endocarditis  of  the  aortic  valve." 


900  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 


III.    DISEASES    OF   THE    ARTERIES 

I.  Arteriosclerosis. — A  chronic  inflammatory  and  degenera- 
tive disease  of  the  vascular  system,  usually  involving  the  arteries 
(arteriosclerosis),  sometimes  the  capillaries  as  well  {arteriocapillary 
fibrosis),  seldom  the  veins  [phlehosclerosis),  or  all  three  {angioscle- 
rosis).  There  is  thickening  of  the  vessel  walls  due  to  fibrous  over- 
growth, affecting  all  three  coats,  but  mainly  the  intima,  of  the  vessel. 
The  process  may  be  diffuse,  involving  the  aorta  and  its  branches 
more  or  less  uniformly ;  or  nodular  and  patchy,  occurring  principally 
in  the  aorta  and  the  larger  arteries.  The  nodular  areas  may  soften 
{atheromatous  abscess)  and  discharge  {atheromatous  ulcer),  subse- 
quently becoming  calcified ;  or  calcareous  deposits  may  take  place  in 
the  sclerotic  plaque  without  softening.  The  diffuse  form  affects  the 
smaller  arteries  rather  than  the  aorta,  but  the  nodular  variety  is  often 
associated. 

Causes. — Either  as  a  result  of  the  normal  loss  of  elasticity  due  to 
old  age,  or  a  similar  loss  resulting  from  the  degeneration  caused  by 
chronic  intoxications,  or  overstretching  by  prolonged  high  arterial 
tension,  the  vessels  become  dilated.  In  order  to  lessen  the  abnor- 
mally large  calibre  of  the  vessel  and  to  restore  the  normal  velocity 
of  the  blood  stream,  the  intima  thickens — practically  a  compensatory 
process.  There  is  in  many  instances  a  congenital  or  inherited  lack 
of  elasticity  in  the  arteries  which  predisposes  toward  their  premature 
senility.     It  is  more  common  in  males. 

The  causes  of  arteriosclerosis  are  old  age ;  gout,  syphilis,  alcohol, 
and  lead ;  muscular  overwork ;  chronic  nephritis,  which  may  be  cause 
or  result;  overeating;  and  rheumatism,  typhoid  fever,  or  scarlet 
fever.  Sclerosis  of  the  pulmonary  artery  and  sometimes  of  the  pul- 
monary veins  may  occur  in  conditions  which  cause  prolonged  high 
pressure  in  the  lesser  circuit,  especially  mitral  stenosis  and  emphy- 
sema ;  and  the  portal  veins  may  be  sclerosed  in  hepatic  cirrhosis. 

Arteriosclerosis  usually  becomes  evident  between  40  and  55  years 
of  age,  but  may  appear  in  the  early  20's  or  as  late  as  60. 

Symptoms. — The  accessible  arteries  are  thickened  or  atheroma- 
tous, the  pulse  is  the  pulsus  tardus  (page  377)  and  of  high  tension. 
Owing  to  the  peripheral  resistance  offered  by  the  more  or  less  ob- 
structed vessels  the  signs  of  left-side  hypertrophy  are  manifest.  The 
apex  beat  is  shifted  to  the  left,  the  impulse  is  forcible  and  heaving, 
and  the  aortic  closure  is  loud,  ringing,  and  accentuated ;  and  if  the 
aortic  valves  and  the  root  of  the  aorta  are  atheromatous,  it  will  be  of 
a  peculiar  harsh  quality  as  well.  Late  in  the  disease  the  evidences 
of  cardiac  dilatation  may  ensue. 


DISEASES  OF  THE  ARTERIES  901 

In  addition  to  the  signs  just  mentioned,  which  are  common  to  all 
cases,  there  are  special  manifestations  depending  upon  the  fact  that 
the  vessels  in  particular  organs  or  regions  may  have  undergone  more 
decided  sclerotic  changes  than  in  other  vascular  areas. 

(1)  The  cardio-vascular  symptoms^  oppression,  palpitation,  and 
dyspnoea,  on  exertion,  may  be  pronounced.  If  the  coronary  arteries 
are  particularly  involved  there  may  be  angina  pectoris,  or  evidences 
of  chronic  myocarditis.  If  dilatation  ensues  there  will  be  dyspnoea, 
cedema,  dropsies  of  serous  cavities,  and  diminished  urine.  Throm- 
bosis of  the  coronary  arteries  or  rupture  of  the  heart,  with  sudden 
death,  and  aneurism  of  the  heart,  are  possible  occurrences ;  so  also 
with  aneurism  in  general.  (2)  Renal  symptoms^  due  to  interstitial 
nephritis  {q.  v.),  may  be  present.  (3)  Cerebral  symptoms  are  com- 
mon. There  may  be  vertigo  (a  frequent  symptom),  headache,  and 
ringing  in  the  ears.  Vertigo  may  coexist  with  attacks  of  faintness, 
epileptiform  seizures,  and  bradycardia.  Temporary  attacks  of  apha- 
sia, hemiplegia,  or  monoplegia  may  occur,  probably  significant  of 
thrombosis  in  the  smaller  almost  obliterated  cerebral  arteries,  or  of 
the  lodgment  of  small  fibrinous  emboli  from  the  roughened  aorta. 
Cerebral  hemorrhage  may  occur,  the  brittle  arteries,  often  the  seat 
of  miliary  aneurisms,  suddenly  rupturing.  (4)  Because  of  oblitera- 
tion, thrombosis,  or  embolism  of  certain  of  the  peripheral  arteries, 
gangrene  of  the  extremities  may  take  place. 

Diagnosis.— Thickened  arteries,  high  tension  pulse,  left  ventricu- 
lar hypertrophy,  and  an  accentuated  aortic  closure  constitute  in- 
dubitable evidence  of  arteriosclerosis.  Hard  arteries  alone  do  not 
necessarily  imply  aortic  changes  unless  the  aortic  second  sound  is  of 

a  harsh  quality. 

When  dilatation  has  occurred  and  the  murmurs  of  relative  aortic 
or  mitral  incompetency  are  found,  it  may  be  difficult  or  impossible 
to  determine,  in  the  absence  of  previous  observation  of  the  case, 
whether  the  condition  is  a  sequel  of  chronic  valvular  disease  or  arises 
from  arteriosclerosis  without  primary  valvular  defects. 

Prognosis  -Ultimately  grave,  although  the  general  health  may 
remain  good  for  manv  years.  The  symptoms  may  come  gradually— 
e.  g.,  with  polyuria,  slight  traces  of  albumin,  and  a  few  hyaline  casts, 
as  in  the  granular  kidney,  due  to  arteriosclerosis ;  or  suddenly,  as  in 

cerebral  hemorrhage. 

II  Aneurism  in  General.-Forms.—A  true  aneurism  is  a 
more  or  less  localized  dilatation  of  an  artery,  the  aneurismal  sac 
consisting  of  one  or  more  of  the  coats  of  the  vessel.  The  dilatation 
may  be  fusiform,  saccular,  or  cylindrical.  A  dissecting  aneurism  is 
one  in  which  the  intima  ruptures  and  the  blood  forces  itself  between 

59 


902  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

the  layers  of  the  vessel  wall.  A  false  aneurism  is  a  circumscribed 
collection  of  blood  outside  of  the  vessel,  and  due  to  rupture  of  the 
latter.  When  an  abnormal  communication  exists  between  an  artery 
and  a  vein  it  constitutes  an  arterio-veiious  aneurism ;  and  the  com- 
munication may  be  direct,  aneurismal  varix,  or  a  sac  may  intervene, 
varicose  aneurism.  The  aneurisms  of  greatest  clinical  interest  to  the 
physician  are  the  true  sacculated  or  fusiform  varieties. 

Causes. — In  the  majority  of  cases  aneurisms  are  due  to  weak- 
ening of  the  arterial  walls  by  arteriosclerosis.  If  the  latter  is  diffuse, 
the  dilatation  is  generally  fusiform  and  irregular ;  if  circumscribed, 
the  yielding  is  saccular.  Of  the  causes  of  sclerotic  changes,  syphilis 
is  the  most  important  in  producing  aneurism.  Prolonged  high  arte- 
rial tension,  as  in  laborious  muscular  work,  cardiac  hypertrophy,  etc., 
predispose.  A  great  and  sudden  strain,  as  in  heavy  lifting  or  violent 
coughing  or  straining,  may  initiate  the  dilatation  if  the  coats  are  weak- 
ened by  previous  disease.  Xon-septic  embolism  of  an  artery  may  cause 
a  dilatation  on  the  proximal  side  of  the  obstruction ;  and,  in  connec- 
tion with  malignant  endocarditis,  acute  inflammatory  or  degenerative 
lesions  leading  to  aneurismal  dilatations  may  result  from  an  extension 
of  the  process  to  the  aorta,  or  the  lodgment  of  infective  emboli  else- 
where. The  arteries  may  be  hereditarily  of  poor  quality.  Aneu- 
risms occur  more  frequently  in  men  than  in  women,  and  most  com- 
monly between  30  and  50  years  of  age. 

According  to  their  site  the  following  varieties  of  aneurism  are 
clinically  recognisable.  Of  all  arteries  the  aorta  is  most  commonly 
the  seat  of  aneurism.  Aneurisms  of  the  thoracic  aorta  outnumber 
those  of  the  abdominal  aorta  by  about  20  to  1. 

III.  Aneurism  of  the  Thoracic  Aorta.— A  majority  of  tho- 
racic aneurisms  are  saccular  and  involve  the  ascending  portion  of  the 
arch,  starting  not  infrequently  at  the  very  root  of  the  vessel.  Xext 
most  frequent  are  those  of  the  transverse  and  descending  portions  of 
the  arch  and  the  descending  thoracic  aorta,  in  the  order  of  mention. 

Symptoms. — Depending  upon  the  size,  site,  and  direction  of  growth 
of  the  aneurism,  the  condition  may  be  latent,  even  with  large  dila- 
tations, or  may  be  manifested  by  distinct  pressure  effects.,  with  or 
without  external  physical  signs.  Aside  from  the  physical  signs, 
later  to  be  described,  the  most  prominent  general  pressure  symptoms 
are  pain,  dyspnoea,  cough,  changes  in  the  voice,  and  dysphagia.  In 
greater  detail  these  and  other  symptoms  are  as  follows : 

Pain,  which,  although  variable,  is  usually  an  early  and  constant 
symptom,  is  apt  to  occur  in  paroxysms.  It  may  be  steady  and  boring, 
often  very  severe  if  pressure-erosion  of  bone  is  occurring ;  frequently 
it  is  sharp,  radiating,  and  neuralgic,  and  is  reflected  to  the  neck  or 


DISEASES  OF  THE  ARTERIES  903 

down  the  arm  (aneurism  of  arch),  or  along  the  intercostal  nerves 
(aneurism  of  descending  aorta),  and  attacks  resembling  angina  pec- 
toris are  not  infrequent,  especially  if  the  ascending  portion  of  the 
arch  is  dilated.  Dyspnoea  and  stridulous  respiration,  together  with 
a  dry,  paroxysmal,  brazen,  ringing,  or  wheezy  cough,  and  hoarseness 
or  aphonia  are  significant  of  pressure  on  a  recurrent  laryngeal  nerve, 
generally  the  left,  and  causing  spasm  or  paralysis  of  the  correspond- 
ing vocal  cord,  by  aneurism  of  the  transverse  portion  of  the  arch. 
Dyspnoea  and  cough  are  also  due  to  pressure  upou  the  trachea  or  the 
left  main  bronchus,  and  the  cough  may  be  accompanied  by  a  thin  or 
thick  expectoration  if  bronchitis  or  bronchiectasis  results  from  the 
compression  of  the  air  tubes.  Dysphagia  arising  from  pressure  upon 
or  spasm  of  the  esophagus  is  a  somewhat  infrequent  symptom. 
Spitting  of  blood  in  small  quantities,  sometimes  persistent,  may 
occur,  coming  from  the  congested  and  altered  mucous  membrane  of 
the  trachea  at  the  point  of  compression ;  large  hemorrhages  may 
arise  from  rupture  of  the  sac  into  the  trachea,  bronchi,  or  lung. 
Owing  to  irritant  pressure  on  the  sympathetic  there  may  be  dila- 
tation of  one  pupil,  perhaps  with  pallor  of  the  same  side  of  the  face  ; 
or  miosis,  due  to  paralyzing  pressure,  perhaps  with  unilateral  con- 
gestion and  sweating  of  the  face.  There  may  be  distention  of  the 
veins  and  oedema  of  the  head  and  arm  due  to  pressure  on  the  superior 
vena  cava,  or  of  the  right  arm  alone  from  encroachment  upon  the 
subclavian  vein.  Clubbed  fingers  and  incurved  nails,  perhaps  of  one 
hand  only,  may  occur. 

Physical  Signs. — Stress  is  to  be  laid  upon  a  careful  inspection 
from  various  points  of  view  aided  by  direct  and  oblique  illumination 
in  order  to  detect  slight  pulsations  or  pulsating  prominences  (Fig. 
82,  page  326).  If  present,  pulsation,  with  or  without  swelling,  is  seen 
most  commonly  in  the  first  and  second  interspaces  to  the  right  of  the 
sternum,  much  less  commonly  in  the  same  interspaces  to  the  left ;  and 
if  the  innominate  participates  in  the  dilatation  it  may  be  visible  on 
the  right  side  of  the  neck  or  in  the  episternal  notch.  Occasionally 
pulsation  and  swelling  are  seen  posteriorly  to  the  left  of  the  spine. 
The  swelling,  which  may  be  hardly  perceptible,  or,  on  the  other  hand, 
exceed  a  large  orange  in  size,  may  involve  the  sternum  and  the  adja- 
cent costal  cartilages.  The  overlying  skin  may  be  greatly  thinned  or 
may  have  ulcerated  through,  thus  revealing  the  fibrinous  layers  of  the 
sac  wall,  from  which  blood  may  ooze.  The  tumour  may  be  impressi- 
ble and  fluctuating ;  more  commonly,  depending  on  the  thickness  of 
the  deposit  of  fibrin,  it  is  firm  and  resistant.  The  pulsation  of  the 
swelling  is  expansile — the  sac  enlarging  in  every  direction— and 
often  forcible  and  heaving.     If  there  is  no  visible  swelling  or  pulsa- 


904  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

tion,  firm  pressure  with  the  fingers  of  one  hand  in  front,  opposed  by 
the  other  hand  placed  posteriorly,  may  develop  it  to  the  accustomed 
touch.  There  may  be  a  systolic  thrill ;  and  a  diastolic  shock,  often 
well  marked,  is  an  important  physical  sign.  The  apex  beat  may  be 
carried  downward  and  to  the  left,  most  commonly  by  reason  of  the 
pressure  of  a  large  aneurism  ;  less  frequently  because  of  simple 
cardiac  hypertrophy  due  to  overwork. 

Percussion  is  negative  except  in  aneurisms  of  a  certain  size 
which  approach  the  chest  wall  sufficiently  to  cause  dulness.  The 
percussion  sound  is  flat  and  resistant,  and  the  area  of  dulness  varies 
in  position  according  to  the  seat  of  the  aneurism,  as  will  be  subse- 
quently described.  Auscultation  may  reveal  a  systolic  murmur, 
largely  dependent  upon  the  thickness  and  irregularities  of  the 
fibrinous  layers,  loudest  over  the  aneurismal  sac,  and  transmitted  to 
the  arteries  of  the  neck,  but  which,  taken  alone,  is  of  little  diagnostic 
value.  When  a  double  murmur  is  heard  the  diastolic  component  is 
usually  due  to  coexisting  relative  or  organic  aortic  insufficiency. 
Unless  the  murmur  of  the  latter  replaces  it,  the  aortic  second  sound 
is,  in  aneurisms  of  the  arch,  accentuated,  ringing  and  snappy — the 
auditory  equivalent  of  the  palpable  diastolic  shock — an  important 
diagnostic  sign.  Occasionally  a  diastolic  murmur  alone  may  be 
heard,  and  perhaps  also  a  systolic  whiff  in  the  trachea.  The  ptdse, 
in  the  arteries  beyond  the  sac,  is  delayed  and  altered  in  character,  so 
that  if  the  innominate  is  involved  the  beat  of  the  right  radial  may  be 
appreciably  later  than  that  of  the  left ;  but  if  the  dilatation  is  beyond 
the  innominate  the  converse  is  true.  Tracheal  tugging  (page  265), 
an  extremely  useful  sign  in  otherwise  obscure  cases,  may  be  detected. 

Diagnosis. — (1)  Of  the  Aneurism. — In  the  cases  which  present 
well-marked  pressure  symptoms  phts  a  pulsating  swelling,  the  diag- 
nosis can,  as  a  rule,  be  safely  made,  especially  if  arteriosclerosis  is 
present  or  its  causes  operative,  and  the  patient  is  between  30  and  45 
years  of  age.  But  if  the  aneurism  is  small  or  deep-seated,  or  if 
pressure  symptoms  alone,  without  physical  signs,  are  present,  par- 
ticularly when  slight,  scanty,  or  indefinite,  the  diagnosis  is  always 
difficult  and  may  be  impossible. 

(2)  Of  its  Site. — In  the  ascending  portion  of  the  arch  the  physical 
signs  often  predominate — e.  g.,  external  tumour  and  dulness,  mani- 
fest usually  to  the  right,  rarely  to  the  left,  of  the  sternum,  over  the 
2d  and  3d  interspaces.  The  veins  of  the  neck,  head,  and  upper 
extremities  may  be  swollen  from  pressure  upon  the  superior  cava ; 
occasionally  there  is  oedema  of  the  right  arm  alone  from  pressure  on 
the  subclavian ;  and  there  may  be  swelling  of  the  lower  extremities 
if  the  aneurism  is  sufficiently  large  to  compress  the  inferior  cava. 


DISEASES  OF  THE  ARTERIES  905 

The  innominate  artery  rarely  participates.  The  heart  may  be  dis- 
placed to  the  left.  Aphonia  and  dyspnoea,  due  to  pressure  on  the 
right  recurrent  laryngeal,  are  common. 

In  the  transverse  portion  of  the  arch  the  pressure  symptoms  often 
dominate  the  physical  signs.  Thus  there  may  be  dyspncea  and 
cough  from  pressure  on  the  trachea ;  dysphagia  from  pressure  on  the 
esophagus ;  bronchitis,  bronchiectasis,  perhaps  pulmonary  abscess, 
from  pressure  on  a  bronchus ;  brassy  cough  and  aphonia  from  pres- 
sure on  the  left  recurrent  laryngeal  nerve ;  pupillary  changes  from 
pressure  on  the  upper  dorsal  or  lower  cervical  ganglia;  and  rapid 
loss  of  flesh  due  to  compression  of  the  thoracic  duct.  A  tumour,  if 
present,  appears  in  the  middle  line  or  to  the  right  of  the  sternum, 
the  manubrium  having  been  eroded ;  rarely  to  the  left  of  the  sternum. 
The  innominate  or  left  carotid  and  subclavian  arteries  may  be  in- 
volved, with  corresponding  delay  and  alteration  in  the  radial  or 
carotid  pulses.  Gldema  of  the  left  side  of  the  head  and  neck  indi- 
cates pressure  on  the  left  innominate  vein. 

In  the  descending  portion  of  the  arch  the  aneurism  exerts  pressure 
against  the  vertebrae  (3d  to  6th  dorsal)  with  resulting  erosion  and 
destruction.  The  pain  caused  by  this  process  is  extreme  ;  and  finally 
a  large  swelling  may  appear  posteriorly  in  the  scapular  region. 
Paraplegia  may  result  from  compression  of  the  cord  after  the  verte- 
bral canal  has  been  opened.  Dysphagia  from  pressure  on  the  esopha- 
gus is  common ;  and  from  pressure  on  the  left  bronchus,  bronchiec- 
tasis, abscess,  or  gangrene  may  ensue.  In  aneurism  of  the  descending 
thoracic  aorta  a  tumour  may  appear  posteriorly  over  or  to  the  left  of 
the  lower  dorsal  vertebrae. 

Differential  Diagnosis.— The  following  conditions  may  require  to 
be  discriminated  from  thoracic  aneurism  : 

(1)  Mediastinal  Tumour.— li  may  be  quite  impossible  to  make 
this  distinction,  for  if  the  tumour  is  deep-seated  the  pressure  symp- 
toms are  practically  identical  with  those  of  an  aneurism  in  the  same 
locality.  But  if  it  be  a  growth  there  is  absence  of  the  tracheal  tug- 
ging, the  accentuated  aortic  second  sound,  and  the  differences  in  the 
radial  pulse  so  often  associated  with  aneurism.  A  tumour  may  also' 
appear  externally  and  perhaps  pulsate,  but  the  expansile  character  of 
the  pulsation  is  absent ;  so  also  is  the  strong  palpable  systolic,  and 
especially  the  diastolic,  impulse  or  shock  of  the  heart  sounds.  More- 
over, in  tumour  pain  is  more  common,  the  cervical  or  axillary  lymph 
glands  may  be  enlarged  and  hard,  and  cachexia  may  be  manifest, 
whereas  the  aneurismal  patient  is  often  strong  and  robust. 

(2)  Pulsating  Empijema  Necessitatis.— The  history  of  a  pleurisy, 
the  absence  of  the  diastolic  shock  and  firm  expansile  pulsation,  the 


906  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

presence  of  the  tumour  farther  to  the  left  than  is  customary  in 
aneurism,  the  usual  flatness  at  the  base  posteriorly,  the  absence  of 
pressure  symptoms  or  alterations  in  the  pulse,  and,  finally,  the  find- 
ing of  pus  by  puncture  with  a  hypodermic  needle,  will  speak  against 
aneurism. 

(3)  Aortic  Insufficiency. — In  this  there  may  be  strong  visible  and 
palpable  pulsation  of  the  aorta,  with  or  without  slight  dilatation  (not 
sufficient  to  be  considered  a  fusiform  or  cylindrical  aneurism)  of  the 
vessel,  possibly  also  an  increase  of  dulness  over  its  course.  The  dif- 
ferentiation may  be  very  difficult,  especially  as  aneurism  of  the  arch 
may  coexist  with  aortic  insufficiency.  A  positive  diagnosis  of  aneu- 
rism should  not  be  made  under  these  circumstances  unless  a  distinct 
tumour  with  expansile  pulsation  is  present,  or  well-marked  pressure 
symptoms  are  manifest. 

(4)  Neurotic  {Dynamic)  Pulsation  of  the  Aorta. — A  case  of  this 
kind  came  under  observation,  in  which  at  first  there  was  much  un- 
certainty as  to  the  presence  of  an  aneurism  in  spite  of  the  fact  that 
the  patient  was  a  woman,  had  no  arterial  sclerosis,  and  was  not  of 
the  alcoholic  or  labouring  class.  There  was  forcible  throbbing  and 
actual  swelling  in  the  episternal  notch  and  behind  the  right  sterno- 
mastoid  muscle  ;  the  heart  sounds,  especially  the  aortic  closure,  were 
abnormally  distinct  and  accentuated,  and  there  was  a  systolic  bruit ; 
but,  on  the  other  hand,  there  was  increased  objective  and  subjective 
pulsation  of  many  peripheral  arteries,  retinal  pulsation,  throbbing  in 
the  head,  paroxysms  of  tachycardia  (200  and  over),  and  many  neu- 
rotic manifestations.  At  the  present  time  the  throbbing  has  prac- 
tically disappeared,  coincidently  with  improvement  in  the  ataxic 
condition  of  the  vasomotor  nerves — an  improvement  to  which  the 
administration  of  suprarenal  extract  has  been  distinctly  contribu- 
tory. 

(5)  Other  Conditions. — Displacement  of  the  heart  and  aorta  by 
tuberculous  or  other  retraction  of  the  right  lung,  or  by  lateral 
curvature  of  the  spine,  may  cause  a  strong  pulsation  to  the  right  of 
the  sternum.  If  an  aneurism  compresses  a  bronchus,  causing  bron- 
chiectasis or  abscess,  with  cough  and  fever,  it  may  be  mistaken  for 
tuberculosis,  but  the  absence  of  bacilli  and  the  presence  of  other 
signs  and  symptoms  of  aneurism  will  usually  prevent  this  error. 

Terminations  and  Prognosis. — The  aneurism  may  perforate  ex- 
ternally and  terminate  fatally  by  repeated  small,  or  sudden  and  large, 
hemorrhages,  or  rupture  into  the  pleura,  pericardium,  superior  cava, 
trachea,  bronchi,  lung,  or  esophagus,  or  death  take  place  by  asthenia. 
The  prognosis  is  always  bad,  although  life  may  be  prolonged,  under 
constant  threat  of  sudden  death,  for  a  number  of  years. 


DISEASES  OF  THE  ARTERIES  907 

IV.  Aneurism  of  the  Abdominal  Aorta. — May  be  fusiform 
or  sacculated,  rarely  multiple,  aud  is  seated  most  commonly  imme- 
diately below  the  diaphragm  in  the  vicinity  of  the  coeliac  axis. 

Symptoms. — The  principal  subjective  symptom  is  pain.  If  the 
tumour  grows  backward,  causing  erosion  of  the  vertebrae,  there  may 
be  a  dull  boring  pain  in  the  back,  usually  with  darting  neuralgic 
pain  in  the  abdomen  and  lateral  and  posterior  lumbar  regions. 
From  pressure  on  the  cord  there  may  be  numbness  and  tingling  of 
the  lower  extremities,  followed  by  paraplegia.  If  the  tumour,  as  is 
more  commonly  the  case,  grows  forward,  there  may  be  gastralgic 
paroxysms,  colicky  pains,  vomiting,  or  diarrhoea,  usually  due  to  pres- 
sure, infrequently  to  embolism  of  the  superior  mesenteric  artery. 
Jaundice  has  been  noted. 

Physical  Signs. — Usually  there  is  marked  epigastric  pulsation, 
sometimes  with  a  palpable  thrill.  There  may  be  a  distinct,  fixed 
(exceptionally  freely  movable)  tumour  with  a  firm,  expansile  pulsa- 
tion ;  occasionally,  when  the  tumour  is  in  contact  with  the  dia- 
phragm and  receives  the  direct  thrust  of  the  heart,  the  pulsation  is 
double.  If  the  aneurism  is  of  suflicient  size  there  may  be  an  area  of 
dulness  which  is  continuous  with  that  of  the  left  lobe  of  the  liver. 
Although  the  tumour  presents  most  commonly  in  the  epigastric 
region,  it  may  be  found,  depending  on  the  direction  in  which  it 
increases,  in  the  left  hypochondrium  or  lateral  and  posterior  lumbar 
regions.  A  large  aneurism,  if  seated  just  beneath  the  diaphragm, 
may  not  be  palpable.  A  systolic  bruit  is  usually  heard  over  the 
swelling,  but  its  point  of  maximum  audibility  may  be  over  the  back. 
A  soft  diastolic  murmur  has  been  noted.  The  pulse  in  the  femoral 
arteries  is  usually  small  and  delayed. 

Diagnosis. — It  is  to  be  remembered  that  visible  and  palpable 
pulsation,  often  violent,  is  very  common,  while  aneurism  of  the 
abdominal  aorta  is  a  quite  infrequent  condition.  A  diagnosis  of 
aneurism  is  not  to  be  made  unless  a  distinct  tumour  is  found  which 
can  be  seized  by  the  hand  and  presents  a  strong  expansile  pulsation. 
Xeurotic  or  dynamic  throbbing  of  the  aorta  occurs  in  anaemic  and 
neurasthenic  states,  particularly  in  women,  and  may  be  so  strong  as 
to  suggest  almost  irresistibly  the  presence  of  an  aneurism.  But  the 
latter  should  be  the  very  last  cause  assigned  as  an  explanation  of 
abnormal  epigastric  pulsation.  An  enlargement  or  tumour  of  the 
left  lobe  of  the  liver,  or  a  tumour  of  the  pylorus  or  pancreas,  may  simu- 
late aneurism,  but  the  pulsation  is  not  heaving  and  expansile,  and 
with  the  assumption  of  the  knee-elbow  posture  the  tumour  falls  for- 
ward and  the  transmitted  pulsation  usually  disappears. 

Terminatiojis  and  Prognosis.— Exceipt  in  rare  instances  of  spon- 


908  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

taneous  cure  the  prognosis  is  grave,  death  resulting  in  most  cases 
from  rupture  into  the  pleura,  peritoneum,  or  retroperitoneal  tissues 
and  intestines,  especially  the  duodenum,  compression  of  the  spinal 
cord,  closure  of  the  vessel  by  deposits  of  fibrin,  or  intestinal  infarc- 
tion from  embolism  of  the  superior  mesenteric  artery  (Osler). 

V.  Aneurism  of  the  Splenic  Artery. — A  diagnosis  is  rarely 
possible.  The  symptoms  resemble  those  of  gastric  uber,  viz.,  epi- 
gastric pain,  vomiting,  and  haematemesis.  There  may  be  a  tumour  in 
the  left  hypochondrium,  or  apparent  increase  of  splenic  dulness. 
The  tumour  may  pulsate  and  present  a  systolic  bruit. 

VI.  Arterio- venous  Aneurism. — An  aneurism  of  the  ascend- 
ing portion  of  the  aortic  arch  may  open  into  the  superior  vena  cava. 
The  physical  signs,  in  addition  to  those  of  the  aneurism  proper,  are 
the  abrupt  development  of  venous  distention,  oedema,  and  cyanosis 
of  the  head,  neck,  arms,  and  upper  thorax.  There  may  be  a  thrill, 
and  a  humming  or  buzzing  murmur,  continuous,  but  intensified  dur- 
ing the  systole  of  the  heart. 


SECTION   V 

DISEASES   OF   THE   BLOOD   AXD   DUCTLESS   GLAXDS 

Prepaked  by  Henry  P.  De  Forest,  M.  D. 

I.  ANvCMIA 

A  DISEASE  of  the  blood  characterized  by  a  reduction  of  the- 
amount  of  the  blood  as  a  whole,  or  of  the  cells,  or  of  the  haemo- 
globin or  albumin.  Two  forms  are  recognised :  secondary  and  pri- 
mary. 

I.  Secondary  Aneemia. — Causes. — Any  condition  or  disease 
which  abstracts  the  blood  from  the  body  or  deprives  it  of  any  one  of 
its  essential  ingredients  may  cause  a  secondary  anaemia,  such  as  acute 
and  severe  or  gradual  and  long-continued  hemorrhages  (gastric  or 
intestinal  ulcers,  bleeders) ;  or  the  drain  upon  the  albuminous  ingre- 
dients of  the  blood  due  to  nephritis,  prolonged  lactation,  tubercu- 
losis, suppuration,  or  malignant  neoplasms ;  or  inanition  from  any 
cause ;  or  the  action  of  poisons,  either  inorganic,  such  as  mercury 
lead,  antimony,  arsenic,  or  the  organic  poisons  of  malaria  or  syphilis. 
High  temperature  (fever,  sunstroke)  interferes  with  the  action  of  the 
haematopoietic  organs.  Blood  Examination. — In  hemorrhages  the 
red  cells  are  diminished  in  number  and  size  and  there  is  a  moderate 


DISEASES  OF   BLOOD  AND   DUCTLESS  GLANDS  909 

poikilocytosis.  Normoblasts  appear,  and  there  is  a  moderate  leuco- 
cytosis.  The  haemoglobin  is  diminished  in  greater  proportion  than 
the  red  cells.  In  disorders  causing  a  continued  drain,  like  nephritis 
or  tuberculosis,  the  blood  coagulates  slowly,  there  is  a  marked  poiki- 
locytosis, a  few  normoblasts,  and  a  moderate  or  extreme  leucocytosis. 

II.  Primary  Anaemia. —Disease  of  the  blood  itself.  Two 
varieties  are  recognised  :  chloro-ancemia  and  jjernicious  ancemia. 

(I)  Chlorosis, — This  is  essentially  a  disease  of  young  girls  between 
the  ages  of  14  and  17,  when  secondary  sexual  changes  are  taking 
place.     Kecurrences  may  take  place  later  in  life. 

Symptoms. — As  a  rule  these  develop  slowly.  Menstrual  disturb- 
ances, delayed  menstruation  or  amenorrhoea,  may  first  attract  atten- 
tion. Languor,  malaise,  anorexia,  and  palpitation  are  common  symp- 
toms. Systolic  haemic  murmurs  at  both  apex  and  base,  and  venous 
murmurs,  are  common ;  diastolic  murmurs  are  rare.  The  pulse  is 
usually  soft  and  full,  but  as  a  result  of  the  altered  condition  of  the 
blood  and  the  enfeebled  circulation,  thrombosis  and  embolism  are  not 
infrequent  complications.  Fever  of  a  mild  type,  cold  hands  and 
feet,  fainting,  neuralgia,  and  shortness  of  breath,  perhaps  severe  dysp- 
noea after  slight  exertion,  are  common  symptoms.  The  appetite 
is  variable.  Acids  seem  to  be  especially  desired,  though  hyperacidity 
of  the  gastric  juice  is  the  rule.  Digestion  is  slow.  So  frequent, 
obstinate,  and  habitual  is  the  constipation  that  by  some  it  is  re- 
garded as  the  real  cause  of  the  disease.  The  skin  is  often  puffy  and 
edematous,  and  the  oedema  of  the  face  and  ankles  may  suggest 
Bright's  disease.  A  yellowish-green  tinge,  oftentimes  pathognomonic, 
is  added  to  the  general  pallor  of  the  skin.  The  eyes  are  bright,  the 
sclerotics  bluish. 

Hmmal  Symptoms.— The  blood  flows  slowly  and  with  difficulty, 
clots  quickly,  and  is  distinctly  paler  than  normal  blood.  The  essen- 
tial change  is  in  the  amount  of  haemoglobin,  which  is  diminished  far 
more  in  proportion  than  are  the  erythrocytes.  Twenty  to  thirty  per 
cent  of  the  normal  amount  of  haemoglobin  is  by  no  means  unusual, 
while  the  red  cells  may  remain  at  80  or  90  per  cent  of  the  normal. 
Aside  from  their  pallor,  the  erythrocytes  may  show  no  changes,  but 
in  severe  cases  poikilocytosis  is  marked,  normoblasts  appear,  and  a 
slight  leucocytosis  is  the  rule. 

Diagnosis.— The  peculiar  colour  of  the  skin,  the  history  of  a  radi- 
cal change  of  climate,  poor  food,  bad  ventilation,  nervous  and  emo- 
tional disturbances,  and  persistent  constipation,  combined  with  the 
hsemanalysis,  render  the  diagnosis,  as  a  rule,  easy.  Chlorosis  is  to  be 
discriminated  from  chronic  nephritis  by  urinalysis,  although  the  two 
conditions  may  coexist,  and  pulmo7iary  triberculosis,  which  produces 


910  DIAGNOSIS,   DIRECT  AND   DTFFEREXTIAL 

pallor  of  the  skin  and  bluish  sclerotics  very  apt  to  be  mistaken  for 
chlorosis.  Careful  physical  examination  and  the  sputum  analysis 
will  establish  the  true  diagnosis. 

(II)  Progressive  Pernicious  AnsBinia.— Persons  of  middle  age  are 
usually  affected,  males  more  frequently  than  females. 

Symptoms. — It  is  difficult  to  improve  upon  Addison's  description  : 
"  It  makes  its  approach  in  so  slow  and  insidious  a  manner  that  the 
patient  can  hardly  fix  a  date  to  the  earliest  feeling  of  that  languor 
which  is  shortly  to  become  so  extreme.  The  countenance  gets  pale, 
the  whites  of  the  eyes  become  pearly,  the  general  frame  flabby  rather 
than  wasted,  the  pulse  perhaps  large,  but  remarkably  soft  and 
compressible,  and  occasionally  with  a  slight  jerk,  especially  under 
the  slightest  excitement.  There  is  an  increasing  indisposition  to 
exertion,  with  an  uncomfortable  feeling  of  faintness  or  of  breath- 
lessness  on  attempting  it ;  the  heart  is  readily  made  to  palpitate ; 
the  whole  surface  of  the  body  presents  a  blanched,  smooth,  and  waxy 
appearance ;  the  lips,  gums,  and  tongue  seem  bloodless,  the  flabbi- 
ness  of  the  solids  increases,  the  appetite  fails,  extreme  languor  and 
faintness  supervene,  breathlessness  and  palpitation  are  produced 
by  the  most  trifling  exertion  or  emotion  ;  some  slight  oedema  is  prob- 
ably perceived  about  the  ankles  ;  the  debility  becomes  extreme — the 
patient  can  no  longer  rise  from  the  bed ;  his  mind  occasionally  wan- 
ders ;  he  falls  into  a  prostrate  and  half-torpid  state,  and  at  length 
expires;  nevertheless,  to  the  very  last,  and  after  a  sickness  of  several 
months'  duration,  the  bulkiness  of  the  general  frame  and  the  amount 
of  obesity  often  present  a  most  striking  contrast  to  the  failure  and 
exhaustion  observable  in  every  other  respect." 

Palpitation  (common),  haemic  murmurs  (constant),  visible  arte- 
rial pulsation,  full  water-hammer  pulse,  a  capillary  and,  not  infre- 
quently, a  venous  pulse  are  the  principal  circulatory  symptoms. 
Hemorrhages,  petechial  or  ecchymotic,  in  the  skin,  mucous  mem- 
branes, and  retina  are  not  infrequent.  Anorexia,  dyspepsia,  nausea, 
vomiting,  diarrhcea,  becoming  progressively  worse,  are  nearly  always 
present.  The  specific  gravity  of  the  urine  is  low  and  the  colour 
pale.  Xot  infrequently  the  excess  of  iron  and  the  resulting  colour- 
ing matter  in  the  liver  and  other  parts  of  the  body  produce  an  excess 
of  urobilin  and  make  the  urine  a  dark  sherry  red.  The  body  is 
rarely  emaciated.  The  complexion  is  pale,  smooth,  waxy,  and  of 
a  marked  lemon-yellow  colour. 

Haemal  Symptoms. — The  red  corpuscles  are  notably  diminished ; 
even  to  150,000  per  cubic  millimetre.  The  haBmoglobin  is  relatively 
increased — a  condition  exactly  opposite  to  that  found  in  chlorosis 
and  in  some  of  the  secondary  anaemias.     A  constant  symptom  is  a 


DISEASES  OF  BLOOD  AND  DUCTLESS  GLANDS  911 

wide  variation  in  the  size  and  character  of  the  erythrocytes ;  micro- 
cytes,  megalocytes,  normoblasts,  and  gigantoblasts  are  all  found  in 
varying  numbers;  poikilocytosis  is  the  rule.  The  leucocytes  are 
unchanged  or  occasionally  diminished ;  in  grave  cases  the  mononu- 
clear forms  increase,  and  the  polynuclear  forms  decrease. 

Diagnosis. — The  rapid  course  of  the  disease,  its  apparent  gravity, 
the  characteristic  colour  of  the  skin,  and  the  results  of  haemanalysis 
are  the  cardinal  symptoms.  In  the  blood  itself  the  relative  increase 
of  hsemoglobin,  and  the  presence  of  the  larger  forms  of  cells  (megalo- 
cytes and  gigantoblasts)  are  of  especial  importance. 

Differential  Diagnosis. — Chlorosis. — In  the  "green  sickness"  the 
appearance  of  the  patient  is  widely  different,  and  the  results  of 
the  heemanalysis  make  confusion  difficult,  if  not  impossible. 

Secondary  Anmmias. — Each  of  the  secondary  anaemias  has  a  defi- 
nite cause  and  associated  symptoms.  Pregnancy,  parturition,  atro- 
phy of  the  stomach,  parasites  (bothriocephalus,  anchylostoma),  and 
the  malarial,  typhoidal,  and  cancerous  cachexias  produce  conditions 
that  closely  simulate  idiopathic  pernicious  anaemia,  but  the  micro- 
scope will  usually  reveal  the  difference. 

Prognosis. — The  majority  of  patients  die,  but  with  recent  meth- 
ods of  treatment  (arsenic)  recoveries  have  become  more  common. 
The  predominance  of  normoblasts  (indicating  regenerative  changes) 
is  a  favourable  sign ;  an  excess  of  gigantoblasts  or  of  mononuclear 
leucocytes  indicates  a  graver  prognosis. 

II.    LEUCiCMIA 

The  majority  of  all  cases  occur  in  early  adult  life  (20  to  40  years) ; 
60  per  cent  are  males.  Two  types  occur  :  sple no-medullary  or  myeloge- 
nous, and  lymphatic  leucaemia  {lymphwmia).  Usually  well  marked, 
but  transitional  or  combination  forms  are  occasionally  observed. 

I.  Spleno-medullary  Form.— By  far  the  most  common. 

Symptoms.— The  spleen  gradually  enlarges,  ultimately  it  may 
become  enormous,  occupying  fully  one  half  of  the  abdominal  cavity. 
It  may  be  immobile  from  adhesions,  or  freely  movable  within  the 
peritoneal  cavity.  Usually  the  free  and  notched  border  is  plainly  felt 
or  even  seen  below  the  free  border  of  the  costal  cartilages.  A  sense 
of  weight,  dragging,  and  oppression  in  the  left  side  are  often  the  first 
symptoms  for  which  relief  is  sought.  Rupture  has  occurred  from 
the  intense  hypersemia.  At  times  a  splenic  bruit  can  be  heard ;  in 
other  cases  the  vessels  entering  the  hilus  are  so  enlarged  that  a 
marked  thrill  may  be  felt  over  the  organ.  Owing  to  the  pressure  of 
the  enlarged  spleen  the  apex  beat  may  be  displaced  upward  and  to 
the  left.     Other  cardiac  symptoms  are  rare.    The  pulse  is  usually 


912  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

rapid,  soft,  compressible,  but  of  good  volume.  As  a  result  of  the 
feeble  circulation,  oedema  of  the  feet,  general  anasarca,  or  abdom- 
inal ascites  may  develop.  Epistaxis  is  common ;  haemoptysis  rare  ; 
haematemesis  (not  common)  may  be  the  first  symptom,  and  the  loss 
of  blood  so  great  as  to  cause  death.  Bleeding  gums,  extensive  pur- 
pura of  skin  and  mucous  membranes,  leucsemic  retinitis,  and  intra- 
cranial hemorrhages  have  been  recorded. 

Gastro-intestinal  symptoms  often  develop  early  in  the  disease. 
Besides  haematemesis,  intestinal  hemorrhages  may  occur,  or  a  dysen- 
teric process  develop  in  the  colon.  Xausea  and  vomiting  are  early^ 
frequent,  and  persistent  symptoms.  Jaundice  occasionally  occurs, 
and  diarrhoea  (even  fatal)  is  not  infrequent.  Toward  the  end  of  the 
disease  pulmonary  oedema  or  pneumonia  may  develop  and  be  the  im- 
mediate cause  of  death.  The  movements  of  respiration  may  be 
restricted  because  of  the  mechanical  pressure  of  the  hypertrophied 
spleen.  Dyspnoea,  an  early  and  characteristic  symptom,  is  due  to  the 
anaemia ;  so  also  are  the  headache,  dizziness,  or  fainting  spells  fre- 
quently observed.  As  a  rule  the  organs  of  special  sense  suffer  more 
severely  than  does  the  general  nervous  system.  With  the  occur- 
rence of  intracranial  extravasation  of  blood  various  sensory  or  motor 
disturbances  arise  according  to  the  location  of  the  exudate  ;  coma 
(rare),  deafness  (common),  and  optic  neuritis  (rare)  are  the  chief 
symptoms  recorded.  Priapism  is  not  infrequent.  There  is  no  con- 
stant urinary  symptom.  Haematuria  (occasional)  and  an  excess  of 
uric  acid,  nearly  always  present,  seem  to  bear  a  direct  relation  to  the 
size  of  the  spleen  and  to  the  excess  of  leucocytes. 

An  extraordinary  hyperplasia  of  the  red  bone  marrow  occurs  in 
this  form  of  the  disease,  and  as  a  result  the  internal  tension  in  cer- 
tain of  the  long  and  flat  bones  (sternum,  ribs)  may  become  so  great 
that  nodular  tumours  develop  along  the  course  of  the  bone.  These 
swellings  may  be  sensitive  to  the  touch  or  even  become  the  seat  of 
more  or  less  inflammation.  The  change  in  the  bone  marrow  is  char- 
acteristic of  this  type  of  the  disease,  for  from  this  source  arise  the 
abnormal  forms  of  leucocytes  (myelocytes)  which  are  diagnostic  of 
leucaemic  blood.  By  many,  indeed,  the  disease  is  called  "  myeloge- 
nous leucaemia,"  and  it  is  held  by  some  that  the  role  played  by  the 
spleen  is  purely  passive, 

Hmmal  Symptoms. — Although  anaemia  is  not  a  necessary  symp- 
tom, it  sooner  or  later  appears,  and  the  changes  which  can  then  be 
observed  in  an  accurate  haemanalysis  constitute  the  most  character- 
istic evidence  of  the  disease.  The  leucocytes  are  enormously  in- 
creased, in  some  instances  even  exceeding  the  erythrocytes  in  num- 
ber, those  which  are  derived  from  the  red  bone  marrow  (myelocytes) 


DISEASES  OP  BLOOD  AND  DUCTLESS  GLANDS  913 

characteristically  and  greatly  predominating.  The  other  forms  of 
leucocytes  are  often  in  normal  proportion,  or  even  relatively  dimin- 
ished. In  general  the  number  of  red  corpuscles  is  markedly  dimin- 
ished, but  rarely  becomes  less  than  2,000,000  per  cubic  millimetre. 
Normoblasts  and  true  gigantoblasts  are  present  in  considerable  num- 
bers. The  amount  of  haemoglobin  is  relatively  reduced  still  further 
than  are  the  erythrocytes.  The  alkalinity  of  the  blood  is  diminished 
and  the  fibrin  increased ;  as  a  result  the  fibrin  network  on  a  blood 
slide  is  unusually  thick  and  dense.  Owing  to  the  enormous  increase 
in  the  leucocytes,  the  blood  clots  more  quickly  than  usual  and  the 
coagulum  has  a  pale  or  even  puslike  colour. 

II.  Lympliatic  Form. — Lymphatic  leucaemia  (lymphaemia)  is 
rare ;  it  is  more  rapid  and  fatal  than  the  form  just  described ;  it 
occurs  in  younger  subjects,  and  occasionally  develops  acutely  and 
terminates  fatally  in  from  2  to  3  months. 

Symptoms. — In  this  form  of  the  disease  there  is  a  general  lym- 
phatic enlargement.  All  of  the  superficial  groups  may  be  involved, 
but  never  to  the  extent  that  occurs  in  pseudo-leucaemia,  nor  do  the 
glands  become  matted  together ;  they  are,  as  a  rule,  soft,  isolated, 
movable,  and  may  vary  considerably  in  size  during  the  course  of  the 
disease.  The  tonsils  and  the  lymph  follicles  of  the  pharynx,  tongue, 
and  mouth  may  be  enlarged.  Lymphoid  growths  may  occur  in  the 
liver,  spleen,  omentum,  thymus  gland,  and  skin.  The  bone  marrow 
is  often  replaced  by  lymphoid  tissue. 

Hcemal  Sijmptoms.—ln  this  type  of'the  disease  the  lymph  glands, 
not  the  bone  marrow,  are  the  seat  of  hyperplastic  proliferation.  As 
a  result  the  blood  usually  shows  a  complete  absence  of  myelocytes 
but  an  enormous  increase  of  lymphocytes  (as  high  as  98  per  cent). 
Eosinophiles  and  normoblasts  are  rare. 

III.  Diagnosis  and  Prognosis  of  Leucaemia.— Haemanaly- 
sis,  the  only  means  of  making  a  diagnosis  of  leucaemia,  discovers  the 
enormous  increase  of  leucocytes ;  with  preponderance  of  myelocytes 
in  the  spleno-medullary  form ;  of  lymphocytes  in  the  lymphatic 
form.  As  the  clinical  features  of  leucaemia,  pseudo-leucaemia,  and 
splenic  anemia  may  be  identical,  hamanalysis  alone  will  differentiate 
them.  Most  cases  prove  fatal  in  from  1  to  3  years.  In  acute  leu- 
caemia death  may  occur  in  2  months  from  the  onset. 

III.    PSEUDO-LEUCiCMIA 
About  one  third  of  all  cases  of  Hodgkin's  disease  occur  in  per- 
sons under  30  years  of  age;  one  third  between  30  and  40;  three 
fourths  in  males^.     It  mav  prove  to  be  of  infectious  origin. 
Symptoms.— Enlargement  of  the  cervical   glands   is   usually   the 


914  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

first  symptom  noticed,  Xext  in  order  of  frequency  the  axillary, 
inguinal,  and,  ultimately,  all  the  lymphatic  glands  of  the  body,  both 
deep  and  superficial,  progressively  enlarge.  In  women  the  chain  of 
glands  in  direct  communication  with  the  breasts  may  first  attract 
attention.  Primarily  the  glands  are  isolated  and  easily  movable ; 
later  they  fuse  together  in  large  masses,  and,  by  thickening  and  ad- 
herence of  the  adjacent  connective  tissue,  may  become  firmly  fixed. 
The  cervical  glands  may  become  enormous,  obliterating  the  neck 
and  giving  the  head  a  pyramidal  appearance.  The  resulting  pres- 
sure upon  the  trachea  often  causes  extreme  dyspncBa.  In  the  axilla 
or  groin  the  masses  are  large,  even  pedunculated,  and  by  pressure 
upon  vessels  or  nerves  may  cause  pain  and  oedema  of  the  extremities. 
The  thoracic  and  mediastinal  glands  may  give  rise  to  marked  pres- 
sure symptoms,  i.  e.,  paroxysmal  dyspnoea,  paralysis  of  one  or  both 
vocal  cords  with  loss  of  speech,  pulmonary  congestion  or  oedema,  and 
necrosis  of  the  sternum.  The  large  intrathoracic  vessels  may  be  sa 
compressed  that  a  collateral  circulation  is  established  through  the 
mammary  and  epigastric  veins.  Of  the  abdominal  glands  the  retro- 
peritoneal are  most  commonly  involved,  and  various  visceral  displace- 
ments often  result.  The  ureters,  the  iliac  vessels,  the  sacral  and 
lumbar  nerves  may  suffer,  and  the  uterus  may  be  so  pressed  forward 
and  surrounded  by  the  large  lobular  masses  as  to  closely  simulate  a 
uterine  fibro-myoma.  Even  the  mesenteric  or  hepatic  glands  may 
give  rise  to  a  variety  of  pressure  symptoms,  dependent  upon  the  site 
of  the  abdominal  tumour.  In  any  of  these  glands  suppuration  and 
necrosis  due  to  pressure,  while  not  common,  may  develop  late  in  the 
disease. 

The  spleen  is  hypertrophied  in  three  fourths  of  all  cases,  and  usu- 
ally contains  marked  lymphoid  growths.  The  patient  may  complain 
of  a  sense  of  weight  and  dragging  in  the  side  of  his  abdomen,  or  may 
accidentally  feel  the  tumour  mass.  Palpation  usually  discloses  the 
splenic  tumour,  reaching,  in  many  cases,  to  or  below  the  navel. 

In  the  early  stages  the  blood  remains  normal,  but  as  the  disease 
progresses  the  haemoglobin  diminishes.  Xext  follows  a  diminution 
in  the  number  of  erythrocytes,  and  ultimately  the  severest  grades  of 
anaemia  may  be  reached.  The  qualitative  changes  found  in  severe 
secondary  anaemia  may  be  present.  It  occasionally  happens  that 
masses  of  the  enlarged  glands  suppurate,  or  pneumonia  develops,  or 
some  similar  cause  gives  rise  to  a  well-marked  leucocytosis.  If  this 
occurs  the  eosinophiles  are  usually  decreased,  and,  if  the  cachexia  be 
marked,  small  numbers  of  myelocytes  may  be  found.  Leucocytosis 
is,  however,  to  be  regarded  as  an  accidental  concomitant. 

The  tonsils  usually  enlarge  late  in  the  disease,  and  lymphoid 


DISEASES  OF  BLOOD  AND  DUCTLESS  GLANDS  915 

growths  or  polypi,  developing  in  the  pharynx  or  larynx,  give  rise  to 
symptoms  of  nasal  or  laryngeal  obstruction.  Deafness  due  to  closure 
of  the  Eustachian  tubes  is  not  infrequent.  Xosebleed  is  common, 
and  ulceration  of  the  mucous  membrane  of  the  air  passages  not  un- 
common. Dyspnoea,  palpitation,  or  haemic  murmurs  are  present  as 
the  anaemia  increases.  The  glandular  masses  may  displace  the  heart. 
Digestive  symptoms  are  not  marked.  Dysphagia  may  be  present 
from  pressure  upon  the  gullet  or  ulceration  of  the  mucous  mem- 
brane. Pressure  or  irritation  of  the  sympathetic  may  cause  irregu- 
larity of  the  pupils,  or  bronzing  or  pigmentation  of  the  skin  ;  the 
latter  may  be  caused  also  by  interference  with  the  capillary  circula- 
tion.    Intense  itching  sometimes  occurs. 

Fever  is  usually  more  or  less  marked,  even  from  the  onset  of  the 
disease.  It  may  be  of  a  hectic  type,  or  simulate  the  paroxysms  of 
malaria.  Apyrexia,  for  periods  of  a  week  or  so,  alternating  with  fever, 
has  occasionally  been  noted. 

Diagnosis. — Progressive  enlargement  of  the  lymphatic  glands 
and  of  the  spleen,  together  with  a  nearly  normal  state  of  the  blood, 
constitute  the  distinctive  complex  of  pseudo-leucaemia.  It  may  re- 
quire discrimination  from  the  following  conditions  : 

(1)  Tuberculous  adenitis^  especially  of  the  cervical  group  of 
glands,  is  at  first  extremely  difficult  to  differentiate.  The  tubercu- 
lous process  is  more  common  in  the  young,  and  involves  the  sub- 
maxillary group  more  frequently  than  the  glands  lying  in  the  ante- 
rior and  posterior  cervical  triangles,  which  are  usually  first  to  be 
involved  in  Hodgkin's  disease.  Tuberculous  glands,  moreover,  even 
when  very  small,  tend  to  become  fused  into  a  firm  mass  and  suppura- 
tion develops  early.  In  tuberculosis  of  the  cervical  glands  one  side 
only  may  be  affected;  in  pseudo-leucaemia  both  sides  are  usually 
involved.  Removal  of  the  glands  and  inoculation  experiments  may 
be  necessary  at  times  to  make  a  positive  diagnosis. 

(2)  SypJnHHc  adenitis  may  present  the  same  gross  appearance, 
but  the  history  and  the  ready  response  to  treatment  will  serve  for 
differentiation. 

(3)  Leuccemia,  especially  of  the  myelogenous  type,  is,  as  a  rule, 
readily  distinguished  from  pseudo-leucaemia  by  haemanalysis,  though 
the  gross  anatomical  changes  may  be  indistinguishable.  Rare  cases 
have  been  observed  in  which  pseudo-leucaemia  has  ultimately  merged 
into  leucaemia  by  transitional  changes. 

(4)  Splenic  anwmia  may  be  at  times  confused  with  Hodgkin's  dis- 
ease, but  careful  examination  of  the  blood  will  enable   a   correct 

diagnosis. 

Prognosis.— The  duration  of  the  disease  varies  from  a  few  months 


916  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

to  several  years,  but  practically  all  cases  die.     The  usual  causes  of 
death,  in  the  order  of  frequency,  are  asthenia,  pressure,  and  coma. 

IV.    PURPURA 

Symptoms. — The  essential  feature  of  this  condition  is  the  appear- 
ance upon  the  skin  or  mucous  membranes  of  minute  punctate  ex- 
travasations of  blood  beneath  the  skin  (petechige),  or  larger  and  more 
diffuse  extravasations  (ecchymoses).  All  these  are  at  first  bright 
red,  but  as  absorption  takes  place  the  colour  gradually  becomes 
darker  and  purple,  finally  fading  to  a  brownish  discoloration.  With 
these  various  forms  of  blood  Extravasation  there  may  or  may  not  be 
associated  other  conditions  affecting  the  joints,  nerves,  or  general 
functions  of  the  body.  The  Hood  is  changed  in  its  fibrin-forming 
elements  and  coagulation  is  retarded  for  10  or  15  minutes. 

Vaeieties. — Purpura,  whatever  form  it  may  take,  is  of  itself  a 
symptom,  and  as  such  is  indicative  of  a  large  number  of  varied  con- 
ditions. The  pathological  classification  of  purpura  is  as  yet  indeter- 
minate, but  the  following  divisions  are  practically  convenient : 

I.  Purpuric  Diseases  of  the  Newborn. — (I)  SypldUs  Hcem- 
orrhagica  Neonatorum. — This  may  not  be  manifest  at  the  time  of 
birth,  but  shortly  thereafter  there  appear  extensive  bloody  extravasa- 
tions in  the  skin  and  mucous  membranes ;  often  a  definite  hemor- 
rhage from  the  navel  takes  place.  Jaundice  is  usually  severe. 
Marked  syphilitic  changes  exist  in  the  liver  and  elsewhere. 

(II)  Hcemoglohinuria  Neonatorum. — This  is  characterized  by 
marked  jaundice  with  accompanying  gastro-intestinal  symptoms, 
■constipation,  fever,  rapid  pulse  and  respiration,  and  sometimes  cyano- 
sis. Punctate  hemorrhages  appear  in  different  parts  of  the  body.  In 
the  urine,  from  similar  hemorrhages  occurring  within  the  substance 
of  the  bladder  and  kidneys,  there  is  albumin  and  methaemoglobin. 
This  disease  is  doubtless  infectious,  as  it  is  often  epidemic  in  hospi- 
tals, but  its  true  nature  has  not  yet  been  determined. 

(III)  Morbus  Maculosus  Neonatorum.. — This  is  a  form  of  hemor- 
rhagic disease  in  which  bleeding  occurs  from  many  of  the  mucous 
surfaces  of  the  body.  The  blood  may  come  from  the  bowels,  the 
stomach,  the  mouth,  or  the  navel,  singly  or  combined,  usually  within 
the  first  week  after  birth.  Marked  jaundice  may  be  associated  with 
this  bleeding ;  fever  is  usually  present. 

II.  Symptomatic  Purpura. — This  may  be  due  to  a  variety 
■of  causes.  Infectious  diseases — i.  e.,  pyaemia,  septicaemia,  typhus  fever, 
measles,  scarlet  fever,  and  especially  certain  forms  of  malignant 
•endocarditis  and  smallpox — are  often  accompanied  by  more  or  less 
well-marked  purpuric  exudations.      Toxic  purpura  may  follow  the 


DISEASES  OP   BLOOD  AND  DUCTLESS  GLANDS  917 

entrance  into  the  blood  of  a  great  number  of  poisons ;  snake  bites, 
mercury,  quinine,  copaiba,  ergot,  and  even  the  various  iodides,  some- 
times give  rise  to  this  condition. 

Cachexia  induced  by  a  number  of  severe  and  wasting  diseases  is, 
in  the  terminal  stages,  marked  by  purpura,  as  in  Hodgkin's  disease, 
chronic  nephritis,  tuberculosis,  scurvy,  or  even  in  general  debility. 
Neuroses  such  as  hysteria  (stigmata),  Raynaud's  disease,  locomotor 
ataxia,  myelitis,  and,  at  times,  severe  neuralgias,  may  show  this 
symptom.  Mechanical  causes  followed  by  venous  stasis  (whooping 
cough,  eclampsia,  epilepsy)  may  give  rise  to  blood  extravasations. 

III.  Arthritic  Purpura. — This  form,  known  also  as  rheumatic 
purpura,  is  an  occasional  accompaniment  of  certain  joint  affections, 
and  may  be  classed  under  three  groups  : 

(I)  Purpura  Simplex. — This  is  most  common  in  children,  and  is 
characterized  by  more  or  less  pain,  petechise  or  ecchymoses  on  the 
legs  (common)  or  trunk  (rare),  fever,  diarrhoea  (occasional),  and  rheu- 
matism affecting  the  joints  (common). 

(II)  Purpura  Rheumatica. — Schmleiii's  disease  is  characterized  by 
multiple  arthritis  and  an  eruption,  either  a  simple  urticaria  or  a  dis- 
tinct purpura,  sometimes  a  combination  of  the  two  (purpura  urti- 
caris).  (Edema  may  be  excessive  and  general,  and  bloody  blebs  may 
form  {pemphigoid  purpura).  The  joint  conditions  are  not,  as  a  rule, 
severe  or  painful.  The  urine  may  be  scanty  and  albuminous.  This 
condition  is  by  many  regarded  as  a  special  affection. 

(III)  Purpura  Erythematosa. — Henoch's  purpura  is  found  chiefly  in 
the  young,  and  is  characterized  by  gastric  pain,  vomiting,  and  diarrhoea, 
more  or  less  severe  joint  involvement,  an  erythematous  form  of  skin 
lesion,  and  marked  hemorrhages  from  the  mucous  membranes.  If  the 
kidneys  are  involved,  blood  and  haemoglobin  may  be  found  in  the 
urine  and  acute  or  chronic  nephritis  result.  The  spleen  may  enlarge. 
Angioneurotic  oedema  may  coexist.  One,  two,  or  more  of  these  symp- 
toms may  be  absent.     All  may  appear  in  a  paroxysmal  form. 

IV.  Hemorrhagic  Purpura.— This  disease  {Morbus  maculo- 
sus  Werlhofii)  is  most  commonly  seen  in  delicate  girls.  General 
weakness,  diffuse  purpura  of  both  skin  and  mucous  membranes  first 
occur.  The  blood  extravasation  becomes  more  and  more  dissemi- 
nated, leading  to  epistaxis,  haematemesis,  hasmaturia,  and  haemoptysis, 
each  more  or  less  severe.  The  resulting  anaemia  may  be  profound, 
leading,  in  the  so-called  purpura  fulminans,  to  death,  within  24  hours. 

Diagnosis. The  severer  forms  of  purpura   must   be   discrim- 
inated from  scur\7  by  the  absence  of  gum  symptoms,  and  the  man- 
ner of  development ;  and  from  hemorrhagic  smallpox,  scarlet  fever, 
or  measles,  by  the  history  and  higher  fever  of  these  infectious  diseases. 
60 


918  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 


V.    H/EMOPHILIA 

Symptoms. — The  cardinal  symptom  of  this  curious  and  rather 
rare  condition  is  a  profuse  and  uncontrollable  bleeding  following  the 
most  trivial  injury.  Often,  indeed,  the  worst  hemorrhage  conies 
from  the  merest  scratch,  and  may  even  occur  spontaneously. 

External  bleedings  may  be  spontaneous,  but  more  commonly  fol- 
low cuts  or  wounds  of  the  skin  or  mucous  membranes.  Bleeding 
from  the  nose  is  most  common ;  next  in  order  of  frequency  from  the 
mouth,  intestines,  stomach,  urethra,  and  lungs.  Xo  part  of  the  body 
is  exempt.  Interstitial  bleedings  occur  in  the  form  of  large  extravasa- 
tions of  blood  (haematomata)  following  slight  bruises,  or  appear 
spontaneously  as  petechial  spots.  The  joints  are  not  infrequently 
involved,  particularly  the  larger  ones,  and  the  lesion  may  closely 
simulate  an  attack  of  acute  articular  rheumatism.  Pain,  fever,  or 
hemorrhage  from  other  parts  of  the  body  may  soon  follow  the  ar- 
thritis. 

The  blood  shows  a  marked  slowness  in  coagulation,  and  the  blood 
plates  may  be  scanty  or  absent.  If  severe  hemorrhage  has  occurred 
the  usual  signs  of  a  traumatic  anaemia  will  be  found. 

Diag?iosis. — The  disease  is  more  common  in  females  than  in 
males  (10  to  1)  and  usually  develops  before  puberty.  In  making  the 
diagnosis  the  family  history  is  of  great  importance,  as  a  marked 
heredity  is  characteristic  of  the  disease.  The  tendency  is  transmitted 
through  the  female  to  the  male,  though,  strangely  enough,  neither 
pregnancy  nor  menstruation  are  influenced  by  the  condition. 

Certain  cases,  limited  in  their  occurrence  to  newborn  children,, 
while  simulating  this  condition,  are  distinguished  from  it  by  rapid 
cessation  of  the  bleeding  and  by  the  coincident  appearance  of  jaun- 
dice and  fever.  Purpura  rheumatica  and  haemorrhagica,  and  scurvy 
have  much  in  common  with  haemophilia  but  lack  the  peculiar  family 
history,  and  occur  usually  in  persons  debilitated  by  improper  living. 
The  joint  affections  may  be  confounded  with  tuberculous  disease, 
but  ecchymoses  and  the  history  of  atavism  are  lacking  in  the  latter. 

VI.    SCURVY 

Scorbutus  is  essentially  a  disease  dependent  upon  improper  diet 
continued  for  a  considerable  period  of  time,  and  hence  affecting  the- 
entire  organism.  The  age  of  the  patient  is  an  important  factor  in 
determining  the  symptoms,  and  two  well-marked  varieties  are  de- 
scribed :  the  scurvy  of  infants,  and  the  scurvy  of  adults. 

I.  Infantile  Scurvy. — This  disease  usually  becomes  manifest 
before  the  child  is  a  year  old. 


DISEASES  OF  BLOOD  AND  DUCTLESS  GLANDS  919 

Symptoms. — Bottle-fed  children,  without  reference  to  their  home 
surroundings,  may  develop  this  disease  as  a  result  of  living  upon 
food  in  which  certain  essential  ingredients  are  lacking.  Malted  milk, 
condensed  milk,  and  the  various  baby  foods  on  the  market  are  the 
chief  causes  of  the  malady. 

The  recognition  of  this  disease  as  an  entity  is  so  recent,  and  the 
symptoms  described  by  Barlow  in  his  monograph  are  so  clearly 
described  that  they  are  here  quoted :  "  So  long  as  it  is  left  alone  the 
child  is  tolerably  quiet ;  the  lower  limbs  are  kept  drawn  up  and  still ; 
but  when  its  diapers  are  changed,  or  it  is  placed  in  its  bath,  or  other- 
wise moved,  there  is  continuous  crying,  and  it  soon  becomes  evident 
that  the  pain  is  connected  with  the  lower  limbs.  At  this  period  the 
arras  may  be  handled  with  impunity,  but  any  attempt  to  move  the 
legs  or  thighs  gives  rise  to  screams.  Next  some  obscure  swelling 
may  be  detected,  first  on  one  lower  limb  and  then  on  the  other, 
though  it  is  not  absolutely  symmetrical.  The  swelling  is  ill-defined, 
but  is  suggestive  of  thickening  around  the  shafts  of  the  bones,  begin- 
ning above  the  epiphyseal  junctions.  Gradually  the  bulk  of  the 
limbs  affected  becomes  visibly  increased,  and  the  position  assumed 
becomes  somewhat  different  from  what  it  was  at  the  outset.  Instead 
of  being  flexed  they  lie  everted  and  immobile,  in  a  state  of  pseudo- 
paralysis. About  this  time,  if  not  before,  great  weakness  of  the  back 
becomes  apparent.  A  little  swelling  of  one  or  both  scapulas  may 
appear,  and  one  or  both  arms  show  similar  changes,  though  rarely  as 
marked  as  in  the  legs.  The  joints  are  free.  In  severe  cases  another 
symptom  may  now  be  found,  namely,  crepitus  in  the  region  adjacent 
to  the  junction  of  the  shafts  with  the  epiphyses.  The  upper  and 
lower  extremities  of  the  femur  and  the  upper  end  of  the  tibia  are 
the  common  sites  of  such  fractures,  but  the  upper  end  of  the 
humerus  may  also  be  affected.  A  very  startling  appearance  may 
now  be  observed  over  the  front  of  the  chest;  the  sternum,  costal 
cartilages,  and  a  portion  of  the  adjacent  ribs  seem  to  have  been 
forcibly  jammed  back  toward  the  spinal  column.  Occasionally  thick- 
enings of  varying  extent  may  be  observed  on  the  surface  of  the  skull, 
or  even  on  some  of  the  bones  of  the  face.  A  remarkable  eye  symp- 
tom may  appear ;  proptosis  of  one  eyeball,  with  puffiness  and  very 
slight  staining  of  the  upper  lid.  In  a  day  or  two  the  other  eye  pre- 
sents the  same  appearance.  Little  ecchymoses  may  appear  on  the 
conjunctiva.  Coincident  with  these  symptoms,  and  proportional  to 
the  amount  of  limb  involved,  a  very  profound  anaemia  develops. 
The  complexion  becomes  sallow  or  earthy  coloured,  and  small  ecchy- 
moses, or  more  rarely  petechiae,  appear  on  various  parts  of  the  body. 
Emaciation  is  not  a  marked  feature— in  fact,  during  the  early  stages 


920  DIAGNOSIS,    DIRECT   AND   DIFFERENTIAL 

of  the  disease  the  child  may  appear  to  be  unusually  plump  and  well 
nourished.  Asthenia  is,  however,  well  marked.  The  temperature  is 
erratic ;  it  is  often  raised  for  a  day  or  two  when  successive  limbs  are 
involved,  but  is  rarely  above  103°.  If  teeth  have  appeared,  the  gums 
may  become  spongy  and  bleed  freely ;  some  of  the  teeth  may  even 
fall  out." 

Diagnosis. — The  cardinal  symptom  is  the  extravasation  of  blood 
beneath  the  periosteum,  with  resulting  thickening  and  tenderness  of 
the  shaft  of  the  bone.  The  pain  in  the  legs,  their  position,  and  the 
spongy  and  bleeding  gums  are  symptoms  of  nearly  equal  impor- 
tance. The  disease  may  be  suspected  in  any  child  who  has  diflS- 
culty  or  pain  in  moving  the  legs,  or  in  whom  paralysis  is  suspected. 
The  character  of  the  child's  diet  is  of  great  importance. 

Differential  Diagnosis. — This  is  to  be  made  from  : 

Acute  Articular  Rheumatism. — The  joints,  not  the  shafts  of  the 
bones,  are  involved ;  crepitus  does  not  exist ;  the  fever  is  much 
higher,  and  the  characteristic  symptoms  of  scurvy  are  absent. 

Rachitis. — In  this,  although  the  early  stages  may  be  indistinguish- 
able, there  soon  develops  the  rachitic  rosary  and  the  enlargement  of 
the  ends  of  the  long  bones ;  pain  is,  as  a  rule,  absent,  and  ecchymoses, 
petechias,  and  spongy  gums  are  not  observed.     Both  may  coexist. 

Purpura. — There  is  an  absence  of  the  history  of  improper  feed- 
ing in  most  cases,  and  the  rapid  improvement  under  treatment  seen 
in  scurvy  is  not  common  in  purpura. 

Infantile  Paralysis. — This  has  a  sudden  onset  accompanied  by 
fever,  certain  special  groups  of  muscles  are  affected,  and  the  electri- 
cal reactions  differ  in  the  two  diseases. 

Syphilis. — In  syphilitic  pseudo-paralysis  the  onset  is  sudden,  and 
there  is  loss  of  motion  in  the  upper  or  lower  limbs,  or  both,  by 
reason  of  the  separation  of  the  cartilage  at  the  end  of  the  diaphysis. 
There  is  usually  much  pain  and  crepitation  on  motion.  The  differ- 
ence in  the  history  is  still  more  marked. 

Asthenia  and  Ancemia. — Some  early  cases  of  scurvy  can  not  be 
recognised,  and  are  regarded  as  cases  of  anaemia  or  asthenia. 

Prognosis. — When  the  disease  is  recognised  and  appropriate  treat- 
ment instituted  at  an  early  date  nearly  all  cases  recover. 

II.  Scurvy  in  Adults. — All  ages  are  attacked  by  the  disease, 
but  the  old  are  more  susceptible  to  it.  More  males  than  females  are 
subject  to  it,  probably  because  of  greater  exposure  to  unfavourable 
conditions  of  food,  weather,  and  work. 

Symptoms. — These  develop  slowly,  after  a  period  of  exposure  to 
cold,  fatigue,  poor  and  damp  quarters,  and  a  diet  deficient  in  green 
vegetables.     Weight  and  strength  are  progressively  lost.     A  marked 


DISEASES  OP  BLOOD  AND  DUCTLESS  GLANDS  921 

pallor  becomes  apparent,  and  the  skin  gets  rough  and  dry.  The 
breath  is  offensive;  the  tongue  is  swollen,  red,  and  furred;  the 
gums  become  spongy,  bleed  easily,  and  the  teeth  loosen  and  may  fall 
out.  There  may  even  be  ulceration  and  loss  of  tissue  from  the  gums 
and  necrosis  of  the  maxillary  bones. 

The  hlood  shows  nothing  characteristic.  Interstitial  hemorrhages, 
petechial  in  character,  soon  begin  to  appear,  at  first  around  the 
ankles,  then  extending  up  the  legs  to  the  trunk  and  arms.  The  mu- 
cous membranes  of  the  mouth,  bowels,  and  urinary  tract  are  also  the 
site  of  similar  lesions.  On  the  surface  of  the  body  the  hair  follicles 
are  especially  the  seat  of  hemorrhages.  Still  larger  extravasations  are 
determined  by  insignificant  bruises.  As  in  infants,  subperiosteal 
extravasation  of  blood  may  occur,  but,  owing  to  the  firmer  structure 
of  the  bony  tissue,  results  in  the  formation  of  nodes  rather  than  fusi- 
form swellings.  Actual  hemorrhages  may  occur,  of  which  epistaxis 
is  the  most  common,  hasmaturia  and  bleeding  from  the  bowels  are 
next  in  frequency,  while  haemoptysis  and  haematemesis  are  rare.  A 
curious  condition  of  the  skin  is  produced — "  scurvy  sclerosis  " — a 
firm,  inelastic  induration  of  the  subcutaneous  tissues  with  a  purplish 
discoloration  of  the  surface  from  multiple  petechiae.  Large  inter- 
muscular clots  may  break  down  and  indolent  ulcers  result. 

The  circulatory  symptoms  are  those  due  to  a  poorly  nourished 
heart,  namely,  palpitation,  with  a  feeble  and  iiTegular  impulse. 
Haemic  murmurs  are  common.  The  nervous  symptoms  are  those  of 
low  vitality,  slow,  unresponsive,  and  depressed  mentality,  headache,  or, 
with  the  occurrence  of  extravasation  into  the  various  tissues  of  the 
brain,  convulsions  or  hemiplegia.  The  chief  osseous  symptoms  which 
have  been  observed  are  necrosis,  separation  of  the  epiphyses  or  of  the 
costal  cartilages,  destruction  of  a  recent  callus,  and  effusion  of  blood 
into  the  larger  joints.  The  appetite  is  lost  or  uncertain,  and  there 
is  nausea  or  repugnance  to  the  mere  sight  of  food ;  vomiting,  de- 
layed digestion,  constipation,  or  diarrhoea.  The  latter  may  be  so 
severe  that,  with  the  addition  of  the  blood  oozing  from  the  intestinal 
mucous  membrane,  there  may  be  a  condition  simulating  a  severe  dys- 
entery. The  respiratiofi  is  normal  but  shallow.  Dyspnoea  may  occur, 
and  infarctions  of  the  lung  have  been  found  post  mortem. 

Diagnosis. — With  increased  care  of  the  rations  scurvy  has  almost 
disappeared,  even  on  the  smaller  ocean  craft.  The  history  of  crowded 
and  damp  quarters,  overwork,  cold,  hardships,  and  poor  food  should 
at  once  suggest  the  diagnosis.  Isolated  cases  are  more  difficult  to 
decide  upon,  and  are  with  difficulty  separated  from  some  forms  of 
purpura.  The  rapidity  of  recovery  when  the  food  is  properly  reg- 
ulated will  establish  the  diagnosis  in  many  instances. 


922  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

VII.    STATUS   LYMPHATICUS 

{See  page  29) 

VIII.    ADDISON'S    DISEASE 

Causes. — Addison's  disease  is  usually  due  to  tuberculosis  of  the 
suprarenal  capsules,  and  the  symptoms  depend  upon  the  loss  of 
function  of  these  bodies.  Most  cases  occur  between  20  and  40  years 
of  age.     It  predominates  in  males  (2  to  1). 

Symptoms. — Its  onset  is,  as  a  rule,  insidious.  A  light  yellow  or 
light  brown  pigmentation  of  the  skin  is  usually  the  first  symptom 
to  attract  attention.  It  progressively  deepens  over  the  entire  body, 
and  is  especially  marked  over  the  pigment-bearing  areas,  the  areolas 
of  the  nipples,  and  the  genitals.  Finally,  a  marked  bronzing  of  the 
entire  skin  surface  is  observed,  with  circumscribed,  sometimes  ex- 
tensive, areas  of  a  dark  brown  or  black  colour.  The  exposed  or 
irritated  skin  surfaces  are  also  deeper  in  colour.  Patches  of  leuco- 
derma  are  occasionally  observed.  The  mucous  membranes  are  also 
pigmented. 

Addison  called  attention  to  the  irritability  of  the  stomach  in 
these  cases.  Nausea,  vomiting,  anorexia,  abdominal  pain,  retraction 
of  the  abdominal  walls,  and  more  or  less  profuse  diarrhoea  occur, 
but  all  vary  greatly  in  severity  and  frequency.  General  languor  and 
debility,  slight  at  first  but  progressively  increasing,  are  symptoms 
which  occur  before  the  discoloration  of  the  skin  suggests  the  true 
nature  of  the  disease.  These  increase  in  severity  till  asthenia  becomes 
the  most  characteristic  feature  of  the  disease.  Lassitude  and  muscular 
prostration  are  marked  even  in  well-nourished,  robust,  and  muscu- 
lar persons.  The  heart's  action  becomes  remarkably  feeble,  irregu- 
lar, or  paroxysmal.  There  are  accompanying  vascular  disturbances, 
such  as  vertigo,  syncope,  headache,  coma,  or  convulsions ;  the  syn- 
cope may  even  be  fatal.  Although  anaemia  was  at  one  time  regarded 
as  an  essential  and  characteristic  symptom,  it  is  by  no  means  so  com- 
mon as  was  once  supposed.  The  number  of  erythrocytes  or  the 
amount  of  haemoglobin  may  even  be  increased.  As  a  rule  the  leuco- 
cytes show  no  marked  changes,  although  in  a  few  instances  melanin 
has  been  observed  in  them. 

Complications. — Acute  general  miliary  tuberculosis  may  develop 
at  any  time  during  the  course  of  the  disease.  This  is  due  to  the  fact 
that  the  new  growth  within  the  suprarenal  capsule  is  nearly  always 
tuberculous,  and  the  involvement  of  some  one  of  the  blood  vessels 
may  lead  to  the  dissemination  of  the  tubercle  bacilli  to  various  parts 
of  the  body.  Symptoms  develop  according  to  the  distribution  of  the 
new  foci  of  disease. 


DISEASES  OF  BLOOD  AND  DUCTLESS  GLANDS  923 

Diagnosis. — The  cardinal  symptoms  upon  which  the  diagnosis 
jests  are  pigmentation  of  the  skin  with  marked  and  progressive 
asthenia  ;  in  doubtful  cases  the  response  to  the  tuberculin  test. 

Differential  Diagnosis. — Pigmentation  of  the  skin  may  develop 
from  a  great  variety  of  causes  and  conditions  :  abdominal  neoplasms, 
particularly  melano-sarcoma ;  pregnancy,  uterine  disease,  torpidity  or 
disease  of  the  liver,  ulcer  or  dilatation  of  the  stomach,  exophthalmic 
goitre,  splenic  leucaemia,  pseudo-leucsemia,  scleroderma,  comedones  ; 
even  dirt  and  the  resulting  irritation  of  the  skin,  have  all  at  times 
given  rise  to  sufficient  discoloration  or  pigmentation  of  the  skin  to 
lead  to  the  diagnosis  of  Addison's  disease.  In  argyria  the  history 
and  the  absence  of  the  asthenia  will  establish  the  diagnosis. 

Prognosis. — Thus  far  the  cases  reported  have  had  a  fatal  termi- 
nation. The  use  of  suprarenal-capsule  extract  may  in  the  future 
modify  the  mortality. 

IX.    DISEASES    OF   THE    SPLEEN 

"We  here  consider  changes  developing  jt?nwari7^  in  the  spleen. 

I.  Movable  Spleen. — Symptoms. — These  vary  with  the  degree 
of  mobility  and  size  of  the  gland.  Some  cases  are  accidentally  dis- 
covered by  palpation  and  give  rise  to  no  subjective  symptoms  what- 
ever. In  other  instances,  especially  if  the  organ  is  enlarged  as  well 
as  displaced,  there  is  a  sense  of  weight  and  dragging  in  the  left  side, 
which,  when  the  cause  is  discovered,  gives  nervous  patients  much 
anxiety.  Barely  torsion  of  the  pedicle  occurs,  and  swelling,  pain, 
fever,  and  even  necrosis  may  follow.  The  diagnosis  is  easily  made  by 
palpation,  unless  adhesions  exist.  Exploratory  laparotomy  may  be 
necessary  in  obscure  cases. 

II.  Rupture  of  the  Spleen.— In  the  excessive  degree  of  hyper- 
emia sometimes  present  in  typhoid,  malarial,  and  other  fevers,  spon- 
taneous rupture  may  occur.  Traumatism  is  a  more  common  cause. 
The  symptoms  of  acute  and  severe  intra-abdominal  hemorrhage 
at  once  develop.  Abdominal  section  confirms  the  diagnosis.  The 
mortality  is  high ;  an  immediate  operation  saves  a  small  proportion. 

III.  infarct,  Abscess,  and  New  Growths  of  the  Spleen.— 
An  infarct  of  tlie  spleen  may  occur  as  a  result  of  emboli  or  throni- 
bosis  in  endocarditis,  typhoid,  and  similar  affections.  Splenic  pain, 
tenderness,  and  swelling  occurring  in  pyaemia  may  cause  a  suspicion 
of  the  condition,  but,  as  a  rule,  the  diagnosis  is  practically  impossible ; 
so  also  with  the  rare  abscesses,  cysts,  and  neoplasms  of  the  gland, 
unless  they  reach  such  a  size  as  to  be  evident  upon  percussion  or 
palpation.  The  true  nature  of  the  enlargement  is  only  to  be  deter- 
mined by  an  exploratory  operation. 


924  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

IV.  Splenic  Anaemia. — Primitive  splenomegaly  occurs  at  all 
ages,  but  is  more  common  in  males  than  in  females.  • 

Symptoms. — The  spleen  is,  as  a  rule,  very  large,  but  aside  from 
mechanical  discomfort  this  gives  rise  to  no  symptoms.  Haemateme- 
gis  is  common,  and  is  often  the  symptom  for  which  the  patient  first 
seeks  relief.  Haematuria  and  purpura  have  also  been  observed.  Me- 
chanical obstruction  is  probably  the  cause  of  all  of  these  symptoms. 
Ascites  is  not  infrequent,  due  either  to  the  enlarged  spleen  or  to 
the  associated  anaemia.  (Edema  of  the  extremities  or  general  anasarca 
may  occur  (rare).  Pigmentation  of  the  skin  (melanoderma)  is  seldom 
observed ;  in  some  instances  the  colour  has  been  as  dark  as  in  pro- 
nounced cases  of  Addison's  disease. 

The  anaemia  may  cause  only  a  slight  pallor,  or  it  maybe  as  intense 
as  that  of  progressive  pernicious  anaemia.  A  relatively  high  red  cell 
count  is  found  (average  3,400,000),  with  a  relatively  low  amount 
of  haemoglobin  (average  45  per  cent) ;  and  the  leucocyte  count  is  low 
(2,500),  with  an  extreme  leucopenia  (500)  in  about  half  of  all  cases. 
The  differential  count  of  the  leucocytes  shows  nothing  of  importance. 
The  red  corpuscles  are  changed  somewhat ;  poikilocytosis  is  common ; 
normoblasts  and  megaloblasts  are  not  infrequent. 

Diagnosis. — The  cardinal  symptoms  are  primitive  splenomegaly, 
with  anaemia  and  without  enlargement  of  the  lymph  glands. 

Pernicious  Anmnia. — The  differentiation  may  be  extremely  diffi- 
cult, but  the  small  size  of  the  spleen  and  the  relatively  high  amount 
of  haemoglobin  are  characteristic  of  pernicious  anaemia. 

Splenic  Leuccemia. — Those  cases  of  leucaemia  in  which  the  leuco- 
cytes gradually  diminish  and  remain  at  their  normal  number  for  pro- 
tracted periods  are  difficult  to  differentiate.  As  a  rule  the  blood 
examination  will  determine  the  diagnosis. 

Pseudo-leucmmia. — The  haemanalysis  and  the  size  of  the  spleen 
may  be  identical  in  the  two  conditions,  but  the  progressive  enlarge- 
ment of  the  lymph  glands  is  characteristic  of  Hodgkin's  disease. 

Cirrhosis  of  the  Liver  with  Enlarged  Spleen. — Whether  the  cirrho- 
sis be  due  to  alcoholism  or  to  syphilis,  the  spleen  is  often  enlarged ; 
even  a  simple  hypertrophy  of  the  liver  may  be  followed  by  splenic 
enlargement.  The  two  conditions  may  coexist.  A  knowledge  of  the 
history  and  progress  of  each  disease  is  essential  to  accurate  separa- 
tion of  such  cases ;  so  also  is  their  behaviour  under  appropriate 
treatment  (e.  g.,  mercury). 

Malaria  with  enlargement  of  the  spleen  and  paludal  cachexia,  may 
be  excluded  by  the  history,  the  absence  of  the  plasmodium  from  the 
blood,  and  the  differences  observed  on  haemanalysis. 


DISEASES  OF  BLOOD  AND  DUCTLESS  GLANDS  925 

X.   DISEASES    OF   THE   THYROID    GLAND 

I.  Goitre.  —  Symptoms.  —  One  lobe,  both  lobes,  or  the  entire 
gland,  may  progressively  enlarge  and  form  a  bilobed  tumour  extend- 
ing across  the  front  of  the  neck.  This  tumour  may  be  of  varying 
composition  :  vascular,  cystic,  or  parenchymatous  with  colloid  degen- 
eration. In  each  instance  the  resulting  disfigurement  may  be  at  first 
the  only  cause  for  complaint.  Later,  as  the  mass  increases  in  size, 
pressure  symptoms  develop  according  to  the  structures  involved — 
pain,  dyspnoea,  aphonia  from  paralysis  of  one  or  both  vocal  cords, 
or  even  sudden  death  from  compression  of  the  vagus  on  one  or  both 
sides. 

This  same  group  and  train  of  symptoms  develop  if  the  gland  be- 
comes the  seat  of  a  new  growth.  Adenomata,  carcinomata,  and  sar- 
comata are  the  forms  of  neoplasm  most  frequently  found  in  this 
locality.  Abscess  of  the  thyroid,  a  condition  rarely  observed,  may 
give  rise  to  similar  symptoms. 

Diagnosis. — Inspection  reveals  the  enlargement,  but  its  exact 
nature  can  only  be  determined  by  a  surgical  operation.  The  prog- 
nosis  depends  entirely  upon  the  size  of  the  tumour  and  the  mechan- 
ical disturbances  caused  by  it. 

II.  Exophthalmic  Goitre. — Graves's,  Basedow's,  or  Parry's  dis- 
ease is  most  frequent  in  early  adult  life,  between  20  and  30,  prepon- 
derating in  women  (3  to  1).  Several  in  the  same  family  may  suffer. 
It  is  probably  due  to  excessive  thyroid  action  (hyperthyrea). 

Symptoms. — Four  cardinal  symptoms  characterize  this  disease : 
enlargement  of  the  thyroid  gland,  exophthalmos,  tachycardia,  and 
tremor.  These  do  not  always  develop  in  the  same  order,  but  ulti- 
mately all  are  well  marked. 

Enlargement  of  the  Thyroid.— As  in  simple  goitre,  one  or  both 
sides  may  be  affected,  although  the  size  of  the  growth  is  not  so 
extreme.  The  thyroid  vessels  become  dilated,  and  a  noticeable  thrill 
may  be  felt,  or  even  seen,  and  various  murmurs  heard  over  the 
tumour  mass. 

Exophthalmos.— SynchTonons\j,  as  a  rule,  with  the  thyroid  en- 
largement one  or  both  eyes  become  more  prominent.  At  first  this 
may  be  due  merely  to  the  infrequent  winking  and  to  the  altered 
adjustment  of  the  eyelid,  whereby  a  line  of  the  white  eyeball 
appears  above  and  below  the  cornea.  In  looking  downward  the 
upper  lid  does  not  follow  the  movement  of  the  eyeball.  Soon  an 
actual  protrusion  of  the  eyeball  becomes  apparent;  this  becomes 
more  and  more  marked,  and  an  actual  dislocation  of  the  eye  from  its 
socket  has  been  observed.     Vision  remains  normal,  as  a  rule,  but  the 


-926  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

arteries  of  the  retina  throb,  and  can  be  seen  to  pulsate.  A  general 
inflammation  of  all  ocular  structures  may  destroy  the  eye  (rare). 

Tachycardia. — The  heart  action  progressively  increases  in  ra- 
pidity, although  intermission  is  rare  ;  140  to  160  beats  per  minute,  or 
■even  higher,  are  not  infrequently  observed.  As  a  result  of  this  the 
cardiac  impulse  may  be  felt  over  the  entire  chest,  and  even  heard  at 
a  considerable  distance  (5  feet  in  1  case).  The  pulsation  can  be 
seen  over  the  praecordial  region  and  over  the  vessels  of  the  neck.  A 
general  arterial  distention  occurs,  and  is  a  marked  and  distressing 
.symptom ;  the  patient  may  be  unable  to  sleep  because  of  the  jarring 
«ound  in  the  ears  conveyed  by  the  carotids.  The  arterioles  are 
dilated  and  hot  flushes  with  profuse  sweats  occur.  The  arterial  pulse 
can  be  felt  in  the  finger  tips.  A  well-marked  venous  pulse  has  been 
observed  (rare).  Tremor  is  a  well-marked  cardinal  symptom,  fine, 
general,  involuntary,  and  appearing  early. 

Miscellaneous  Symptoms. — The  skin  may  show  a  pigmentation 
closely  simulating  that  of  Addison's  disease,  and  leucoderma,  severe 
pruritus,  or  urticaria.  In  the  underlying  connective  tissue  patches  of 
solid  oedema  or  of  myxcedema  may  appear.  As  a  result  of  this 
excess  of  moisture  in  the  skin  and  underlying  structures  a  marked 
■diminution  in  electrical  resistance  has  been  noted. 

Vomiting  and  diarrhoea,  in  paroxysmal  attacks,  are  not  infrequent. 
As  a  result  of  impaired  nutrition,  anaemia,  emaciation,  and  slight  fever 
progressively  increase.  Marked  changes  occur  in  the  nervous  system. 
The  mind  may  remain  unaffected,  but  irritability,  change  of  disposi- 
tion, mental  depression,  melancholia  (rare),  or  acute  mania  (more 
■common)  have  been  noted.  This  last  symptom,  when  it  does  occur, 
is  of  considerable  importance,  for  death  sometimes  rapidly  super- 
venes. Glycosuria,  albuminuria,  or  diabetes  may  be  observed.  These 
various  symptoms  vary  markedly  in  intensity  from  time  to  time  and 
in  different  individuals.    ■ 

Diagnosis. — Bearing  in  mind  the  four  cardinal  symptoms  just 
described,  the  diagnosis  is  usually  easy.  Acute  or  chronic  forms 
occur.  A  certain  proportion  of  recent  cases  recover,  but  recovery  in 
"well-established  cases  is  rare. 

III.  Myxoedema. — In  goitre  and  exophthalmic  goitre  there  is 
an  excessive  action  of  the  thyroid  gland  (hyperthyrea) ;  but  in  the 
conditions  about  to  be  described  the  opposite  state  prevails  (athyrea). 

(I)  Cretinism. — Symptoms. — May  develop  immediately  after  birth, 
or  at  any  time  up  to  puberty.  In  the  sporadic  type  of  the  disease 
the  thyroid  gland  is  either  congenitally  absent  or  deficient,  or  fails 
to  develop.  The  child  usually  appears  like  other  children  until 
about  6  months  of   age.      About  that  time  marked  developmental 


DISEASES  OF  BLOOD  AND  DUCTLESS  GLANDS  927 

defects  begin  to  be  manifest.  Growth  of  body  and  mind  is  re- 
tarded. The  fontanels  do  not  close ;  the  hair  is  thin,  the  skin  dry, 
the  tongue  lolls  loosely  from  the  mouth  and  appears  to  be  too  large. 
The  pale  and  yellowish  face  is  swollen,  and  the  toadlike  eyes  peer 
through  a  mere  slit  between  the  puffy  lids  (Fig.  20,  page  156).  The 
nose  is  flat,  and  the  few  teeth  appear  late,  at  infrequent  intervals, 
and  promptly  decay.  The  hands  and  feet  of  this  pot-bellied  child 
are  stubby  and  nearly  useless  appendages  to  the  short  and  stumpy 
limbs.  The  mind  is  as  deformed  as  the  body ;  idiocy  and  imbecility 
are  common  terminal  stages.  In  certain  parts  of  the  world  (Switzer- 
land, France,  and  Italy)  an  endemic  form  of  this  disease  exists,  asso- 
ciated with  goitre.  The  resulting  symptoms  are  much  the  same  as 
in  the  sporadic  cases,  but  there  is  doubtless  a  difference  in  the  pri- 
mary cause  not  clearly  understood  at  present. 

Diagnosis. — Is,  as  a  rule,  easy,  provided  the  existence  of  this  dis- 
ease be  borne  in  mind.  Owing  to  its  rarity  in  America  unrecognised 
■cases  doubtless  occur.  The  non-deposition  of  lime  salts  in  the  bones, 
giving  rise  to  the  condition  known  as  foetal  rickets,  and  the  perma- 
nent preservation,  in  the  adult,  of  childlike  characteristics  of  body 
and  mind,  infaiitilism,  can  easily  be  differentiated.  Formerly  nearly 
«very  case  died.  Of  the  few  who  survived  there  resulted  a  curious 
form  of  dwarfs,  with  short  legs,  big  joints,  and  the  toadlike  and 
repulsive  facial  expression  described. 

(II)  Juvenile  Myxoedema. — It  occasionally  happens  that  in  a  child 
who  up  to  the  age  of  6  or  8  years  has  been  healthy  and  normally 
developed,  the  occurrence  of  some  of  the  infectious  diseases,  or  of  a 
direct  septic  involvement  of  the  thyroid,  causes  the  gland  to  atrophy 
or  its  function  to  be  suspended.  The  same  symptoms  then  develop, 
.save  for  the  differences  in  age,  as  are  about  to  be  described. 

(III)  Myxoedema  in  Adults.— As  in  exophthalmic  goitre,  women 
^re  much  more  subject  to  the  disease  than  men  (6  to  1).  It  is  more 
common  in  adults  between  the  ages  of  20  and  40  years. 

Symptoms.— In  women  these  bear  no  direct  relation  to  menstru- 
ation, pregnancy,  or  the  menopause.  The  body,  as  a  whole,  becomes 
more  bulky  and  appears  to  be  generally  swollen  or  edematous,  but 
the  swelling  is  firm,  inelastic,  and  does  not  pit  on  pressure.  The 
skin  is  dry  and  rough.  The  wrinkles  are  obliterated,  and  this 
change  in  the  face  gives  rise  to  a  curiously  stolid  expression  (Fig. 
22,  page  157).  The  features  change,  the  nose,  lips,  and  cheeks 
broaden,  the  mouth  is  enlarged,  and  the  tongue  appears  too  big. 
Red  patches  may  mark  the  skin  over  the  nose  and  on  the  cheeks. 
The  hair  is  dry,  stiff,  and  sparse.  The  muscles  of  the  body  become 
flabby,  and  a  slow  and  hesitating  gait  develops. 


928  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Headache,  defective  memory,  delayed  mentality,  an  irritable  and 
suspicious  disposition,  and  finally  delusions,  hallucinations,  dementia, 
and  coma,  follow  the  course  of  the  disease  within  the  brain.  The 
thoracic  and  abdominal  viscera  remain  normal,  though  the  power  of 
resistance  to  malign  influences  is  diminished.  Tuberculosis  is  there- 
fore a  common  cause  of  death.  The  thyroid  progressively  dimin- 
ishes in  size,  finally  the  glandular  elements  disappear,  and  only  a 
shriveled  and  fibrous  structure  marks  the  location  of  the  glands 
Exophthalmic  goitre  sometimes  develops  coincidently  with  myx- 
cedema,  and  the  symptoms  of  the  two  conditions  may  be  combined. 

Diagnosis. — The  diagnosis  of  uncomplicated  myxoedema  is  usually 
easy  if  the  causes  and  symptoms  be  carefully  studied.  Bright's 
disease  is  the  ailment  most  commonly  confounded  with  myxoedema 
and  the  urinary ,  symptoms  may  be  very  similar  in  each  affection. 
The  solid  character  of  the  swelling  and  the  fact  that  it  does  not  pit 
on  pressure  as  does  renal  oedema,  the  loss  of  hair,  the  dryness  of  the 
skin,  and  the  peculiar  mental  state  are  the  chief  features  by  which 
the  true  nature  of  the  lesion  can  be  best  determined. 

Prognosis. — With  proper  treatment  (thyroid  extract)  the  per- 
centage of  recoveries  has  greatly  increased  within  the  past  decade. 

(IV)  Operative  Myxoedema. — As  a  result  of  operations  in  which 
the  thyroid  has  been  entirely  removed  a  condition  of  myxoedema 
(cachexia  strumipriva)  develops  in  about  one  sixth  of  all  cases.  Al- 
lowing small  portions  of  the  gland  to  remain,  or  the  presence  of 
accessory  glands  (not  infrequent),  may  prevent  the  occurrence  of 
the  characteristic  symptoms,  but  when  the  gland  is  quite  obliterated 
the  myxoedematous  cachexia  develops  with  comparative  rapidity. 

XI.    DISEASES    OF   THE   THYMUS    GLAND 

Symptoms. — The  functions  of  this  gland  are  unknown,  the  disor- 
ders caused  by  its  disease  are  rare,  and  the  resulting  symptoms  ob- 
scure. Such  symptoms  as  do  arise  develop,  as  a  rule,  before  the  age 
of  puberty.  If  the  gland  persists  after  the  15th  year  instead  of  under- 
going atrophy  in  the  normal  manner,  or  if  the  gland  is  unusually  large 
(hypertrophy  of  the  thymus),  or  if  it  be  invaded  by  tuberculous, 
syphilitic,  or  neoplastic  deposits,  or  if  hemorrhage  occurs  or  an  ab- 
scess develops  within  the  substance  of  the  gland,  and  by  any  of  these 
means  the  size  of  the  gland  be  made  disproportionate  to  its  normal 
relations  at  the  root  of  the  neck,  various  symptoms  due  to  pressure 
may  develop.  Pressure  upon  the  trachea  may  cause  dyspnoea ;  upon 
the  adjacent  nerve  trunks,  thymic  asthma,  spasm  of  the  glottis,  or 
laryngismus  stridulus ;  if  the  large  blood  vessels  are  compressed, 
congestion  or  oedema  may  result. 


DISEASES  OF  THE  KIDNEY  929 

Diagnosis.— MsiTked  increase  in  the  size  of  the  gland  may  give 
rise  to  an  increased  area  of  dulness,  on  percussion,  along  the  left 
sternal  border  from  the  2d  to  the  4th  ribs.  The  exact  relationship 
existing  between  this  purely  mechanical  pressure  and  thymic  asthma, 
laryngismus  stridulus,  exophthalmic  goitre,  spasm  of  the  glottis,  or 
acute  dyspnoea  is  so  indefinite,  that  at  the  present  time  accurate 
diagnosis  of  thymic  disorders  is  without  any  firm  basis. 


SECTION   VI 

DISEASES   OF   THE  KIDXEY 

Pbepared  by  Heney  Goodwin  Webster,  M.  D. 

(See  also  pages  475  to  480  and  681  to  648) 

Movable  Kidney. — Symptoms. — These  are  frequently  lacking. 
In  some  cases  there  is  dragging  pain  in  the  lumbar  and  sacral 
regions,  occasionally  colicky  abdominal  pain,  intercostal  and  lumbo- 
abdominal  neuralgia,  and,  rarely,  the  kidney  itself  is  tender.  Movable 
kidney  is  often  associated  with  the  multiple  symptoms  of  hysteria, 
neurasthenia,  and  hypochondriasis,  and  serious  mental  anxiety  often 
dates  from  the  discovery  of  the  condition.  The  various  forms  of 
nervous  dyspepsia  often  coexist,  and  there  may  be  prolapse  of  the 
stomach  (gastroptosis),  rarely  dilatation,  or  descent  of  many  abdom- 
inal viscera  (splanchnoptosis)  of  which  movable  kidney  is  a  part. 
Constipation  is  common,  intestinal  obstruction  and  jaundice  (from 
pressure)  are  rare.  The  characters  of  the  urine  in  movable  kidney 
have  been  described  elsewhere  (page  645). 

Attacks  of  severe  abdominal  pain  wnth  chills,  fever,  nausea,  vom- 
iting, and  prostration  (Dietl's  crisis)  may  occur,  probably  from  twist- 
ing or  kinking  of  the  ureter.  The  occurrence  of  oliguria  during  the 
attack,  perhaps  with  swelling  of  the  kidney  (hydronephrosis),  fol- 
lowed by  an  excessive  flow  of  clear  urine  with  subsidence  of  pain  and 
swelling,  renders  this  explanation  plausible,  at  least  in  cases  attended 
by  the  symptoms  just  described. 

Differential  Diagnosis.— The  kidney  may  be  palpable,  or  movable 
as  far  down  as  the  navel,  or  floating,  in  which  case  it  may  be  carried 
to  various  parts  of  the  abdomen  below  the  level  of  the  umbilicus. 
The  diagnosis  depends  upon  the  physical  examination  (page  477). 

A  movable  kidney  may  be  mistaken  for  an  enlarged  gall  bladder, 
but  the  latter  descends  with  inspiration  and  can  not  be  moved  ex- 


930  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

cept  in  the  arc  of  a  circle  with  its  centre  at  the  end  of  the  8th  rib, 
whereas  the  movable  kidney  can  be  carried  downward.  Moreover, 
a  distended  gall  bladder  when  pushed  backward  tends  to  return  to 
its  former  position,  while  the  movable  kidney  when  reposited  will 
frequently  elude  subsequent  palpation.  In  rare  instances  a  tumour 
of  the  intestine  or  the  ovary  may  give  rise  to  doubt,  but  a  careful 
physical  examination,  together  with  the  history,  is  usually  sufficient 
to  settle  the  question.  In  the  large  majority  of  cases  movable  kid- 
ney occurs  in  women,  and  it  is  the  right  kidney  which  is  prolapsed. 

II.  Renal  Congestion  {Hyper cemia). — Presenting  as  the  initial 
stage  of  nephritis,  or  in  the  course  of  the  infectious  and  contagious 
diseases,  or  associated  with  the  inorganic  poisons,  it  is  really  a  part 
of  one  or  the  other  of  these  affections.  An  acute  and  a  chronic 
hyperaemia  are  recognised. 

(1)  Acute  Congestion. — This  may  occur  after  exposure  to  cold, 
after  poisoning  by  turpentine,  cantharides,  and  the  like,  and  after 
operations  upon  the  urethra,  bladder,  or  kidney.  The  symptoms 
are  diminution  or  suppression  of  the  urine,  which  may  contain 
blood,  albumin,  or  casts,  separately  or  together.  More  or  less  pros- 
tration is  present.  In  severe  cases,  after  nephrectomy,  the  patient 
may  pass  into  the  typhoid  condition  with  delirium.  After  injury, 
collapse  may  supervene  with  suppression.  A  single  attack  of  acute 
congestion  is  not  in  itself  dangerous,  but  repeated  attacks  tend  ta 
induce  nephritis.  Where  serious  complications  do  not  exist  the  out- 
look is  good. 

This  condition  is  not  likely  to  be  mistaken,  it  being  merely  neces- 
sary to  distinguish  it  from  its  accompanying  conditions. 

(2)  Chronic  Congestion. — Chronic  hypersemia  of  the  kidney  being 
due  to  chronic  disease  of  the  heart  or  lungs  with  vascular  inter- 
ference ;  or  to  pressure,  as  by  tumours,  ascitic  fluid,  pericardial  effu- 
sion, pregnancy,  and  the  like,  presents,  for  the  most  part,  the  symp- 
toms of  its  associated  disease.  Diminished  secretion  of  urine  is  the 
most  constant  symptom  (see  also  (3),  page  646). 

The  prognosis  depends  largely  on  the  causative  condition,  but 
from  the  tendency  of  chronic  congestion  to  produce  permanent 
changes  in  the  kidney  structure  and  so  induce  chronic  nephritis,  it 
is  serious.  Indeed,  some  writers  do  not  attempt  to  separate  this  con- 
dition from  diffuse  nephritis. 

III.  Uraemia. — This  name  is  given  to  a  congeries  of  symptoms 
occurring  in  the  course  of  acute  or  chronic  nephritis,  puerperal 
eclampsia,  some  cases  of  obstructed  urinary  excretion,  and  occasion- 
ally in  patients  with  pronounced  vascular  changes  alone. 

Symptoms. — These,  as  usually  described,  include  headache  and. 


DISEASES  OP  THE  KIDNEY  931 

sleeplessness,  paralyses,  amaurosis,  convulsions,  mania,  vomiting,  de- 
lirium, coma,  increased  arterial  tension,  and  dyspnoea.  Often  there  i» 
marked  fever.  Sometimes  muscular  spasm  is  present.  Many  patienta 
develop  repeated  acute  attacks  of  uraemia  of  varying  intensity,  or  the 
disease  may  pursue  a  chronic  course.     See  also  (17),  page  647. 

Mentioned  somewhat  more  in  detail,  headache,  usually  occipital 
and  generally  severe,  may  be  the  only  symptom,  and  may  be  continu- 
ous for  a  long  period.  Associated  with  sleeplessness  it  may  lead 
to  mania.  Other  nervous  phenomena,  such  as  itching,  numbness^ 
and  cramps,  may  accompany  it.  It  is  often  conjoined  with  high 
arterial  tension.  Paralysis  may  take  any  form,  though  hemiplegia^ 
monoplegia,  and  aphasia  are  perhaps  most  frequent.  The  first  and 
last  are  often  associated  with  or  succeeded  by  coma. 

Amaurosis  is  not  infrequently  present  in  puerperal  eclampsia. 
It  appears  suddenly  and  lasts  for  a  short  time  only. 

Convulsions,  typical  of  eclampsia,  may  be  mild  or  severe,  single 
or  multiple  in  type.  In  children  they  are  usually  dependent  on 
acute  Bright's  disease  and  are  not  necessarily  grave  ;  in  adults  they 
are  frequent  in  the  later  stages  ol  chronic  nephritis,  when  oedema 
has  set  in  and  the  heart  is  failing ;  or  they  may  appear  suddenly  at 
any  time  in  the  chronic  interstitial  form.  These  seizures  may  closely 
simulate  epilepsy.  The  patient  may  complain  of  prodromal  headache 
and  restlessness,  though  often  the  attack  occurs  without  warning. 
During  the  short  intervals  between  the  convulsions  unconsciousness- 
is  the  rule.  The  temperature  varies.  It  may  be  subnormal  during 
the  seizure,  but  has  a  tendency  to  rise  subsequently.  Increased  ar- 
terial tension  with  congestion  is  usually  present.  As  already  noted, 
children  respond  readily  to  treatment,  so  that  the  appearance  of  con- 
vulsions in  such  cases  need  not  cause  undue  anxiety,  but  in  older 
patients  their  occurrence  is  always  grave. 

Mania  may  appear  suddenly  in  persons  in  whom  nephritis  is  not 
suspected  and  who  have  never  displayed  indications  of  mental 
trouble.  This  is  especially  true  of  puerperal  cases,"  in  which  attacks 
may  accompany  successive  pregnancies. 

Vomiting  may  be  only  a  consequence  of  the  general  disturbance 
dependent  upon  the  disordered  vascular  system,  but  is  sometimes 
seen  as  the  only  marked  symptom  of  an  apparently  slight  nephritis. 
In  such  instances  its  onset  is  abrupt,  its  course  intense,  and  its  out- 
come not  infrequently  fatal.  At  times  diarrhoea,  or  catarrhal  or 
membranous  colitis,  may  accompany  such  attacks.  A  form  of 
stomatitis  with  furred  tongue,  foul  breath,  oedema,  hyperaemia,  and 
swelling  of  the  lips  and  buccal  mucosa,  is  described  as  peculiar  to 
uraemia. 


932  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Delirium  and  coma  are  usually  associated,  and  commonly  appear 
toward  the  end  of  chronic  nephritis.  The  onset  is  gradual,  remis- 
sions may  occur,  but  the  course  is  toward  a  fatal  termination. 

Increased  arterial  tension  of  varying  degree  is  very  generally  pres- 
ent in  the  uraemic  state,  many  of  the  uraemic  symptoms,  such  as 
headache,  being  associated  with  it.  Dyspnoea  may  be  due  to  me- 
chanical causes,  such  as  ascites,  pleuritic  effusion,  pulmonary  oedema, 
and  the  like,  but  that  peculiar  to  uraemia  is  probably  dependent  on 
circulatory  changes.  It  may  simulate  bronchial  asthma  in  all  but 
the  characteristic  "  wheezing."  It  is  paroxysmal  at  first,  increases  in 
frequency,  and  at  last  is  continuous,  the  patient  being  unable  to  lie 
down.  Toward  the  end  the  Cheyne-Stokes  type  of  breathing  may 
occur.  The  condition  may  persist  for  years,  and  is  at  first  amenable 
to  treatment  directed  to  the  circulatory  trouble. 

Diagnosis. — From  alcoholic  or  opium  coma,  see  pages  68,  69. 

Cases  of  uraemic  coma  coming  on  slowly,  with  fever,  and  with- 
out convulsions,  muscular  spasms,  and  the  like,  may  be  mistaken  for 
typhoid,  but  a  positive  Widal  reaction  may  make  the  diagnosis  clear. 
'  Perhaps  the  most  difficult  differentiation  is  from  cerebral  disease. 
Uraemic  hemiplegia  and  monoplegia  occur,  as  previously  noted,  with- 
out cerebral  lesions ;  but  a  suffused  face,  stertorous  breathing,  eyes 
turned  toward  the  side  of  the  hemorrhage,  full,  slow  pulse,  and  hemi- 
plegia should  suggest  apoplexy.  In  rare  instances  it  is  possible  for 
meningitis  to  be  confused  with  uraemia. 

Prognosis. — This  is  always  grave,  but  mild  cases  may  recover  and 
the  patient  survive  for  years. 

IV.  Acute  Bright's  Disease. — Causes. — Acute  diffuse  nephri- 
tis follows  cold  and  exposure ;  the  acute  infectious  diseases,  espe- 
cially scarlet  fever,  typhoid,  diphtheria,  and  the  like ;  the  ingestion 
of  poisons,  such  as  arsenic,  turpentine,  cantharides,  and  carbolic 
acid ;  occurs  sometimes  as  a  result  of  extensive  cutaneous  burns,  and 
more  frequently  in  the  course  of  pregnancy. 

Symptoms. — The  clinical  symptoms  include  some  or  all  of  the 
following  manifestations  :  More  or  less  general  serous  effusion,  anae- 
mia, chills,  pain,  nausea  and  vomiting,  sometimes  fever,  and,  most 
characteristic  of  all,  urinary  changes. 

The  effusion  may  vary  from  simple  puffiness  about  the  ankles  or 
the  eyelids  to  general  anasarca,  or  there  may  even  be  ascites  or  pleu- 
ral effusion.  The  amount  of  fluid  present  is  no  indication  of  the  in- 
tensity of  the  nephritis,  as  violent  and  rapidly  fatal  disease  of  the 
kidneys  may  be  accompanied  with  little  swelling.  Pulmonary  oedema 
is  of  not  infrequent  occurrence,  and  even  oedema  of  the  glottis  has 
been  noted.     The  skin,  however,  is  dry.     Anaemia  appears  early  and 


DISEASES  OF  THE  KIDNEY  933 

is  very  generally  present.  Chills  occur  in  some  instances,  particu- 
larly when  the  disease  is  dependent  on  exposure,  but  are  by  no  means 
frequent — a  statement  which  also  applies  to  nausea  and  vomiting. 

There  is  no  temperature  curve  peculiar  to  acute  Bright's  disease. 
The  fever  may  run  high,  especially  in  children,  or  there  may  be  but 
little  rise  of  temperature.  The  pulse  may  in  some  instances  be  hard, 
of  increased  tension  and  increased  rapidity.  Kapid  cardiac  dilatation 
with  fatal  issue  has  been  reported.  Uraemia  is  occasionally  seen. 
Hemorrhagic  retinitis  occurs. 

As  a  rule,  the  urinary  symptoms  (see  (4),  page  648)  are  the  only 
ones  which  afford  a  clew  to  the  real  nature  of  the  cases. 

Kegarding  the  course  of  the  disease  no  fixed  rule  applies,  as  its 
duration  and  intensity  vary  greatly.  The  cases  running  the  most 
acute  course  are  usually  those  subsequent  to  scarlet  fever,  when  sup- 
pression and  oedema  are  the  rule,  although  rapidly  fatal  cases  may 
lack  the  latter,  and  haematuria  may  be  the  first  cardinal  symptom. 

Differential  Diagnosis. — Recognition  of  this  condition  should  not 
be  difficult.  Of  course  the  alert  practitioner  will  be  on  the  look- 
out for  it  as  a  sequel  of  scarlet  and  typhoid  fevers,  and  as  a  manifes- 
tation in  the  course  of  pregnancy.  Following  exposure  and  the 
eruptive  fevers,  its  onset  is  usually  sufficiently  marked  to  call  atten- 
tion to  the  real  nature  of  the  trouble,  but  in  many  cases  of  pregnancy, 
and  when  it  appears  in  young  children,  it  may  begin  so  insidiously  as 
to  escape  attention,  and  an  eclamptic  seizure  may  be  the  first  symp- 
tom noted.  It  must  be  borne  in  mind  that  simple  febrile  albumi- 
nuria, with  a  few  hyaline  casts,  does  not  constitute  Bright's  disease. 

Prognosis. — This  is  always  serious,  a  fatal  issue  sometimes  ensu- 
ing as  early  as  the  2d  or  3d  day.  An  increase  in  the  dropsical  symp- 
toms, with  small,  rapid,  low-tension  pulse  and  increasing  albumin, 
are  grave  symptoms,  while  increased  urinary  secretion  and  diminish- 
ing albumin  are  hopeful  signs.  The  tendency  to  chronicity  must 
not  be  forgotten.  Scarlatinal  nephritis  should  show  an  improvement 
in  from  7  to  10  days,  with  complete  recovery  after  3  or  4  weeks  in 
favourable  cases.  A  much  longer  course — 8  to  10  weeks — is  not 
incompatible  with  a  perfect  restoration  of  structure  and  function. 

T.  Chronic  Bright's  Disease.— Different  authorities  recog- 
nise a  number  of  sub-varieties  of  this  disease,  but  for  purposes  of 
clinical  diagnosis  it  is  sufficient  to  describe  a  chronic  diffuse  or 
2)arenchijmatous,  and  a  chronic  interstitial  form.  Amyloid  degenera- 
tion is  not  a  distinct  form  of  Bright's  disease,  but  an  incident  in 
either  of  the  forms  of  chronic  nephritis,  or  a  manifestation  of  some 
one  of  the  cachexias,  such  as  .that  of  tuberculosis,  carcinoma,  and 
the  like.  It  will  receive  separate  mention. 
61 


934  DIAGNOSIS,    DIRECT  AXD  DIFFERENTIAL 

(I)  Chronic  Diffuse  Nephritis. — Pathologically,  the  large  white 
kidney — chronic  diffuse  or  parenchymatous  nephritis  with  exudation. 

Symptoms. — As  previously  stated,  an  acute  nephritis  may  merge 
into  a  chronic  nephritis,  or  the  chronic  form  may  be  primary  and 
develop  insidiously.  If  it  follows  the  acute  form  the  symptoms  will 
be  similar  but  of  modified  intensity.  Developing  as  a  primary  af- 
fection, possibly  dependent  upon  chronic  alcoholism,  syphilis,  febrile 
diseases,  and  the  like,  its  first  indication  may  be  a  gastro-intestinal 
crisis.  Moderate  oedema  of  the  feet  or  about  the  eyelids  calls  atten- 
tion to  a  possible  nephritis,  and  urinalysis  makes  the  diagnosis  cer- 
tain. The  cardinal  symptoms  of  chronic  diffuse  nephritis  are  dropsy, 
anaemia,  and  the  urinary  changes.  Associated  with  them  may  be 
uraemic  symptoms,  headache,  nausea,  and  vomiting.  A  distinctive 
facies,  due  to  the  pufflness  about  the  eyes  and  the  marked  anaemia, 
is  insisted  on  by  some  writers  as  peculiar  to  this  form  of  nephritis. 
Eecurring  attacks  of  bronchitis  are  of  frequent  occurrence.  The 
tension  of  the  pulse  increases,  the  arteries  gradually  become  stiff, 
and  the  left  ventricle  hypertrophied.  There  may  be  hemorrhagic 
retinitis.     For  the  urinary  clianges  see  (5),  page  646. 

Prognosis. — This  is  always  grave.  Recovery  may  take  place, 
especially  in  young  subjects,  but  the  course  is  for  the  most  part 
toward  a  fatal  issue,  either  from  uraemia,  oedema  of  the  lungs,  or 
intercurrent  disease. 

(II)  Chronic  Interstitial  Nephritis. — Pathologically  this  is  vari- 
ously termed  cirrhosis  of  the  kidney,  chronic  productive  nephritis 
without  exudation,  contracted  kidney,  etc. 

Causes. — Chronic  parenchymatous  nephritis  may  merge  into  this 
form  (small  white  kidney) ;  it  may  result  from  arteriosclerosis,  gout, 
alcoholism,  or  syphilis ;  or  it  may  occur  spontaneously. 

Symptoms. — Its  early  stages  pass  unrecognised,  though  it  may 
well  be  looked  for  in  hearty  eaters  where  a  habit  of  high  arterial 
tension  exists.  Although  essentially  a  disease  of  middle  life  and  old 
age,  it  is  occasionally  met  with  in  young  children.  Its  symptoms  are 
manifested  in  the  uropoietic,  circulatory,  respiratory,  nervous,  and 
digestive  systems,  and  in  the  eyes,  ears,  and  skin.  The  urinary  mani- 
festations are  described  in  (6),  page  646. 

Of  the  early  manifestations,  increased  arterial  tension  is  the  most 
important.  It  may  be  the  only  cardinal  symptom  in  a  congeries 
which  includes  headache,  palpitation,  bronchial  cough,  tinnitus 
aurium,  muscae  volitantes,  dizziness,  malaise,  anorexia,  and  a  number 
of  kindred  subjective  phenomena.  Closely  following  it  we  find 
hypertrophy  of  the  left  ventricle,  with  eventual  enlargement  of  the 
entire  organ,  and  corresponding  changes  in  the  character  of  the  apex 


DISEASES  OF  THE  KIDNEY  935 

beat.  Reduplication  of  the  first  sound  is  not  uncommon,  while  the 
second  sound,  as  heard  over  the  aortic  area,  is  accentuated  and  has  a 
peculiar  ringing  quality.  A  systolic  murmur,  heard  at  the  apex  and 
transmitted  to  the  left,  may  develop  later ;  and  toward  the  end,  when 
dilatation  succeeds  and  compensation  fails,  any  or  all  of  the  symp- 
toms of  chronic  endocarditis  and  myocarditis  may  appear.  The 
central  nervous  changes  are  those  noted  under  uraemia.  Retinitis, 
choked  disc,  and  amaurosis  are  frequent  ocular  symptoms,  and  ring- 
ing in  the  ears  and  sudden  deafness  may  occur. 

G  astro-intestinal  symptoms  such  as  anorexia,  nausea,  vomiting, 
and  diarrhoea  are  almost  always  present  in  greater  or  less  degree. 
The  tongue  is  generally  coated.  It  may  be  red,  dry,  and  cracked,  or 
moist  and  glazed,  or  covered  with  a  brownish  scum,  or  furred  and 
foul.  Uraemic,  and  often  cardiac,  dyspnoea  is  of  frequent  occur- 
rence ;  bronchitis  is  a  very  regular  accompaniment ;  oedema  of  the 
lungs  is  often  seen  toward  the  last ;  and  oedema  of  the  glottis  may 
occur.  Eczema,  dry  and  itching  skin,  "  pins  and  needles,"  cramp, 
numbness,  and  other  cutaneous  and  nervous  manifestations  occur, 
although  oedema  is  rare.  Where  present  it  is  generally  merely  a 
slight  puffiness  of  the  feet  and  ankles. 

Differential  Diagnosis.— The  distinction  must  be  carefully  drawn 
between  cases  of  diabetes  insipidus,  the  "urina  spastica"  of  neu- 
rotic and  hysterical  patients,  and  cases  of  interstitial  nephritis  with 
a  large  output  of  thin,  clear  urine.  Daily  examination  of  concen- 
trated specimens  of  the  latter  will  show  sooner  or  later  the  casts 
and  albumin  which  distinguish  it.  The  character  of  the  pulse  also 
will  throw  light  on  the  true  nature  of  the  condition.  As  the  onset 
of  the  disease  may  simulate  an  attack  of  dyspepsia,  gastro-enteritis, 
bronchitis,  or  even  cerebral  disease,  the  importance  of  careful  urinal- 
ysis as  a  routine  measure  can  not  be  underestimated. 

Prognosis.— Th\%  is  generally  bad.  While  many  sufferers  from 
chronic  interstitial  nephritis  go  on  in  comparative  comfort  for  many 
years,  there  is  but  one  outcome.  Eventually  the  arteriosclerosis 
determines  cardiac  disease,  and  the  patient  becomes  subject  to  re- 
peated cardiac  or  uremic  attacks  of  increasing  intensity,  or  dies  from 
apoplexv,  oedema  of  the  lungs,  or  intercurrent  disease. 

YI.  Amyloid  Kidney.— The  cases  where  amyloid  disease  is 
manifested  only  in  the  kidney  are  very  rare,  and  in  these  it  is  doubt- 
ful if  the  diagnosis  can  be  made  from  the  urinalysis  alone.  But 
occurring  in  association  with  the  amyloid  degeneration  of  the  liver, 
spleen,  and  other  organs  which  may  follow  the  severe  cachexias,  or 
coming  on  during  a  chronic  nephritis,  it  presents  symptoms  suf- 
ficiently marked  to  permit  a  diagnosis.     Sequent  to  syphilis,  general 


936  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

tuberculosis,  osteomyelitis,  or  the  cancerous  cachexia,  there  may  ap- 
pear a  condition  characterized  clinically  by  certain  urinary  fijuUngs, 
for  which  see  (7),  page  646.  Amyloid  disease  of  the  kidney  is  seldom 
responsible  for  dropsical  symptoms ;  nor  are  cardiac,  arterial,  and 
ocular  symptoms  common.  The  diagnosis  rests  upon  the  combina- 
tion of  polyuria  with  amyloid  degeneration  of  other  viscera. 

VII.  Pyelitis. — Causes. — Consequent  upon  renal  calculus,  local 
tuberculosis,  the  acute  infectious  diseases  (diphtheria,  typhoid  fever, 
scarlet  fever,  gonorrhcea,  and  others),  purulent  cystitis,  obstructed 
ureter,  sarcoma  of  the  kidney,  pregnancy,  and  many  other  conditions, 
the  pelvis  of  the  kidney  may  become  the  seat  of  inflammation  which 
may  be  limited  to  the  pelvis  alone  {pyelitis) ;  or  to  the  pelvis  and 
kidney  substance  {pyelonephritis) ;  or  the  entire  organ  may  be  re- 
placed by  a  single  abscess  cavity  {pyonephrosis). 

Symptoms. — These  are  separable  into  early  and  late,  the  former 
preceding  suppuration,  the  latter  accom^panying  it.  At  the  incep- 
tion of  the  disease,  as  in  the  course  of  typhoid  fever,  there  may  be 
moderate  backache,  tenderness  to  deep  pressure  over  the  kidneys, 
a  marked  rise  of  temperature,  often  decided  chills  and  sweating. 
The  urine  remains  acid,  but  becomes  more  or  less  turbid.  For  the 
urinary  characters  of  the  varieties  of  pyelitis  see  (8),  page  649. 

The  milder  cases  of  pyelitis,  such  as  occur  in  fevers,  often  pass 
unnoticed,  as  they  may  give  no  decided  symptoms,  complete  and 
spontaneous  recovery  occurring,  but  in  those  which  proceed  to  sup- 
puration the  symptoms  become  more  distinctive.  A  chill  with  a 
decided  rise  of  temperature  usually  marks  the  establishment  of  the 
purulent  process,  while  the  increase  of  pus  cells  may  in  extreme 
cases  render  the  urine  almost  milky.  A  septic  temperature,  with 
very  marked  accessions  and  remissions  and  repeated  chills,  is  char- 
acteristic of  the  earlier  stages,  and  persists  in  severe  cases,  but  in 
those  of  less  intensity  the  chart  shows  merely  a  small  evening  rise, 
dropping  to  normal  the  next  morning.  This  is  particularly  the  case 
when  the  pyelitis  is  tuberculous.  After  a  longer  or  shorter  time  the 
effect  on  the  general  health  becomes  marked.  The  patient  becomes 
anaemic,  loses  flesh  and  strength,  his  appetite  is  poor,  he  has  night 
sweats,  and  usually  runs  a  constantly  elevated  temperature.  The 
disease  may  exhibit  marked  remissions  and  run  a  course  of  many 
years'  duration. 

In  other  more  virulent  cases  the  kidney  substance  becomes  the 
seat  of  multiple  pus  foci,  which  may  later  coalesce,  and  the  patient 
soon  exhibits  the  effects  of  the  septic  process.  Inspissation  of  the 
pus  may  occur,  thus  blocking  the  ureter,  or  occlusion  may  result 
from  the  presence  of  a  calculus  or  other  mechanical  or  inflammatory 


DISEASES  OF  THE   KIDNEY  937 

cause.  The  consequent  accumulation  of  pus  causes  distention  of 
the  kidney  into  a  tender  tumour  which  may  be  readily  perceptible  in. 
the  loin.  Irregular  high  temperature,  delirium,  and  rigours  mark 
such  severe  cases.  Unless  relieved,  the  patient  succumbs  to  septic 
poisoning.  In  a  fevr  instances  spontaneous  cure  arises  through  in- 
spissation  of  the  pus,  whereby  masses  are  found  resembling  putty,  in 
which  a  deposit  of  lime  salts  may  take  place. 

A  train  of  symptoms  referable  to  the  central  nervous  system, 
including  dyspnoea  and  other  manifestations,  which  may  simulate 
uraemia,  is  sometimes  encountered. 

Diagnosis. — This  is  not  always  easy,  but  the  occurrence  of  chills 
and  a  rise  of  temperature  in  the  course  of  the  infectious  diseases, 
with  a  close  watch  on  the  urine,  should  usually  enlighten  the  prac- 
titioner. The  differentiation  between  the  calculous  and  tuberculous 
forms  may  often  be  made  with  accuracy  by  means  of  the  Roentgen 
ray,  and  catheterization  of  the  ureter  is  of  great  value  for  diagnosis 
as  well  as  treatment.  While  tubercle  bacilli  may  occasionally  be 
demonstrated,  the  microscopical  examination  of  the  urine  is  more 
often  negative  than  otherwise.  Suppurative  cystitis  usually  differs 
from  pyelitis  in  the  tenesmus  and  vesical  pain  and  the  alkaline  con- 
dition of  the  urine  (  (18),  page  647),  the  urine  of  pyelitis  being  more 
often  acid,  though  cases  may  occur,  especially  in  men,  in  which  both 
conditions  are  present  and  differentiation  is  impossible.  Lumbar 
pain  and  tenderness  over  the  kidney  are  suggestive  of  pyelitis,  al- 
though the  symptoms  are  in  some  cases  more  vesical  than  renal. 

Perinephritic  abscess  differs  from  pyonephrosis  in  that  the  pus 
does  not  escape  through  the  urine,  and  cedema  in  the  skin  over  the 
lumbar  region  and  fluctuation  may  often  be  made  out. 

Prognosis. — Mild  cases,  especially  those  of  febrile  origin,  usually 
resolve  spontaneously.  The  suppurative  varieties  may  occasionally 
be  self-limiting,  but  more  often  are  progressive  and  demand  surgical 
relief.  It  must  always  be  borne  in  mind  that  the  condition  may  be 
bilateral,  while  it  not  infrequently  happens  that  anomalies  exist  and 
death  may  result  from  removal  of  the  only  kidney. 

VIII.  Hydroneplirosis.—Caws^s.— Dilatation  of  the  kidney, 
its  pelvis  and  calyces,  may  be  unilateral,  rarely  bilateral ;  congenital, 
or  due  to  obstruction  of  the  ureter  by  kinking,  valves,  cicatricial 
bands,  or  calculi ;  may  be  continuous  or  intermittent,  and  present  in 
varying  degrees. 

Symptoms.— It  often  exists  for  years  without  attracting  atten- 
tion, and  at  most  simply  presents  a  progressively  enlarging  tumour 
in  the  region  of  the  kidney  which  may  cause  some  dragging  pain. 
When  large,  it  may  cause  pressure  symptoms.     Bilateral  cases  are 


938  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

almost  always  congenital,  and  cause  death  from  uraemia  in  a  few 
days  at  most.  The  symptoms  of  the  intermittent  variety  are  quite 
distinctive.  A  large  tumour  is  found,  corresponding  in  position  to 
the  kidney,  which  suddenly  disappears  with  the  simultaneous  pas- 
sage of  large  quantities  of  clear  urine.  Such  hydronephroses  tend 
to  reaccumulate,  and  the  process  may  be  repeated  indefinitely. 

Differential  Diagnosis. — In  young  children  sarcoma  of  the  kid- 
ney and  enlarged  retroperitoneal  glands  closely  simulate  hydrone- 
phrosis, and  exploration  alone  may  demonstrate  the  true  nature  of 
the  growth.  Ovarian  cystoma  may  be  mistaken  for  hydronephrosis. 
Vaginal  examination  should  help  to  make  the  difference  plain ;  the 
ovarian  tumour  is  more  freely  movable,  fills  the  lower  portion  of  the 
abdomen,  and  tends  to  push  the  intestines  upward,  while  the  ascend- 
ing colon  can  often  be  made  out  passing  over  the  hydronephrotic  sac. 
Erom  pyonephrosis  the  diagnosis  may  be  made  by  the  absence  of 
constitutional  disturbance.  Rare  instances  occur  of  hydronephrosis 
so  large  as  to  be  taken  for  ascites,  while  the  combination  of  a  mova- 
ble kidney  and  hydronephrosis  occurs.  Should  other  means  fail, 
puncture  and  the  examination  of  the  aspirated  fluid  (  (10),  page  653) 
may  be  of  service,  although  (to  be  remembered)  the  characteristics 
of  urine  tend  to  disappear  in  collections  of  long  standing. 

Prognosis. — A  majority  of  cases  never  cause  trouble.  A  certain 
proportion  are  cured  by  spontaneous  evacuation.  In  some  instances, 
however,  the  growth  of  the  tumour  is  such  as  to  cause  serious  incon- 
venience, requiring  surgical  relief.  A  few  cases  of  intra-abdominal 
rupture,  or  even  evacuation  through  the  diaphragm  and  lung,  have 
been  reported.  Infection  and  transformation  into  pyonephrosis  may 
happen. 

IX.  Nephrolithiasis. — Renal  calculus  may  vary  from  a  mere 
"  infarct,"  so  called,  to  a  mass  occupying  the  entire  pelvis.  The 
symptoms  necessarily  depend  upon  the  size  of  the  stone.  The  sim- 
ple infarct  gives  no  symptoms.  Fine  "  gravel "  may  be  passed  by  the 
patient  for  years  and  give  no  other  symptom.  The  size  of  renal 
calculi  passed  j9er  wreMram,  without  discomfort,  maybe  considerable. 
Such  stones  may  appear  but  once,  or  may  be  passed  at  intervals  for 
years.     See  also  (10),  page  647. 

Symptoms. — Many  patients,  however,  are  not  so  fortunate,  and 
attacks  of  renal  colic  result.  The  patient  is  suddenly  seized  with 
pain  of  an  agonizing  character,  having  its  origin  in  the  lumbar  re- 
gion, either  anteriorly  or  posteriorly,  and  following  along  the  course 
of  the  ureter.  It  is  felt  also  in  the  testicle  and  down  the  inner  side 
of  the  thigh,  and  is  at  times  referred  to  the  glans  penis.  Sucli  an 
attack  may  last  only  a  few  minutes,  ceasing  as  the  stone  enters  the 


DISEASES  OF  THE  KIDNEY  939 

bladder,  or  it  may  last  for  hours,  inducing  nausea  and  vomiting, 
sweating,  and  even  syncope  and  collapse.  A  chill  may  accompany 
the  onset,  the  temperature  is  regularly  elevated,  and  the  pulse  be- 
comes rapid  and  feeble.  There  is  often  strangury.  Some  patients 
during  an  attack  void  large  quantities  of  clear  urine.  It  not  infre- 
quently happens  that  suppression,  and  even  uraemia,  supervene, 
although  the  opposite  kidney  is  perfectly  normal.  Following  the 
attack  there  is  a  period  of  prostration.  Aching  pain  may  persist  in 
the  region  of  the  affected  kidney  for  a  considerable  time  after  the 
stone  has  passed.  It  is  rarely  possible  to  demonstrate  the  condition 
by  physical  examination. 

In  the  case  of  calculus  too  large  to  be  voided  by  the  ureter,  its 
continued  presence  in  the  pelvis  of  the  kidney  may  give  rise  to  pain, 
usually  a  dull,  boring  backache,  not  always  referred  to  the  kidney, 
occasionally  paroxysmal,  and  in  certain  cases  simulating  floating  kid- 
ney; to  hgematuria,  by  no  means  a  constant  symptom,  sometimes 
causing  a  smoky  appearance,  often  discoverable  only  by  the  micro- 
scope, and  frequently  aggravated  by  exercise  ;  to  pyelitis  either  sim- 
ple or  purulent ;  and  to  pyuria.  Xon-suppurative  pyelitis  due  to  the 
irritation  of  a  calculus  is  often  recurrent,  the  backache,  chill,  fever, 
and  high-coloured  urine  closely  simulating  malaria. 

Differential  Diagnosis. — Kenal  colic  may  closely  resemble  biliary 
colic  (when  occurring  on  the  right  side),  intestinal  colic,  floating 
kidney,  and  sometimes  vesical  calculus.  The  direction  and  localiza- 
tion of  the  pain,  which  in  renal  colic  is  referred  to  the  testicle,  the 
latter  becoming  tender  and  retracted,  the  character  of  the  urine, 
and  the  previous  history,  should  distinguish  this  condition  from  the 
hepatic  and  intestinal  varieties,  while  ammoniacal  urine  points  to 
vesical  calculus,  and  physical  examination  will  often  establish  the 
diagnosis  of  floating  kidney.  Several  investigators  have  successfully 
diagnosed  renal  calculus  by  means  of  the  Roentgen  ray. 

Prognosis.— Rei\^\  calculus  may  be  present  for  years  without 
causing  discomfort  to  the  patient.  Repeated  attacks  of  pain  or  the 
occurrence  of  pyelitis  are  a  source  of  danger,  and  call  for  surgical 
interference,  the  increasingly  successful  outcome  of  operations  on 
the  kidney  making  this  method  of  treatment  desirable. 

X.  Tumours  of  the  Kidney.— ^S';/wjo/(wws.— If  benign,  the 
growth  mav  not  be  recognised  until  it  has  attained  such  a  size  as  to 
cause  discomfort  by  reason  of  its  weight  and  the  pressure  exerted 
on  surrounding  organs,  although  it  is  rare  to  find  non-malignant 
growths  of  large  size.  Malignant  growths,  on  the  other  hand,  form- 
ing a  very  large  majority  of  kidney  tumours,  frequently  attain  enor- 
mous dimensions.    This  is  especially  the  case  with  sarcoma,  the  form 


940  DIAGNOSIS,  DIRECT  AND   DIFFERENTIAL 

appearing  most  often  in  young  children,  in  whom  the  tumour  mass 
may  occupy  and  distend  the  entire  abdomen.  The  symptoms  of 
malignant  tumour  of  the  kidney  include  hasmaturia,  pain,  and  ema- 
ciation. The  blood  is  frequently  voided  as  clots,  which  often  show 
as  moulds  of  the  ureter  or  even  of  the  pelvis  of  the  kidney,  or  it 
may  be  passed  in  the  fluid  state.  It  is  claimed  that  detached  por- 
tions of  the  growth  may  be  detected  in  the  urine.  Pain  is  not  always 
present,  but  the  patient  may  complain  of  dull,  aching,  lumbar  pain, 
sometimes  radiating  along  the  course  and  distribution  of  the  genito- 
crural  nerve.  As  in  cancer  elsewhere,  there  is  progressive  emaciation 
and  loss  of  strength.  In  considering  the  question  of  the  probable 
nature  of  the  tumour,  it  must  be  remembered  that  cancer  is  most 
frequent  before  the  3d  and  after  the  40th  year. 

When  sufficiently  large  to  be  palpable,  examination  reveals  a 
deep-seated  mass  in  the  lumbar  region,  which  may  be  movable,  may 
present  a  lobulated  surface,  and  across  which  the  colon  may  be  shown 
to  pass  (Fig.  157,  page  473).    It  does  not  move  with  respiration. 

Differential  Diagnosis. — From  neoplasm  of  the  retroperitoneal 
glands ;  this  is  more  centrally  placed  and  is  quite  immovable.  The 
distinction  may  be  impossible  to  make. 

From  enlargement  of  the  spleen ;  the  characteristic  outline  of 
the  spleen  should  prevent  confusion.  It  also  moves  with  respira- 
tion. 

From  tumour  of  the  gall  bladder ;  the  latter  is  more  superficially 
placed,  and  jaundice  is  a  prominent  symptom. 

From  pedunculated  fibroid  and  ovarian  cystoma ;  the  movability 
of  these  tumours  is  lateral  and  downward,  and  their  pelvic  origin  is 
generally  demonstrable. 

Prognosis. — Benign  neoplasms  rarely  cause  trouble.  The  out- 
look in  cancer  is  of  the  gravest.  If  early  diagnosis  can  be  made,  ex- 
tirpation affords  the  only  chance  of  recovery.  The  percentage  of 
successful  cases  is,  however,  small,  as  recurrences  are  frequent, 

XI,  Cystic  Disease  of  the  Kidney. — Of  pathological  rather 
than  clinical  interest,  as  the  condition  can  rarely  be  diagnosed. 

Four  varieties  occur :  multiple  small  retention  cysts  incident  to 
chronic  nephritis  ;  single  larger  cysts,  probably  of  the  same  origin ; 
combined  cystic  disease  involving  the  liver  and  spleen  in  addition  to 
the  kidneys;  and  the  congenital  variety.  While  most  of  the  latter 
cases  die  antepartum,  or  shortly  after  delivery,  a  few  survive  for 
years,  the  real  condition  being  discovered  post  mortem.  The  cystic 
kidney  is  here  bilateral,  much  distended,  and  presents  a  fluctuating 
tumour  in  both  flanks.  There  is  cardiac  hypertrophy  with  high- 
tension  pulse,  and  death  may  occur  with  the  symptoms  of  chronic 


DISEASES  OF  THE  KIDNEY  941 

interstitial  nephritis.  The  condition  may  simulate  hydronephrosis, 
though  the  latter  in  its  acquired  form  is  rarely  bilateral. 

XII.  Perinepliritic  Abscess. — Causes. — This  disease  has  al- 
ready been  mentioned  under  pyelitis  (page  937).  It  may  occur  pri- 
marily as  a  result  of  traumatism  ;  or  secondarily  as  an  extension  from 
pyelitis,  appendicitis,  spinal  caries,  and  empyema  ;  or  follow  the  acute 
febrile  diseases  ;  and  a  few  cases  seem  to  result  from  invasion  by  the 
common  colon  bacillus  without  traumatism. 

Symptoms. — Following  one  of  the  conditions  just  mentioned,  a 
chill,  fresh  rise  of  temperature,  sweating,  and  deep-seated  lumbar 
pain  radiating  into  the  thigh  and  testicle,  with,  later,  the  finding 
of  a  tender,  fluctuating  mass  in  the  space  between  the  last  rib  and 
the  crest  of  the  ilium,  and  oedema  of  the  skin,  point  to  perinephritic 
abscess.  If  the  collection  of  pus  lies  anteriorly  the  patient  is  more 
apt  to  lie  with  the  thigh  flexed,  and  to  complain  of  pain  radiating 
into  and  about  the  hip-joint  and  the  testis.  Bending  of  the  trunk 
toward  the  affected  side  is  said  to  be  a  valuable  diagnostic  sign.  The 
urine  is  clear  unless  a  pyelitis  coexists.  The  condition,  instead  of 
beginning  abruptly,  may  have  an  insidious  onset  and  a  prolonged 
course  with  very  moderate  constitutional  symptoms. 

Differential  Diagnosis. — From  renal  calculus,  by  the  presence  of 
constitutional  disturbance  and  by  physical  examination.  From  ap- 
pendicitis, by  the  history  and  position  of  the  pain  and  swelling,  which 
also  holds  for  empyema  of  the  gall  bladder.  From  psoas  abscess ; 
the  swelling  and  pain  here  are  anterior  to  the  anterior  axillary  line, 
and  the  pus  tends  to  point  in  the  groin.  From  pyelitis  and  pyone- 
phrosis the  diagnosis  is  sometimes  difficult,  as  they  may  coexist. 
The  presence  of  an  indefinite  fluctuating  mass  points  to  abscess.  In 
doubtful  cases  the  use  of  an  aspirating  needle  would  be  justifiable. 
From  spinal  and  hip-joint  disease,  by  the  characteristic  deformities 
and  limitation  of  motion.  From  lumbago,  by  the  fever,  tenderness 
and  swelling,  and  lateral  inclination. 

Prognosis.— T\d%  is  generally  good  provided  free  drainage  is 
established.  Some  few  cases  of  violent  infection  in  patients  already 
enfeebled  by  old  kidney  trouble  die  in  spite  of  all  treatment. 


942  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

SECTION  VII 
DISEASES   OF   THE   XERYOUS  SYSTEM 

{See  also  pages  4SI  to  559) 

Prep  ABED  by  Smith  Ely  Jelliffe,  M.  D.,  axd  A.  B.  Boxar,  M.  D. 

I.  THE  NEUROSES:    DISEASES  OF   UNDETERMINED  PATHOGENY 

A.    SENSORI-MOTOR    NEUROSES 

I.  Epilepsy. — Causes. — Usually  develops  after  10  and  before  20 
years  of  age,  commonly  between  10  and  15,  and  may  appear  late 
in  life.  In  America  males  are  affected  oftener  than  females.  The 
predisposing  causes  are :  Injuries  at  birth,  heredity,  alcoholism, 
syphilis,  the  intermarriage  of  neurotic  persons,  and  powerful  emo- 
tions during  pregnancy.  Exciting  causes  are  :  Fright,  injuries  to 
the  head,  rickets  at  time  of  dentition,  masturbation,  sunstroke, 
syphilis,  alcoholism,  and  infectious  diseases,  especially  scarlet  fever. 
Reflex  causes  (so-called)  are  worms,  dyspepsia,  lesions  involving  the 
peripheral  nerves,  and  ocular,  auditory,  and  dental  irritations. 

Symptoms. — In  the  grande  mal,  or  major  attacks,  the  patient  may 
for  a  few  hours,  or  perhaps  a  day  before  an  attack,  suffer  from  general 
malaise,  vertigo,  or  irritability.  For  a  description  of  the  attack  see 
page  72.  There  may  be  a  temporary  exhaustive  paralysis  immediately 
following  the  attack,  with  loss  of  knee-jerk.  The  dilatation  of  the 
pupils  subsides  and  they  often  oscillate.  Slight  transient  glycosuria 
or  albuminuria  may  be  present.  The  urea  is  not  increased,  but  the 
earthy  phosphates  are.  One  attack  may  be  followed  by  others,  hour 
after  hour — the  status  epilepticus.  This  condition  usually  lasts  for 
less  than  12  hours,  but  may  last  for  1  or  more  days. 

Minor  attacks  {petit  mal)  may  occur  in  which  the  patient  sud- 
denly stops  whatever  he  may  be  doing,  the  features  become  fixed, 
the  face  is  pale,  the  eyes  are  open  and  the  pupils  dilated,  there  is 
slight  twitching  of  the  muscles  of  the  face  or  limbs,  and  a  momen- 
tary loss  of  consciousness.  The  attack  lasts  only  for  a  few  seconds, 
and  the  patient  may  immediately  continue  his  work  or  conversation 
from  the  point  at  which  it  was  interrupted.  He  does  not  fall,  and  is 
unconscious  of  what  has  occurred  except  that  he  knows  he  has  had 
an  attack.  Occasionally  there  are  forced  movements,  in  which  the 
patient  turns  around  a  few  times,  or  runs,  or  takes  a  few  steps  in  a 
confused  automatic  manner. 

Psychical  epilepsy  may  consist  of  sudden,  violent  automatic  move- 
ments, or  of  sudden  exhibitions  of  maniacal  excitement  following  or 


DISEASES  OF  THE  NERVOUS  SYSTEM  943 

replacing  a  minor  attack.  While  in  this  condition  crimes  of  violence 
may  be  committed.  Earely  patients  may  go  into  a  state  of  som- 
nambulism, in  which  they  perform  automatically  acts  to  which  they 
are  accustomed.  This  has  been  called  somnambulic  epilepsy,  and 
when  it  occurs  without  a  preceding  minor  attack  it  is  by  some  con- 
sidered a  "  psychical  epileptic  equivalent." 

The  aura  may  be  a  feeling  of  prickling  or  numbness  which  be- 
gins in  the  hand  and  goes  upward  until  it  reaches  the  head,  when 
the  patient  becomes  unconscious.  A  sensation  of  something  passing 
from  the  epigastrium  upward  toward  the  throat  is  a  common  aura. 
Psychical  aurse  are  not  infrequent.     (See  also  page  72.) 

The  most  frequent  form  of  epilepsy  is  that  with  severe  attacks  ; 
next  a  combination  of  severe  and  minor  attacks ;  then  minor  attacks 
alone ;  and,  least  frequent,  the  psychical  form.  The  attacks  may 
occur  from  once  or  twice  a  year  to  a  number  of  times  a  day.  Minor 
attacks  may  occur  oftener,  generally  every  day.  It  appears  that  at- 
tacks occur  mainly  in  the  waking  hours.  In  most  cases  of  epilepsy 
there  is  a  gradual  mental  deterioration,  which  may  be  very  slight. 
There  is  irritability  of  temper,  inability  to  fix  the  attention  or  carry 
out  a  purpose,  selfishness,  and  a  weak  memory.  A  lack  of  moral 
sense  and  vicious  impulses  may  appear  in  children  with  epilepsy. 
Epileptics  are  not  of  robust  constitution,  are  undersized,  and  for  the 
most  part  present  some  stigmata  of  degeneration  (page  507). 

Diagnosis.— ^i^ile^sy  must  be  distinguished  from  hysteria  and 
various  symptomatic  and  toxic  convulsions.  The  cardmal  points 
are  :  The  aura,  the  cry,  the  tonic  convulsion,  the  sudden  loss  of  con- 
sciousness, the  biting  of  the  tongue,  the  dilated  pupils,  and  the 
emptying  of  the  bladder.  Hysterical  patients  do  not,  as  a  rule,  bite 
the  tongue  or  hurt  themselves  when  they  fall,  and  their  movements 
are  more  co-ordinate.  Especial  pains  should  be  taken  to  diagnose 
true  epilepsy  from  many  of  the  reflex  epileptic  phenomena  (verti- 
goes, etc.)  which  occur  in  "nervous  children."  These  cases  are 
those  so  frequently  reported  as  being  cured  by  trifling  surgical  pro- 
cedures, such  as  circumcision,  cutting  of  eye  muscles,  et  al. 

Prognosis.— k  small  number  of  epileptics  recover.  Dementia 
or  insanity  develops  in  about  10  per  cent,  and  these  are  incurable. 
In  general  life  is  somewhat  shortened  by  epilepsy.  Death  may  occur 
as  the  result  of  the  staUis  epilepticus,  but  it  is  rare  in  other  phases 
of  the  disease. 

II.  Vertigo.— See  page  58. 

III.  Migraine,  Hemicrania  {Sick  Headache).— This  is  best 
regarded  as  a  constitutional  disease.  Begins  usually  at  puberty, 
sometimes  as  early  as  the  2d  year,  and  is  most  frequent  in  females. 


944  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

It  is  occasionally  hereditary  in  neurotic  families  with  a  history  of 
gout,  rheumatism,  epilepsy,  or  neuralgic  disorders.  Overwork  is  an 
occasional  cause  in  children.  Autotoxaemia  from  uric  acid  and  com- 
plex intestinal  poisons,  errors  in  refraction,  overwork,  shock,  injury, 
and  exhausting  disease  are  causative  factors. 

Symptoms. — There  may  be  premonitory  symptoms,  a  feeling  of 
depression  and  general  malaise,  for  a  few  hours  or  a  day.  The  attack 
usually  begins  during  the  morning,  in  the  forehead  or  occiput,  on 
one  side  of  the  head,  increasing  in  severity  and  extent  until  the  whole 
head  is  affected.  The  pain  is  tense,  throbbing,  blinding,  and  in- 
creased by  jars,  noises,  and  light.  Frequently  there  is  dimness  and 
restriction  of  the  visual  field,  sometimes  hemianopia,  and  flashes  of 
light,  or  light  or  dark  spots  dancing  before  the  eyes.  Xausea  and 
vomiting  are  usually  present.  Xot  infrequently  a  feeling  of  stupor, 
confusion  of  ideas,  disturbances  of  memory,  vertigo,  and  tinnitus  au- 
rium  are  present.  These  headaches  are  often  called  "  bilious  head- 
aches "  from  the  character  of  the  vomited  matter.  Liver  or  gastric 
disturbances,  however,  do  not  cause  migraine.  The  pulse  is  small, 
hard,  and  perhaps  slow,  and  the  patient's  face  is  usually  pale,  rarely 
flushed.  The  length  of  an  attack  varies  from  6  hours  to  2  or  3  days, 
lasting,  as  a  rule,  from  6  to  24  hours.  When  the  pain  becomes  less 
severe  the  patient  goes  to  sleep,  and  usually  awakes  the  next  morning 
feeling  well.  The  attacks  occur  periodically — weekly,  fortnightly, 
or  monthly — and,  in  women,  especially  at  the  time  of  the  menstrual 
period.  The  severity  and  frequency  of  the  attacks  lessen  at  or 
about  the  time  of  the  menopause,  and  generally  then  disappear 
altogether. 

Rheumatism,  anaemia,  or  dyspepsia  may  coexist,  and  neuralgia  be 
added  to  the  ordinary  pain  of  the  disease.  When  the  pains  are  neu- 
ralgic there  are  usually  no  visual  or  aural  disorders,  as  in  migraine. 

Diagnosis. — The  cardinal  points  are  :  heredity ;  periodical  char- 
acter of  the  attacks,  and  their  location  ;  the  visual  and  aural  symp- 
toms ;  and  the  nausea  and  vomiting.  Renal  or  organic  brain  disease 
or  neuralgia  may  coexist  with  migraine.  Multitudinous  abortive  and 
mixed  types  occur.  Some  of  these  may  be  designated  as  migrainoid 
states.     The  prognosis  for  cure  is  not  good. 

IV.  Hysteria. — Causes. — Occurs  most  frequently  between  the 
ages  of  15  and  25  in  females ;  at  a  somewhat  later  age  in  males ;  in 
children,  between  11  and  15,  perhaps  as  early  as  8,  years  of  age.  Fe- 
males are  affected  much  oftener  than  men.  The  chief  predisposing 
cause  is  heredity,  with  a  history  of  the  disease,  or  of  some  psychosis 
or  neurosis  in  the  parents.  Exciting  causes  are  :  powerful  emotions 
(especially  fear),  anxiety,  excitement,  worry,  injuries  accompanied  by 


DISEASES  OF  THE  NERVOUS  SYSTEM  945 

mental  shock,  imitation,  excesses  (mental,  bodily,  sexual),  syphilis, 
lead,  alcohol,  tobacco,  hemorrhages,  and  the  infectious  fevers. 

Symptoms. — la  hysteria  minor  the  patient  is  very  nervous,  with 
hyperaesthesias,  pains,  and  crises  of  an  emotional  character.  Girls 
and  young  women  are  the  usual  subjects  of  hysteria  minor.  The 
patient  becomes  extremely  sensitive,  excitable,  mentally  depressed, 
and  there  is  a  marked  loss  of  emotional  control.  She  yields  to 
impulses,  and  cries  and  laughs  very  easily.  There  may  be  spinal 
pains,  and  severe  and  chronic  vertical  headaches.  When  excited 
there  may  be  sensations  of  tickling,  fulness,  or  choking  in  the  throat 
— the  "globus  hystericus" — and  occasionally  fleeting  attacks  of 
chilliness  and  trembling.  More  rarely  there  are  vasomotor  disturb- 
ances, resulting  in  cold  extremities  and  flushings.  Sleep  is  usually 
more  or  less  disturbed.  Attacks  of  headache  or  vomiting  or  of  great 
mental  excitement  may  occur.  There  may  be  somnambulism  or, 
under  excitement,  attacks  of  cerebral  automatism,  in  which  she  may 
perform  acts  of  which  she  will  be  entirely  ignorant  after  the  seizure. 
After  the  crises  there  is  usually  a  large  quantity  of  light-coloured 
urine  passed.  In  hysteria  minor  there  are,  as  a  rule,  no  anaesthesias, 
paralyses,  or  decided  convulsions. 

Between  the  crises  of  hysteria  major  the  patient  may  be  well,  but 
generally  there  are  characteristic  paralyses,  contractures^  and  setisory 
distil rhances.  Frequently  there  are  anaesthesia  and  hyperaesthesia  of 
the  skin  and  mucous  membranes,  and  anaesthetic  disorders  of  the 
special  senses.  Anaesthesia  of  the  skin  occurs  as  an  hemianaesthesia 
(most  common),  or  a  segmental  or  disseminated  anaesthesia  (Figs. 
192,  page  531 ;  and  194,  page  533).  The  pain  sense  is  chiefly  af- 
fected with  a  lesser  impairment  of  the  tactile  and  thermal  sensibil- 
ities. Ansesthesia  is  found  more  frequently  upon  the  left  side  of  the 
body.  The  skin  reflexes  are  usually  absent.  With  hemianaesthesia 
there  is  usually  some  hemiplegia  and  occasional  tremor,  and  in  seg- 
mental anaesthesia  often  some  paralysis  of  the  part.  There  is  often  an 
anesthetic  condition  of  the  retina,  causing  a  concentric  limitation  of 
the  visual  field  and  a  disturbance  in  the  colour  sense.  Vision  may 
be  impaired  in  both  eyes,  or  completely  lost  in  one  eye,  the  latter 
especially  with  hemianesthesia,  and  on  the  same  side  the  senses  of 
hearing  and  smell  may  be  impaired.  The  sense  of  taste  is  impaired 
or  abolished,  perhaps  only  on  the  back  part  of  the  tongue  and  palate. 

Hyperesthesia  is  found  in  small  patches ;  in  women,  most  com- 
monly over  the  ovaries ;  in  men,  over  the  corresponding  regions  and 
on  the  scrotum.  They  are  also  found  below  the  breasts,  along  the 
spine  and  in  the  epigastrium,  and  are  sensitive  to  pressure,  which 
causes  various  kinds  of  paroxysms— hysterogenic  zones  (Fig.  193). 


946  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Headaches,  chiefly  vertical  or  parietal,  are  frequent,  and  the  pain 
is  of  a  sharp,  boring  kind,  at  times  very  severe.  Facial  and  inter- 
costal neuralgias,  migraine,  and,  more  often,  pains  along  the  spine 
occur.     There  may  be  attacks  of  pseudo-angina. 

Choreic  and  ataxic  movements,  tremor,  contractures,  amyosthe- 
nia,  and  paralyses  occur  in  hysteria  major.  The  paralyses  are  usu- 
ally hemiplegias,  paraplegias,  and  monoplegias.  The  onset  of  hys- 
terical hemiplegia  is  sudden,  and  the  left  side  is  more  often  affected. 
The  face  usually  escapes  and  the  paralysis  is  not  complete.  "When 
walking,  the  patient  drags  the  affected  leg  after  him,  instead  of  swing- 
ing it  around  in  a  half  circle  as  in  organic  hemiplegia.  The  knee- 
jerk  is  usually  not  exaggerated,  and  may  even  be  absent  for  a  time. 
The  monoplegias  rarely  affect  the  face,  usually  an  arm  or  leg,  or 
the  muscles  of  the  larynx  or  of  the  eye.  Electrical  reactions  are 
normal,  and  atrophy,  if  present,  is  slight.  The  adductors  are  involved 
in  hysterical  paralysis  of  the  larynx,  and  the  patient  is  unable  to 
speak  aloud  (hysterical  aphonia,  usually  sudden).  Hysterical  para- 
plegia is  frequent,  often  with  much  pain  in  the  back — the  condition 
of  "  spinal  concussion."  The  knee-jerks  may  be  normal  or  increased, 
never  lost.  There  may  be  a  short  or  false  clonus,  and  the  sphincters 
are  not  involved.  Amyosthenia  is  frequent,  the  patient's  legs  sud- 
denly becoming  weak  or  paralyzed,  or  the  arm  giving  out  when  lift- 
ing some  object.     This  symptom  usually  precedes  a  paralysis. 

In  some  cases  of  hysteria  contractures  of  the  muscles  may  occur 
as  the  result  of  slight  mechanical  irritation.  These  may  be  temporary, 
or  may  last  for  a  long  time.  The  legs,  arms,  and  facial  muscles  are 
most  affected.     Tremor  of  all  varieties  may  be  present. 

In  hysteria  there  is  marked  emotional  instability  and  craving  for 
sympathy,  lack  of  self-control,  and  weakness  of  the  will.  The  mood 
constantly  changes ;  there  is  increased  sensitiveness,  and  exaggera- 
tion of  the  Ego.  There  is  a  limitation  of  the  field  of  consciousness 
as  there  is  of  the  field  of  vision.  The  hysterical  person  can  think  of 
nothing  but  her  personal  feelings.  There  is  an  undercurrent  of 
suggestibility  in  the  mental  state,  through  which  ideas  become 
fixed  and  patients  become  self-hypnotized,  and  believe  they  have 
various  ailments  which  have  no  objective  existence. 

Constipation,  dyspepsia,  anorexia,  and  sometimes  regurgitation 
of  food,  or  vomiting,  occur.  The  specific  gravity  of  the  urine  is 
often  low,  especially  that  of  the  large  amount  of  light-coloured  urine 
which  is  always  passed  after  hysterical  attacks.  There  may  be  re- 
tention of  urine.  The  vasomotor  symptoms  consist  of  flushings 
and  pallor,  and  sometimes  coldness  and  oedema  of  the  extremities. 
The  oedema  may  be  ordinary,  or  have  a  peculiar  bluish  tint  ( "  blue 


DISEASES  OF  THE  NERVOL^S  SYSTEM  947 

oedema  "),  and  not  pit  on  pressure.  The  hands  are  usually  affected, 
and  their  surface  temperature  is  somewhat  below  normal.  The  con- 
dition resembles  Raynaud's  disease,  but  gangrene  never  occurs. 
Anaemia  is  usually  present,  and  there  may  be  irregular  fever. 

The  crises  of  hysteria  major  are  emotional,  convulsive,  neuralgic, 
or  gastric;  paroxysms  of  coughing,  hiccoughing,  or  sneezing;  or 
attacks  of  catalepsy,  amnesia,  cerebral  automatism,  trance,  and 
lethargy.  The  first  group  are  the  most  common.  The  emotional 
crises  are  similar  to  those  which  occur  in  hysteria  minor.  The 
*'  globus  hystericus  "  is  almost  always  present. 

Two  forms  of  convulsions  in  hysteria  major  are  described:  the 
ordinary  form^  which  also  occurs  in  hysteria  minor,  and  the  hys- 
teroid  attack,  or  hystero-epilepsy.  In  the  former  the  patient  suddenly 
falls,  and  various  irregular  movements  of  the  body  occur.  In  a  more 
severe  attack  the  hands,  arms,  and  fingers  are  flexed  and  the  legs 
and  feet  extended.  Usually  the  eyes  are  closed.  The  pupils  are 
dilated,  and  frequently  there  is  convergence,  or  perhaps  irregular 
movements,  of  the  eyeballs.  Sensation  may  be  diminished  over  the 
body  and  on  the  conjunctivae.  The  patient  never  bites  her  tongue  or 
injures  herself  in  any  way,  although  she  may  bite  her  lips.  She  may 
scream  or  make  noises  during  the  attack.  The  attack  may  last 
from  a  half  hour  to  several  hours.  The  convulsion  may  consist 
simply  of  a  chill-like  tremor ;  in  other  cases  simply  a  slight  rigidity 
of  the  body,  or  a  series  of  rhythmical  movements  of  the  limbs  or 
trunk.  Opisthotonus  may  be  the  chief  manifestation ;  in  others  the 
patient  falls  and  lies  unconscious,  as  if  sleeping,  for  some  minutes, 
or  it  may  be  an  hour.  Marked  mental  excitement  may  accompany 
or  follow  the  attack.  During  the  attacks  there  is  usually  a  con- 
sciousness of  what  is  going  on,  and  if  spoken  to  sternly  the  patient 
will  often  respond.  Pressure  upon  a  hysterogenic  zone  may  cause 
the  attack  to  cease,  especially  in  women. 

Hystero-epilepsy  is  not  epilepsy,  but  is  a  true  hysteria.  In  this 
form  of  hysterical  attack  there  is  a  prodromal  stage ;  an  epileptoid 
stage,  lasting  from  1  to  3  minutes ;  a  stage  of  contortions  and  grand 
movements  lasting  1  to  3  minutes ;  an  emotional  stage,  lasting  from 
5  to  15  minutes ;  and,  at  times,  a  stage  of  delirium. 

Diagnosis.— The  cardinal  points  are:  The  hysterical  temperament 
of  the  patient,  the  history  of  previous  hysterical  crises,  the  presence 
of  some  of  the  various  stigmata  of  hysteria,  the  transient  and  vary- 
ing character  of  the  paralyses,  anaesthesias,  and  other  stigmata,  and 
the  condition  of  the  deep  reflexes.     See  also  (2),  page  73. 

Pro^«05i>.— Favourable  in  children.  In  hysteria  minor  the  prog- 
nosis depends  upon  the  severity  of  the  disease.     In  hysteria  major 


948  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

and  hysteria  associated  with  organic  disease,  the  prognosis  is  very 
unfavourable.     Males  frequently  recover  if  treated  vigorously. 

V.  Neurasthenia. — Causes. — Occurs  most  frequently  between 
the  ages  of  20  and  50,  but  may  occur  between  the  ages  of  10  and  20, 
and  also  between  50  and  70.  Men  and  women  are  equally  affected. 
The  disease  is  found  more  frequently  in  cities,  and  among  the  edu- 
cated classes.  The  chief  predisposing  cause  is  the  inheritance  of 
a  neuropathic  tendency.  The  exciting  causes  are :  severe  shocks, 
with  or  without  injury,  as  many  cases  of  so-called  "  traumatic  neuro- 
ses "  are  simply  neurasthenia ;  overwork  and  worry ;  excessive  use  of 
stimulants  and  narcotics ;  sexual  excesses  ;  dietetic  imprudences  ;  and 
the  infections  of  syphilis,  malaria,  typhoid,  influenza,  or  other  debili- 
tating diseases.  Auto-intoxication  and  the  uric-acid  diathesis  are 
also  put  forth  as  causes  of  neurasthenia  by  many  writers. 

Symptoms. — These  are  mainly  subjective.  The  initial  symptoms 
are  usually  headache  or  mental  depression.  The  headache  is  more 
commonly  occipital  or  diffuse  in  character  and  is  chronic  and  persist- 
ent. It  begins  in  the  morning  and  lasts  all  day,  but  does  not  keep 
the  patient  awake  at  night.  There  may  be  a  feeling  of  general  men- 
tal depression,  inability  to  concentrate  the  mind  upon  work,  mental 
confusion,  marked  irritability,  excessive  sensitiveness  and  morbid  re- 
serve, or  undefinable  fears.  Sleep  is  not  good,  and  there  may  be  per- 
sistent insomnia,  or  the  sleep  is  not  refreshing.  There  are  various 
parassthesiae  of  the  head,  mainly  feelings  of  constriction,  tenderness, 
burning,  or  pressure.  Paresthesias  of  the  hands  and  limbs  occur, 
and  there  may  be  pain  or  a  feeling  of  weakness  in  the  back  of  the 
neck  and  along  the  spine.  Slight  but  frequent  vertigo  is  occasion- 
ally present,  and  there  may  be  buzzings  in  the  ears  and  head  and 
spots  before  the  eyes. 

There  is  a  general  muscular  weakness  in  a  large  proportion  of  the 
cases.  The  patient  may  not  appear  weak,  but  he  tires  quickly.  There 
is  often  a  tremor  of  the  hands,  tongue,  lips,  and  eyelids,  and  some- 
times twitching  of  the  muscles  of  the  face  and  tongue.  The  deep 
reflexes  are  usually  much  exaggerated,  and  the  skin  reflexes  increased. 
The  condition  of  the  reflexes,  however,  varies  greatly.  The  patient's 
eyes  tire  easily,  although  his  vision  is  good.  Astigmatism,  hyper- 
metropia,  and  asthenopias  are  frequent.  The  field  of  vision  is  not 
contracted.  The  pupils  are  frequently  dilated,  and  in  some  cases 
are  sluggish  to  light.  Occasionally  there  is  excessive  mobility  of 
the  iris,  inequality  of  the  pupils  ;  and  hyperacusis  or  dysacusis.  The 
sexual  function  is  irritable  and  weak.  Xocturnal  emissions  are  fre- 
quent, and  there  may  be  partial  or  complete  impotence.  The  pulse 
is  often  markedly  accelerated  from  a  slight  cause. 


DISEASES  OP  THE  NERVOUS  SYSTEM  949 

Symptoms  due  to  vasomotor  disturbance  are  cold  feet  and  hands, 
palpitation  of  the  heart,  hot  flashes,  pseudo-angina,  dermographic 
skin,  fulness  and  noises  in  the  head,  vertigo,  a  fluttering  feeling  in 
the  abdomen,  and  paroxysms  of  profuse  perspiration.  In  neuras- 
thenics there  is  much  stomach  and  intestinal  indigestion  and  con- 
stiijation.  A  "  mucous  enteritis  "  sometimes  occurs.  At  times  a 
temporary  albuminuria  or  a  transient  glycosuria  may  be  found. 

Diagnosis. — The  disease  must  be  distinguished  from  hypochon- 
driasis, melancholia,  the  initial  stage  of  general  paresis,  hysteria 
(major  and  minor),  simulation,  and  the  effects  of  some  other  consti- 
tutional disease.  The  border  line  between  neurasthenia  and  most  of 
these  conditions  is  not  very  distinct  in  the  initial  stages. 

The  following  are  some  of  the  different  forms  of  neurasthenia : 
Hystero-neurasthenia,  traumatic  neurasthenia,  primary  neurasthenia, 
acquired  neurasthenia  and  lithaemia,  climacteric  neurasthenia,  spinal 
irritation,  neurasthenia  with  fixed  ideas  or  the  anxiety  neurosis,  neu- 
rasthenia gravis,  and  angiopathic  neurasthenia. 

Prognosis. — The  disease  is  usually  chronic,  and  runs  a  course  of 
from  1  to  8  or  9  years.     Eecovery  is  frequent,  so  also  are  relapses. 

YI.  Traumatic  Neuroses. — C«ws?«.— Trauma  may  be  the  ex- 
citing cause  in  the  following  conditions :  (1)  The  nervous  condition 
following  railway  and  other  injuries,  especially  when  associated  with 
fright.  (2)  Xeurasthenia.—"  Traumatic  neurasthenia"  or  "neuro- 
sis," or  "railway  spine,"  does  not  differ  from  neurasthenia  due  to 
other  causes  except  that  coincident  surgical  troubles  may  be  present. 
It  is  described  under  neurasthenia.  (3)  Hysteria.— "  Traumatic 
hysteria  "  does  not  differ  from  hysteria  due  to  other  causes  except  by 
the  presence  of  surgical  troubles,  and  in  its  sudden  appearance.  It 
usually  takes  the  form  of  hysteria  major.  (4)  Trauma  may  also 
produce  minute  multiple  hemorrhages  throughout  the  nervous  cen- 
tres. The  resulting  organic  symptoms  are  added  to  the  hysterical 
and  neurasthenic  symptoms  usually  present. 

Stj mpf am s.— These  are  headache  and  vertigo,  with  lessened  power 
of  application,  depression,  irritability,  and  hypochondriasis.  The 
sight  is  disturbed,  and  there  may  be  a  contracted  field  of  vision  and 
sometimes  optic  atrophy.  Tremor,  inco-ordination,  numbness,  prick- 
ling, and  anesthesia,  not  limited  to  one  half  of  the  body,  may  be 
present.  The  reflexes  are  apt  to  be  exaggerated.  The  muscular  move- 
ments  are  slow  and  weak.  Control  of  the  bladder  may  be  impaired, 
and  there  may  be  some  stiffness  and  pain  in  the  back.  The  condi- 
tion may  resemble  that  of  multiple  sclerosis.  Traumatism  may  be 
the  exciting  cause  of  tabes,  insanity,  and  inebriety  in  those  predis- 
posed to  these  diseases,  or  of  a  cerebral  tumour.  The  shock  and  the 
62 


950  DIAGNOSIS,   DIRECT  AXD  DIFFERENTIAL 

mental  impression  are  more  powerful  factors  in  the  production  of 
functional  neuroses  than  the  physical  injury. 

Diagnosis. — Malingering  must  be  guarded  against.  The  essentials 
are  the  history  of  trauma  and  the  points  already  given  under  the 
headings  of  neurasthenia  and  hysteria. 

B.    MOTOR    NEUROSES 

I.  Chorea  (St.  Vitus'' s  Dance^  Sydenham'' s  Chorea). — Causes. — Oc- 
curs most  frequently  between  the  ages  of  5  and  15,  but  may  appear 
after  20  or  even  in  old  age.  Girls  are  affected  more  often  than  boys. 
It  occurs  with  the  greatest  frequency  in  the  spring,  next  in  the 
autumn,  winter,  and  summer.  There  is  some  slight  heredity.  The 
exciting  causes  are  mental  worry,  rheumatism,  fright,  and  injury 
(seldom).  Endocarditis  frequently  develops.  Other  causes  are  preg- 
nancy ;  infectious  fevers ;  reflex  irritation  from  nasal  disease,  or 
sexual  disorders ;  overstudy ;  and  intestinal  irritation  from  worms. 
Anaemia  and  malnutrition  are  frequent  predisposing  causes,  and  ma- 
laria may  be  a  factor.  There  is  a  widespread  belief  in  its  being  a 
bacterial  disease,  but  a  definite  organism  is  not  yet  known. 

Symptoms. — The  onset  is  usually  slow,  lasting  1  or  2  weeks,  but 
may  be  sudden.  There  are,  at  first,  irregular  twitchings  of  the  hand 
of  one  side,  and  the  patient  may  drop  his  knife  or  fork.  Winking, 
grimacing,  and  twitching  of  the  facial  muscles  become  manifest. 
After  a  time  the  child's  foot  and  leg  are  involved  and  he  may  stum- 
ble in  walking.  In  a  week  or  so  the  other  side  of  the  body  is  also 
affected,  usually  not  to  the  same  extent.  The  disease  reaches  its 
height  in  from  3  to  4  weeks.  At  this  time  the  movements  are  nearly 
continuous,  the  child  can  hardly  use  his  hands,  and  walking  is  dif- 
ficult. The  speech  is  indistinct,  confused,  and  difficult,  and  the 
muscles  of  respiration  may  be  affected.  Usually  the  movements 
continue  whether  the  muscles  are  at  rest  or  acting.  In  some  cases 
they  are  present  only  when  the  limbs  are  at  rest,  in  others  chiefly 
when  volitional  acts  are  attempted.  During  sleep  the  twitching 
generally  stops.  In  severe  cases  there  may  be  attacks  of  mental  ex- 
citement or  delirium.  The  most  common  mental  impairment  is  irri- 
tability of  temper  and  some  dulness  of  intellect. 

The  general  physical  condition  is  impaired,  there  are  anorexia, 
constipation,  loss  of  flesh,  and  ansemia.  Excitement  or  exertion 
increases  the  movements.  The  reflexes  are  diminished  and  the  knee- 
jerk  may  be  absent.  There  is  no  real  paralysis,  although  the  muscles 
are  weak.     Their  electrical  irritability  is  somewhat  increased. 

In  maniacal  chorea  there  is  delirium  with  delusions  and  hallucina- 
tions.    The  mania  after  a  week  or  so  is  succeeded  by  a  condition  of 


DISEASES  OF  THE  NERVOUS  SYSTEM  951 

apathy  and  dulness.  This  form  usually  occurs  in  adult  females  and 
is  serious.  In  paralytic  chorea  (usually  in  children)  one  arm  sud- 
denly becomes  weak  and  powerless,  perhaps  with  slight  twitchings. 
In  cJiorea  of  adult  life  and  in  senile  chorea  men  are  more  often 
affected  than  women,  and  it  is  apt  to  become  chronic. 

The  duration  of  chorea  may  be  from  6  weeks  to  6  months,  but 
usually  it  lasts  from  10  to  12  weeks.  The  disease  may  continue  for 
years,  each  improvement  being  followed  by  a  relapse.  Relapses  occur 
in  nearly  one  half  of  the  cases. 

Diagnosis.— The  peculiar  twitching  movements  are  characteristic. 
The  disease  must  be  distinguished  from  hysterical  spasms,  which 
include  myoclonus,  saltatory  chorea,  convulsive  tic,  and  chorea  major. 

Prognosis.— 'Sea.T\y  all  cases  recover.  In  very  few  instances  the 
disease  in  adults  has  a  fatal  termination. 

II.  Huntington's  (Hereditary)  Chorea.— Cawses.— Occurs 
with  about  equal  frequency  in  males  and  females,  and  usually  between 
the  ages  of  30  and  50  years.    The  disease  is  always  directly  hereditary. 

Symptoms. — Twitchings  in  the  face  are  first  noticed,  then  in  the 
arms  and  legs.  There  is  progressive  mental  impairment,  a  tendency 
to  melancholy,  and  finally  dementia.  The  disease  is  chronic,  usually 
lasting  from  10  to  20  years,  and  the  progtiosis  is  bad. 

III.  Habit  Spasm  (or  Chorea). — A  condition  characterized 
by  the  occurrence  of  co-ordinate  movements.  In  different  cases  this 
movement  may  be  a  gesture,  or  a  shrug  of  the  shoulders,  or  a  winking 
of  the  eyes,  or  a  sniff,  or  some  peculiar  grimace.  These  movements 
are  often  seen  in  children,  and  may  be  the  remains  of  an  attack  of 
true  chorea,  or  may  be  a  chronic  convulsive  tic  from  the  beginning. 

IV.  Saltatory  Spasm. — Occurs  in  both  sexes  and  at  all  ages. 
The  patients  are  hysterical  or  neurasthenic.  The  exciting  cause  is 
the  weight  of  the  body  upon  the  feet.  Violent  contractions  of  the 
calf  and  hip  muscles  occur  the  instant  the  feet  touch  the  floor,  but 
all  the  muscles  may  be  involved.  The  peculiar  muscular  contrac- 
tions cause  the  patient  to  jump,  and  may  be  so  violent  as  to  throw 
him  to  the  ground.     The  disorder  is  probably  an  hysterical  spasm. 

V.  Facial  Spasm  {Mimic  T/c).— Intermittent,  involuntary 
twitchings  of  the  facial  muscles.  Always  chronic  and  usually  uni- 
lateral Occurs  in  middle  and  later  life,  more  often  in  women.  Pre- 
disposing cause  is  a  neuropathic  constitution.  Exciting  causes  are 
injury,  shock,  anxiety,  and  exposure.  Occasionally  reflex,  from  irri- 
tation of  the  cervico-brachial  nerves  or  some  branch  of  the  trigem- 
inus. Some  organic  disease  may  cause  a  symptomatic  tic,  e.  g.,  post- 
hemiplegic. Symptoms.— Onset  slow.  The  orbicularis  muscle  and 
zygomatic!  are  the  first  affected.     The  spasm  is  clonic,  the  muscles 


952  DIAGNOSIS,   DIEECT   AND  DIFFERENTIAL 

of  the  face  being  affected  by  a  series  of  quick  twitches,  with  intervals 
of  rest.  Occasionally  the  spasm  is  tonic  and  lasts  for  several  seconds. 
There  is  no  pain,  paralysis,  or  atrophy,  and  no  trophic  or  secretory 
symptoms.  The  spasm  m.ay  become  bilateral  after  a  time.  Diagnosis. 
— It  is  distinguished  from  organic  spasm  by  the  fact  that  in  the  latter 
there  are  always  other  symptoms,  and  it  is  usually  unilateral,  while 
mimic  tic  is  bilateral.  There  is  generally  unconsciousness  in  spasm 
from  cortical  disease.  The  spasm  is  tonic  when  it  follows  hemiplegia, 
and  in  hysterical  facial  spasm.  Prog?iosis. — Generally  incurable. 
The  outcome  is  better  if  the  disease  is  due  to  a  reflex  cause. 

VI.  Torticollis  {Wry?ieck). — A  clonic  or  tonic  spasm  of  the 
muscles  supplied  by  the  spinal  accessory,  sometimes  of  other  muscles 
of  the  neck.  (1)  Congenital  "Wryneck. — Caused  by  injury  to  the 
sterno-cleido-mastoid  during  delivery,  or  due  to  intra-uterine  atrophy. 
It  most  often  follows  foot  or  breech  presentations.  There  is  no 
spasm,  but  the  neck  is  drawn  to  one  side  because  of  the  shortness  of 
the  muscle.  (2)  Symptomatic  Wryneck. — Appears  usually  as  a  symp- 
tom of  rheumatic  myositis,  sometimes  of  tumours,  adenitis,  abscesses, 
or  local  syphilis.  Occurs  principally  in  children.  Tenderness  and 
pain  are  always  present.  (3)  Spurious  Wryneck. — An  apparent  or 
real  spasm  of  the  muscles  of  the  neck.  Usual  cause  is  caries  of  the 
spine.  (4)  Spasmodic  Wryneck. — This  condition  is  purely  nervous. 
There  is  spasm  of  the  muscles  supplied  by  the  spinal  accessory ;  some- 
times of  those  innervated  by  the  upper  cervical  nerves. 

Causes. — It  occurs  in  women  more  often  than  in  men,  and  is  a 
disease  of  early  and  middle  adult  life.  Heredity  and  a  neuropathic 
constitution  are  predisposing  factors. 

Symptoms. — There  are  primarily  slight  feelings  of  discomfort  or 
pain  in  the  neck,  soon  followed  by  spasm,  which  is  at  first  clonic  and 
intermittent.  The  sternomastoid  and  the  upper  fibres  of  the  trape- 
zius are  oftenest  affected.  The  head  is  inclined  toward  the  affected 
side,  the  chin  raised,  and  the  head  rotated  to  the  opposite  side. 
The  superior  obliquus  and  complexus  are  more  rarely  involved.  The 
muscles  of  the  opposite  side  may  be  affected,  most  commonly  the 
splenius.  The  disease  may  start  in  one  muscle  and  gradually  involve 
others.  The  spasm  usually  becomes  more  and  more  constant,  until 
finally  it  may  be  tonic.  The  pain  gradually  disappears.  The  unused 
muscles  undergo  atrophy,  while  the  affected  muscles  hypertrophy. 
Facial  asymmetry  may  or  may  not  occur. 

Prognosis. — Xot  fatal,  rarely  cured,  but  sometimes  much  im- 
proved.    Usually  reaches  a  certain  stage  and  remains  chronic. 

VII.  Spasmus  Nutans  {Nodding  'Spasm). —  A  disorder  charac- 
terized by  rhythmical  nodding  or  oscillatory  movements  of  the  head. 


DISEASES  OF  THE  NERVOUS  SYSTEM  953 

Causes. — Occurs  chiefly  in  poorly  nourished  and  anaemic  children. 
It  may  be  due  to  digestive  disorders,  gross  disease  of  the  brain,  basilar 
meningitis,  or  dentition.     Is  sometimes  a  habit  chorea. 

Sy7ji2)toms. — Onset  usually  sudden.  The  attacks,  sometimes  rather 
violent,  last  for  a  few  minutes,  perhaps  hours,  or  are  constant,  ex- 
cept during  sleep.  The  movements  of  the  head  may  be  from  30  to 
60  a  minute,  or  more  or  less.  The  eyes  and  facial  muscles  may  be 
affected.  An  epileptic  attack  may  follow  a  paroxysm.  The  diag- 
nosis is  easy,  and  the  prognosis  depends  upon  the  cause. 

VIII.  Spasmodic  Tic  -with  Coprolalia  {Gilles  de  la  Tour- 
ette's  Disease). — Occurs  in  neurotic  children,  chiefly  boys  6  to  16 
years  of  age,  with  a  neuropathic  family  history. 

Symjytofns. — There  are  attacks  of  irregular,  perhaps  violent,  move- 
ments, involving  at  first  the  upper  extremities,  head,  and  face,  later 
the  whole  body.  The  spasms  can  be  sometimes  controlled  by  the 
will,  but  are  usually  more  severe  afterward.  They  stop  during  sleep. 
After  a  while  the  patient  makes  inarticulate  cries  during  the  attacks, 
or  he  repeats  words  that  he  hears,  or  utters  obscene  or  profane  words 
or  expressions.  These  utterances  are  made  suddenly  and  automatic- 
ally, accompanied  by  grimaces  and  contortions  of  the  facial  muscles. 
The  disease  is  chronic  and  may  last  for  years. 

IX.  Paralysis  Agitans  {Parkifison's  Disease^  Shaking  Palsy). 
— Causes.— Occurs  between  the  ages  of  40  and  70,  most  frequently 
between  50  and  60.  Less  commonly  it  may  occur  in  early  life  after 
puberty.  Affects  males  more  often  than  females.  Predisposing 
causes  are  anxiety,  prolonged  overwork,  and,  rarely,  hereditary  in- 
fluences. Syphilis,  alcohol,  and  sexual  excesses  do  not  seem  to  enter 
into  the  etiology.  The  exciting  causes  are  fright,  acute  mental 
suffering,  exposure  to  cold  and  wet,  injury,  and,  more  rarely,  sudden 
severe  muscular  strain,  acute  rheumatism,  and  fevers. 

Symptoms.— There  are  at  first  aching  pains  in  the  arm,  usually 
the  left,  and  a  tremor  in  the  fingers  of  the  same  hand.  The  tremor 
gradually  extends  to  the  foot  of  the  same  side,  then  to  the  hand  and 
foot  of  the  other  side.  The  face,  tongue,  and  neck  may  be  affected, 
but  more  rarely  and  only  to  a  slight  extent.  There  now  develops  a 
stiffness  of  the  whole  body,  with  contractures  and  shortening  of  all 
flexor  muscles.  The  attitude  of  the  patient  is.characteristic.  The 
head  and  body  are  bent  forward,  the  trunk  is  flexed  on  the  thighs, 
the  forearms  on  the  arms,  the  fingers  are  straight,  but  are  flexed  as  a 
whole  on  the  metacarpus,  and  the  knees  are  slightly  flexed  on  the 
legs.  He  walks  slowly  with  short  and  shuffling  steps.  It  is  difficult 
for  him  to  rise  from  a  chair,  to  start  to  walk,  to  stop,  or  to  turn  cor- 
ners.    There  is  often  a  feeling  of  propulsion  or  retropulsion,  more 


954  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

rarely  of  lateropulsion.  The  voice  is  characteristically  high-pitched, 
weak,  and  monotonous,  with  difficulty  in  beginning  a  sentence,  but 
when  started  the  patient  talks  rapidly. 

There  may  be  sensations  of  heat,  cold,  fatigue,  nervousness,  and 
restlessness.  There  are  often  aching  pains,  usually  in  the  forearms 
or  legs,  more  rarely  neuralgic  pains.  Muscular  weakness  is  marked, 
coming  on  early  and  slowly  increasing.  There  are  no  paralyses.  The 
deep  reflexes  may  be  exaggerated  and  there  may  be  a  clonus,  but 
usually  they  are  normal.  Often  there  is  profuse  perspiration,  and, 
as  a  rule,  the  face  is  red  and  flushed.  The  tremor  increases  in  ex- 
tent and  the  rigidity  becomes  more  marked,  until  finally  the  patient 
becomes  bedridden. 

The  tremor  of  paralysis  agitans  is  peculiar  in  that  it  continues 
when  the  hand  or  limb  is  at  rest,  but  ceases  upon  voluntary  move- 
ments. In  the  hand,  the  tremor  moves  the  fingers  and  thumb  as 
a  whole  and  they  vibrate  against  each  other  (the  "  bread-crumbling  " 
movement).  Tremor  of  the  head  and  face  muscles  occurs,  but  the 
trembling  of  the  head  usually  seen  is  communicated  from  the  body. 
The  lips  and  neck  muscles  are  sometimes  the  seat  of  tremor. 

The  rigidity  begins  early  and  increases  until  the  patient  is  help- 
less. The  flexors  are  chiefly  affected.  The  muscular  movements  are 
slow.  The  muscles  of  the  face  are  stiffened,  and  there  is  a  peculiar 
expressionless,  masklike  appearance.  The  patient  is  usually  emo- 
tional. There  may  be  polyuria.  The  disease  may  affect  one  limb, 
or  those  of  one  side  only,  or  rigidity  may  be  the  sole  symptom. 

Diagnosis. — The  cardinal  points  are  :  the  tremor,  ceasing  on  vol- 
untary movements,  the  rigidity  of  the  back,  neck,  and  limbs,  the 
masklike  face,  monotonous  voice,  and  the  characteristic  position  of 
the  hands.  The  disease  must  be  distinguished  from  multiple  sclero- 
sis, senile  tremor,  posthemiplegic  tremor,  and  wryneck  affecting  the 
extensors  bilaterally.  In  multiple  sclerosis  the  tremor  is  jerky  and 
"  intentional  "  ;  there  are  scanning  speech,  nystagmus  and  other  eye 
troubles,  and  often  apoplectiform  attacks  and  paralyses.  In  senile 
tremor  the  head  is  affected  first  and  most,  and  the  patients  are  older. 
In  posthemiplegic  tremor  there  is  a  history  of  hemiplegia,  and  the 
increased  reflexes,  paralysis,  and  tremor  are  unilateral.  The  neck 
muscles  and  frontalis  only  are  involved  in  retrocollis. 

Prognosis. — Good  as  regards  life.     The  disease  can  not  be  cured. 

X.  Writer's  Cramp. — Causes. — Occurs  in  men  oftener  than  in 
women,  most  frequently  between  the  ages  of  25  and  40,  seldom  before 
the  age  of  20  or  after  50.  The  predisposing  causes  are  a  neuro- 
pathic constitution,  heredity,  alcoholism,  worry,  and  other  weakening 
influences.    The  chief  exciting  cause  is  excessive  writing,  especially  if 


DISEASES  OF  THE  NERVOUS  SYSTEM  955 

done  under  a  strain.     Other  causes  are  lead-poisoning,  exposure  to 
wet  and  cold,  albuminuria,  and  local  injuries. 

Symptoms.— Onset  usually  slow.  At  first  there  is  a  slight  stiff- 
ness in  the  fingers,  or  occasional  jerky,  uncertain  movements  of  the 
pen  when  writing.  This  condition  may  last  for  months  or  years. 
The  patient  may  be  depressed  and  fearful  of  paralysis.  Finally, 
writing  becomes  impossible.  If  the  attempt  is  made  there  are  spas- 
modic contractions  of  the  fingers  and  even  of  the  arm.  Usually  all 
other  complex  movements  can  be  performed.  The  arm  aches  and 
occasionally  is  tender  to  pressure,  but  there  is  no  active  paralysis  and 
no  anaesthesia.     Xumbness  and  prickling  are  present. 

In  the  spastic  form  of  the  disorder  there  are  muscular  cramps 
in  half  the  cases.  The  muscles  most  affected  are  those  of  the  thumb 
and  first  three  fingers,  the  flexors  in  writers,  the  extensors  in  teleg- 
raphers. The  forefinger,  thumb,  or  little  finger  alone  may  be  in- 
volved ;  frequently  also  the  supinators  and  pronators.  The  spasm 
is  usually  tonic,  and  there  is  inco-ordination  for  writing  movements. 
The  neuralgic  form  is  the  same  as  the  spastic  form,  with  the 
addition  of  severe  pain  and  fatigue  when  writing.  Rarely  a  trem- 
bling movement  of  the  hand  and  arm  develops  on  an  attempt  at 
writing  (an  "  intention  "  tremor),  and  stops  when  the  attempt  ceases. 
In  the  paralytic  form,  also  rare,  an  overpowering  sense  of  weakness 
and  fatigue  develops  in  the  fingers  and  hand  as  soon  as  the  patient 
hegins  to  write.  The  pen  may  drop  from  the  fingers.  The  arm 
aches,  and  may  become  painful  if  the  attempt  is  continued. 

The  patient  may  be  emotional,  nervous,  and  at  times  mentally 
depressed.  There  may  be  vertigo,  insomnia,  sensations  of  numb- 
ness, prickling,  weight,  pressure,  and  constriction,  and  pains  and 
weariness,  perhaps  with  some  hyperaesthesia,  and  occasional  head- 
aches. When  the  nerves  are  involved  there  may  be  local  sweating, 
dryness  of  the  skin,  cracking  of  the  nails,  or  a  passive  congestion 
of  hand  and  arm.  In  severe  cases  the  condition  of  the  fingers  is 
suggestive  of  chilblains.  The  electrical  reactions  are  variable.  In 
the  early  stage  the  irritability  is  increased,  in  the  later  stages  it 
is  decreased,  to  both  forms  of  current. 

Diagnosis. — The  history  of  excessive  writing  and  the  symptoms 
presented  make  the  diagnosis  simple.  The  prognosis  is  not  favour- 
able, although  with  prompt  treatment  recovery  may  result.  The 
disease  is  chronic  and  progressive.  If  the  left  hand  is  used,  that, 
-too,  is  apt  to  become  affected  (three  fourths  of  all  cases). 

Other  occupation  neuroses  of  similar  character  are  musician's 
<3ramp,  in  which  are  included  pianist's,  violinist's,  clarionet- and  flute- 
player's  cramp ;  telegrapher's  cramp ;  sewing  spasm,  affecting  tailors, 


956  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

seamstresses,  and  shoemakers  ;  smith's  spasm,  affecting  those  making- 
penknife  blades,  scissors,  and  the  like ;  and  driver's  spasm,  milker's- 
spasms,  and  ballet-dancer's  cramp.  Occupation  neuroses  also  affect 
billiard  players,  hide  dressers,  dentists,  painters,  weavers,  pedestrians, 
artificial  flower  makers,  stampers,  turners,  type-writists,  etc. 

C.    TROPHONEUROSES 

I.  Raynaud's  Disease. — Eare,  and  occurs  usually  in  children 
and  young  adults,  and  in  women  more  often  than  men.  Predisposing 
causes  are  anaemia,  chlorosis,  and  neurasthenic  conditions.  The  chief 
causative  factors  are  the  acute  infectious  fevers,  menstrual  disturb- 
ances, malaria,  fright,  and  occupations  that  lead  to  exposure.  Syph- 
ilis and  diabetes  may  be  causes. 

Symptoms. — The  onset  is  sudden.  Two  or  three  fingers  of  both 
hands  are  usually  involved.  At  first,  or  in  a  mild  form,  there  is  cold- 
ness, numbness,  and  waxy  pallor  of  the  fingers.  They  feel  as  if  dead, 
the  skin  appears  shrunken,  and  there  is  slight  anaesthesia.  This  condi- 
tion disappears,  but  returns  again,  and  may  become  almost  constant. 
All  the  fingers  may  be  affected,  more  rarely  the  toes,  tip  of  the  nose,, 
and  the  ears.  This  mild  form  {digiti  mortui,  dead  fingers,  local 
syncope)  is  due  to  a  slight  exposure  to  cold. 

In  the  more  severe  form  the  fingers  are  blue  and  swollen.  There 
are  burning  sensations  and  much  pain,  without  anaesthesia.  Gan-^ 
grene  follows  this  "local  asphyxia."  In  the  gangrenous  stage  the 
tips  of  the  fingers  become  the  seat  of  small  blisters,  which  fill  with 
bloody  serum  and  then  dry  up.  Beneath  the  scab  thus  formed  a 
shallow  ulceration  begins,  which  soon  heals  and  leaves  a  scar. 

Occasionally  haematuria  may  be  present.  The  condition  of  digiti 
mortui  may  last  a  few  days  or  weeks,  perhaps  months.  The  gan- 
grenous stage  usually  continues  for  about  three  weeks. 

Diagnosis. — This  disease  must  be  distinguished  from  senile  gan- 
grene, frostbite,  ergot  poisoning,  alcoholic  neuritis,  endarteritis,  and 
obstruction  of  the  nutrient  vessels.  The  course  is  long  and  the  dis- 
ease is  liable  to  recur,  but  most  cases  recover. 

II.  Erythromelalgia  {Red  XeuraJgia  of  the  Feet,  Congestive- 
Neuralgia). —  Causes. — Commonly  affects  men  in  middle  life.  The 
usual  causes  are  severe  physical  exertion  afoot  and  fevers.  It  occurs 
in  diabetes  and  in  the  gouty. 

Sg?nptoms. — There  are  continuous  burning  pains  in  the  ball  or  the 
heel  of  the  foot,  and  all  of  the  plantar  nerve  distribution  on  the  sole 
of  the  foot  is  soon  involved.  The  pain  is  usually  worse  at  night. 
Walking  and  standing  are  painful.  On  exertion  there  is  flushing  of 
the  feet,  and  in  bad  cases  the  parts  affected  present  a  continuous. 


DISEASES  OP  THE  NERVOUS  SYSTEM  957 

dusky,  mottled  redness,  with  some  swelling.  The  hands  may  be 
slightly  involved.  Blisters  and  ulcerations  may  result  from  slight 
injuries.  Lying  down  usually  relieves  the  congestion  and  also  the 
pain.     In  warm  weather  the  symptoms  are  aggravated. 

This  disease  must  be  distinguished  from  alcoholic  and  gouty 
paraesthesias,  reflex  pains,  podalgia,  and  local  disease  of  bone  and 
ligaments.     It  is  not  dangerous  to  life,  but  is  very  chronic. 

III.  Angio-neurotic  (^dein.a. {Circumscribed  (Edema). — Causes, 
— Occurs  most  frequently  between  the  ages  of  20  and  30,  but  is  met 
with  before  and  after  this  period.  Males  are  affected  oftener  than 
females.  The  predisposing  causes  are  exhausting  occupations,  occa- 
sionally hereditary  influences.  The  disease  appears  oftenest  in  win- 
ter. The  exciting  causes  are  fright,  anxiety,  grief,  sudden  exposure 
to  cold,  certain  kinds  of  food,  and  slight  traumatisms. 

Symptoms. — The  onset  is  sudden.  A  circumscribed  swelling  ap- 
pears within  a  few  minutes,  or  an  hour  or  two,  upon  the  face  or  arms 
or  hands.  The  swelling  may  measure  from  ^  to  2  or  3  inches  across. 
It  may  be  pale  and  waxy,  or  rosy,  or  of  a  dark  reddish  colour.  There 
is  slight,  if  any,  pitting  on  pressure.  There  is  no  pain,  but  there 
may  be  sensations  of  itching,  burning,  scalding,  or  tension  and 
stiffness.  The  face  is  most  often  affected,  then  the  hands  and 
extremities,  the  body,  the  larynx  and  throat,  and  the  genitals,  in 
the  ordei-  mentioned.  There  is  usually  only  one  swelling  at  a  time, 
but  there  may  be  several.  This  oedema  lasts  from  an  hour  to  2  or  3 
days,  and  often  returns  at  intervals  varying  from  3  or  4  weeks  to 
several  months.  If  the  disease  affects  the  larynx  and  throat,  seri- 
ous dyspnoea  and  even  suffocation  may  result.  The  patient  is  well 
between  the  attacks. 

Diagnosis.— The  essential  points  are :  the  sudden  appearance  of 
the  circumscribed  oedema,  the  absence  of  pain,  and  the  recurrence  of 
the  swelling  at  intervals.  The  prognosis  is  good  as  regards  life,  but 
not  very  satisfactory  with  reference  to  cure. 

IV.  Progressive  Facial  Hemiatrophy.— This  begins  usu- 
ally  between  the  ages  of  10  and  20  years,  and  is  more  frequent  in 
females.     Occasional  causes  are  injuries  and  infectious  fevers. 

Onset  is  slow.  The  skin  loses  its  pigment,  and  the  hair  falls  out 
in  patches.  Occasionally  the  periosteum  and  bone  are  involved. 
The  disease  affects  the  subcutaneous  tissue  most,  the  muscles  least. 
There  is  atrophy  of  the  bony  parts,  the  lower  jaw  becoming  perhaps 
two  thirds  of  its  normal  size.  The  eye  sinks  in,  the  lid  becomes 
narrow,  and  the  pupil  is  dilated.  The  secretion  of  perspiration  may 
be  increased,  but  that  of  sebum  ceases.  Occasionally  there  may  be 
some  pain.     Anesthesia  is  rare.     Slight  spasms  of  the  muscles  of 


958  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

mastication  may  occur.  The  tongue  may  also  be  affected.  The  diag- 
nosis is  easy  (Fig.  23,  page  158).  The  disease  must  be  distinguished 
from  infantile  hemiplegia  with  atrophy,  atrophy  from  gross  nerve  le- 
sions, and  congenital  asymmetry.  The  disease  is  rapidly  progressive 
at  first  and  then  stationary.     It  is  not  curable,  but  does  not  affect  life. 

V.  Acromegaly  {Marie's  Disease). — Occurs  equally  in  males 
and  females,  and  usually  begins  between  the  ages  of  18  and  26  years. 
Many  cases  are  associated  with  disease  of  the  pituitary  body. 

Symptoms. — There  is  a  gradual  enlargement  of  the  head,  feet, 
and  hands,  accompanied  by  headaches,  malaise,  dulness,  slight  rheu- 
matic pains,  general  weakness,  anaemia,  polyuria,  and  dryness  of  the 
skin.  The  sexual  power  diminishes  in  men  and  menstruation  ceases 
in  women.  The  bones  and  the  soft  parts  are  both  hypertrophied,  the 
enlargement  being  in  width  rather  than  length.  The  hands  and 
feet,  and  the  tongue,  lips,  and  nose  are  enormously  hypertrophied. 
The  lower  jaw  is  often  more  involved  than  the  cranium.  The  ster- 
num is  hypertrophied  and  the  chest  bulging.  The  pelvis  may  be 
enlarged,  but  the  bones  of  the  thigh  and  leg  usually  escape.  The 
arms  and  the  shoulder  girdle,  except  the  clavicle,  are  not  usually 
much  affected.  The  face  (see  (e),  page  156)  is  heavy  and  massive,  the 
hair  coarse  and  dry,  and  the  skin  frequently  pigmented.  There  is  a 
cervico-dorsal  kyphosis.  The  voice  is  altered  and  the  speech  is  slow, 
guttural,  and  embarrassed,  apparently  as  a  result  of  the  enlarged 
tongue.  The  vision  may  be  affected,  and  hemianopia  may  be  present, 
especially  if  the  tumour  of  the  pituitary  body  presses  on  the  optic 
tracts.  The  muscles,  at  first  hypertrophied,  afterward  atrophy. 
Paralyses  and  anaesthesias  do  not  occur. 

Diagnosis. — The  disease  must  be  distinguished  from  osteitis  de- 
formans, congenital  enlargements,  and  the  so-called  giant  growth 
which  affects  only  single  members.  The  disease,  as  a  rule,  can  not 
be  cured,  but  it  may  become  stationary.  Its  course  is  chronic,  and  it 
persists  from  10  to  20  years. 


II.    DISEASES  OF  THE   PERIPHERAL   NERVOUS  SYSTEM 

A.    DISEASES    OF   THE    PERIPHERAL   SENSORY 
NEURONES 

I.  The  Neuralgias. — (I)  Coccygodyiiia.— Xeuralgia  affecting 
the  lower  posterior  branches  of  the  sacral  nerves.  It  occurs  most 
frequently  in  women,  and  is  due  mainly  to  labour,  injury,  and  expo- 
sure. Coccygeal  pains  occur  in  spinal  irritation  and  also  reflexly 
from  pelvic  disease.     The  disease  is  painful  and  interferes  with  walk- 


DISEASES  OP  THE  NERVOUS  SYSTEM  959 

ing  and  sitting.     There  is  tenderness  on  pressure  in  the  parts  and 
also  pain  at  stool. 

(II)  Tarsalgia  {Policeman's  Disease). — This  is  a  neuralgic  affec- 
tion, of  which  incipient  flat  foot  and  stretching  of  the  plantar  liga- 
ments is  the  most  common  cause.  It  occurs  in  people  who  have 
gone  barefoot  for  some  time,  and  who  have  then  been  obliged  to 
stand  or  walk  a  great  deal,  as  in  the  army  or  among  the  police. 

(III)  Morton's  Neuralgia.— This  disease  affects  the  metatarso- 
phalangeal joint  of  the  3d  and  4th  toes.  It  occurs  generally  in 
women.  There  is  a  slight  luxation  with  consequent  pressure  on  a 
digital  branch  of  the  external  plantar  nerve.  It  may  be  due  also  to 
beginning  flat  foot  or  to  shoe  pressure. 

(IV)  Sciatica  {Xeuralgia  of  the  Sciatic  Nerve^  Sciatic  Neuritis). — 
Causes. — Men  are  more  often  affected  than  women.  The  disease 
occurs  most  frequently  between  the  ages  of  30  and  50,  and  in  the 
fall  and  winter.  The  predisposing  causes  are  occupations  that  lead 
to  exposure  and  strain,  the  arthritic  and  gouty  diathesis,  and  a  neu- 
rotic constitution.  The  exciting  causes  are  pressure  from  hard  seats, 
constipation,  pelvic  diseases,  exposure,  and  muscular  strain  from 
heavy  work.  Injury  to  the  nerves,  inflammation,  the  pressure  of 
pelvic  tumours,  vertebral  and  spinal  disease,  may  cause  symptomatic 
sciatica.     It  may  occur  in  phthisis  and  in  diabetes. 

Symptoms. — Onset  usually  sudden,  with  pain  in  the  back  of  the 
thigh,  running  down  the  course  of  the  nerve.  It  may  extend  up 
into  the  lumbar  region,  but  is  most  marked  in  the  thigh.  Motion 
increases  it,  and  consequently  the  pelvis  tilts  up  toward  the  sound 
side  and  the  trunk  leans  over  toward  the  affected  side  {sciatic  scolio- 
sis). The  pain  is  dull  and  almost  continuous,  with  paroxysms  in 
which  it  is  sharp,  lancinating,  burning,  and  of  great  severity.  There 
may  be  sensations  of  tingling,  numbness,  and  a  sense  of  weight  and 
coldness  in  the  affected  limb.  There  are  tender  points  at  the  sciatic 
notch,  the  middle  of  the  hip,  behind  the  knee,  in  the  middle  of  the 
calf,  behind  the  external  malleolus,  and  on  the  back  of  the  foot. 
Earely  there  is  anaesthesia  along  the  course  of  the  nerve.  There 
may  be  weakness  and  muscular  atrophy  in  chronic  cases,  and  occa- 
sionally a  partial  De  E.  The  duration  of  the  disease  is  usually  about 
2  or  3  months,  although  it  may  last  for  a  year  or  more. 

Diagnosis.— ^ci?it\c?i  must  be  differentiated  from  organic  disease 
of  the  Cauda  equina  or  cord,  hip-joint  disease,  muscular  pains  in  the 
hip  or  leg,  and  from  pains  caused  by  tumours.  If  the  leg  is  extended 
and  the  thigh  at  the  same  time  flexed  upon  the  abdomen,  a  sharp  pain 
occurs  at  the  sciatic  notch  which  is  diagnostic  of  sciatica.  Recovery 
occurs  in  the  majority  of  cases  within  6  months. 


960  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

(V)  Plantar  Neuralgia. — Very  rarely  the  pain  of  sciatica  is  limited 
to  the  plantar  nerves.  In  this  condition  there  is  paraesthesia  and 
sometimes  anaesthesia. 

(VI)  Lumbo-abdominal  Neuralgia. — Affects  the  upper  lumbar 
nerves.  Causes. — Occurs  usually  in  women  after  the  30th  year.  In 
addition  to  the  usual  causes  of  neuralgia,  straining,  pelvic  disease, 
and  constipation  are  found  to  be  causative  factors.  Diseases  of  the 
hip  or  of  the  internal  genitals  cause  reflex  pain.  Myalgic  and  reflex 
pains  from  uterine  disorders  are  common.  True  essential  neuralgias 
are  infrequent. 

Symptoms. — The  chief  symptom  is  pain  in  the  back  (frequently 
bilateral),  loins,  and  buttocks,  which  extends  down  to  the  hypogas- 
trium  or  genitals  on  one  side.  Occasionally  painful  points  may  be 
found.  Femoral  or  crural  neuralgia  is  a  form  in  which  the  long 
lumbar  branches  are  affected.  Meralgia  is  a  condition  in  which 
numbness  and  pricking  is  felt  along  the  thigh.  It  is  due  to  a  lesser 
irritation  of  the  long  lumbar  branches,  and  is  a  mild  form  of  femoral 
neuralgia.  The  pain  in  true  femoral  neuralgia  is  in  the  front  of  the 
knee  and  the  anterior  and  outer  parts  of  the  thigh.  There  is  no 
pain  below  the  knee. 

Diagnosis. — The  cardinal  points  are :  the  unilateral  pain,  with  its 
distribution  and  paroxsymal  character,  the  presence  of  tender  points, 
the  absence  of  organic  disease,  and  of  marked  discomfort  on  motion 
or  pressure.  Lumbago  has  a  sudden  onset,  a  history  of  exposure, 
and  is  limited  to  a  single  group  of  muscles  which  are  painful  on  deep 
pressure.  In  lumbar  sprain  there  is  a  history  of  injury,  a  sudden 
onset,  and  marked  local  tenderness. 

(VII)  Mammary  Neuralgia  {Mastodynia). — True  mammary  neu- 
ralgia is  due  to  injury,  pendent  breasts,  anaemia,  and  pressure  from 
badly  fitting  corsets.  It  also  occurs  in  hysterical  women  and  sexu- 
ally precocious  girls,  and  in  pregnancy  and  during  lactation.  It  is 
also  caused  by  local  tumours.  Local  disease  of  the  breast  causes 
many  mammary  pains.  This  form  of  neuralgia  is  unilateral  and  very 
severe.     It  may  cause  mental  depression  from  fear  of  cancer. 

(VIII)  Herpes  Zoster  {Dermatitic  Neuritis,  SJiingles). — An  acute 
dermatitis  secondary  to  a  neuritis  of  the  intercostal  nerves.  The 
most  frequent  causes  are  infections,  wounds,  rheumatic,  syphilitic, 
and  gouty  poisons,  emotional  influences,  and  the  morphine  habit. 
The  onset  is  gradual,  and  characterized  by  pain  and  a  herpetic 
eruption  on  one  side  of  the  trunk.  The  lower  dorsal  nerves  are  usu- 
ally affected,  and  the  eruption  follows  the  course  of  the  nerve.  The 
pain  diminishes  and  the  attack  is  over  in  a  few  weeks. 

(IX)  Intercostal  Neuralgia  {Side  Pains). — This  affection  is  com- 


DISEASES  OF  THE  NERVOUS  SYSTEM  961 

mon  and  occurs  more  frequently  in  women  than  in  men,  usually  in 
the  winter,  and  between  the  ages  of  20  and  35.  The  chief  causative 
factors  are  neurasthenia,  hysteria,  anaemia,  childbearing,  pelvic  dis- 
ease, heart  disease,  dyspepsia,  lead-poisoning,  and  malaria.  Very 
rarely  exposure  and  muscular  strain  are  exciting  causes. 

Symptoms. — The  onset  is  sudden.  The  pain  is  sharp  and  stab- 
bing, and  but  slightly  increased  by  respiratory  movements.  There 
may  be  tenderness  over  the  seat  of  the  pain,  over  the  exit  of  the  dor- 
sal or  the  anterior  branch  of  the  nerve.  The  left  side  is  affected 
more  often  than  the  right.  The  duration  of  the  disease  is  usually 
from  3  to  6  weeks,  but  it  may  last  months. 

Diagnosis. — This  neuralgia  must  be  distinguished  from  myalgic 
pains  by  the  character  of  the  latter,  the  history  of  rheumatism  and  of 
the  cause,  by  the  pain  on  deep  inspiration,  and  by  the  tenderness  on 
pressure.  The  important  points  in  diagnosticating  intercostal  neu- 
ralgia are  the  presence  of  rheumatic  and  reflex  causes,  the  character 
of  the  pain,  the  presence  of  tender  points,  and  the  exclusion  of  pleu- 
risy. The  prognosis  is  good.  The  disease  occasionally  becomes 
chronic,  especially  when  due  to  a  degenerative  neuritis. 

(X)  Cervico-bracliial  Neuralgia.— Not  frequent,  and  occurs  in  early 
adult  and  middle  life,  mainly  in  women.  Caused  by  rheumatism, 
gout,  and  overuse  of  the  arm  in  anaemic  and  neurasthenic  patients. 
It  occurs  as  a  symptom  of  tabes  and  other  cord  diseases,  and  also 
reflexly  from  uterine  disease  and  caries  of  the  teeth. 

Symptoms. — Onset  is  gradual,  with  aching  pains  along  the  course 
of  the  nerves  and  in  the  neck,  shoulder,  and  axilla.  One  arm  only  is 
affected.  The  pains  are  worse  at  night,  and  are  increased  by  expo- 
oure  and  use  of  the  arm.  There  may  be  painful  or  tender  points  in 
the  axilla,  over  the  deltoid,  at  the  lower  end  of  the  scapula,  over  the 
lower  part  of  the  radius,  over  the  ulna  near  the  wrist,  and  occasion- 
ally on  each  side  of  the  lower  cervical  vertebrae.  Paraesthesias  and 
feelings  of  numbness  are  present.  Vasomotor  disturbances,  herpes, 
angesthesia,  and  muscular  weakness  and  atrophy  may  appear. 

(XI)  Digital  Neuralgia.— A  single  finger  may  be  affected.  Neu- 
ritis or  a  local  injury  is  tlie  usual  cause.  Occasionally  the  pain  may 
be  reflex  from  some  distant  trouble  (e.  g.,  uterine).  The  main  point 
is  to  find  the  cause  of  the  neuralgia,  and  to  exclude  organic  disease. 
The  prognosis  is  good  unless  the  neuralgia  is  complicated  with  a 
neuritis,  when  it  is  more  serious.  If  the  neuritis,  however,  is  not 
marked,  or  is  rheumatic  or  gouty,  or  is  secondary  to  injury,  the  prog- 
nosis is  still  good. 

(XII)  Cervico-occipital  Neuralgia  {Xech  Pains).— Causes.— These 
pains  occur  in  migraine,  hysteria,  neurasthenia,  and  spinal  irritation ; 


962  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

as  a  true  neuralgia ;  as  a  result  of  eye  strain,  and  as  a  symptom  of 
brain  tumour,  meningitis,  and  rheumatic  inflammation  of  the  nerves 
and  muscles  of  the  neck.  True  cervico-occipital  neuralgia  occurs- 
more  commonly  in  women  and  between  the  ages  of  20  and  35.  Pel- 
vic disease  often  causes  it  reflexly. 

Symptoms. — In  the  typical  form  the  pain  is  paroxysmal,  unilateral, 
and  sharp,  sometimes  intense,  and  there  are  tender  points  over  the 
nerves.  The  duration  of  the  disease  is  about  5  or  6  weeks,  but  it 
may  become  chronic  if  due  to  a  reflex  cause.  When  due  to  hysteria 
or  spinal  irritation  the  disease  is  central  and  there  is  a  sharp  boring 
pain  below  the  occiput.  Symptoms  of  cerebral  congestion  or  anaemia,, 
and  vertigo  and  faintness,  may  be  present,  but  no  vomiting.  Pain 
of  a  boring  character  points  almost  positively  to  spinal  irritation.. 
The  pain  in  neurasthenia  is  more  like  a  tired  ache. 

(XIII)  Neuralgias  of  the  Trigeminus. — (1)  Symptomatic  Form. — 
This  is  the  most  frequent,  and  includes  supraorbital,  infraorbital,  or 
supramaxillary,  inframaxillary  or  dental,  and  mixed  forms.  Supra- 
orbital neuralgia  is  the  commonest  variety.  It  occurs  in  females 
oftener  than  in  males,  usually  in  the  first  half  of  life.  The  left  side 
is  generally  affected.  The  causes  are  dental  disorders,  exposure,, 
anaemia,  childbearing,  disease  of  the  eyes  or  nose,  syphilis,  gout,, 
rheumatism,  diabetes,  epilepsy,  malaria,  and  trauma. 

The  pains  are  very  sharp  and  severe,  with  exacerbations  and  re- 
missions. They  may  last  for  days  and  then  be  absent  for  a  long 
time,  but  they  come  back  unless  the  cause  is  removed.  There  may  be 
oedema  of  the  eyelids  in  supraorbital  neuralgia.  There  are  tender 
points  along  the  course  of  the  nerve  involved.  The  pain  may  radiate 
from  some  point,  as  the  ear  or  occiput.  The  pupil  is  occasionally 
dilated,  and  there  may  be  a  reflex  facial  spasm. 

(2)  Tic  Douloureux. — This  form  of  neuralgia  occurs  in  middle  or 
advanced  life,  and  is  very  severe.  Exposure,  overwork,  and  depress- 
ing influences  are  causative  factors.  Local  disease  of  the  teeth  or 
jaws  may  cause  it.  The  chief  symptoms  are  the  intense,  unilateral, 
darting  pains,  which  radiate  from  the  side  of  the  nose  or  the  upper  lip, 
through  the  teeth,  or  into  the  eye,  or  even  the  brow  and  head.  The 
pains  come  in  paroxysms,  lasting  for  a  few  minutes,  during  which 
the  face  is  flushed  and  the  eyes  and  nose  run.  There  is  an  expres- 
sion of  agony  on  the  face.  The  patient  is  seldom  free  from  some 
pain,  and  a  breath  of  cold  air,  speaking,  eating,  or  putting  out  the 
tongue  may  bring  on  a  paroxysm.  These  pains  may  come  on  for  a 
certain  length  of  time  each  year.  There  are  often  spasmodic  move- 
ments of  the  face,  tongue,  or  jaws.  Occasionally  there  is  anaesthesia^ 
This  disease  is  very  diflScult  to  cure. 


DISEASES  OF  THE  NERVOUS  SYSTEM  963 

(3)  Trigeminal  ParcBsthesia. — A  thrilling,  formication,  or  numb- 
ness along  the  course  of  the  nerve.  There  is  no  pain.  It  occurs  in 
anaemic,  nervous,  and  hysterical  people. 


B.  DISEASES  OF  THE  PERIPHERAL  MOTOR  NEURONES 

I.  Multiple  Neuritis. — Onset  acute,  but  running  a  subacute 
or  chronic  course,  and  characterized  by  weakness  or  paralysis  of  all 
four  extremities,  accompanied  by  atrophy,  pain,  and  tenderness. 

(1)  The  Motor  Type. — This  is  the  commonest  form.  It  is  a  dis- 
ease of  early  adult  life,  and  occurs  in  women  more  often  than  in  men. 
Occasionally  it  occurs  in  children.  Predisposing  causes  are  exposure 
to  cold  and  wet,  excessive  tea-drinking,  anaemia,  sexual  abuse,  and 
tuberculosis.  The  exciting  causes  include  nearly  all  the  infectious 
fevers  and  malaria,  arsenic,  alcohol  (most  common),  copper,  phos- 
phorus, lead,  rheumatism,  and  diabetes. 

There  may  be  numbness,  slight  pains  and  general  weakness,  espe- 
cially in  the  legs,  for  a  few  weeks  before  the  attack.  The  onset  is 
usually  sudden,  with  pains  and  tenderness  in  the  legs  and  feet  and 
a  fever  for  a  day  or  two.  The  pains  and  weakness  increase  and  the 
muscles  and  nerves  become  very  tender.  The  arms  and  hands  are 
also  affected,  but  not  as  severely.  The  skin  becomes  reddened  or 
slightly  edematous.  The  muscles  of  the  legs  grow  weak,  and  in  a 
week  or  so  there  may  be  a  complete  paralysis  of  the  anterior  muscles 
of  the  legs  and  a  corresponding  loss  of  power  in  the  extensors  of  the 
hands,  but  to  a  less  degree.  There  may  be  a  loss  of  co-ordination. 
The  pains  are  severe.  Nearly  all  the  muscles  of  the  legs  and  fore- 
arms become  more  or  less  involved,  and  atrophy  begins.  Rarely  the 
motor  cranial  nerves  are  affected.  Slight  nystagmus  is  common. 
The  condition  soon  develops  into  that  of  a  paraplegia  with  foot-  and 
wrist-drop.  The  knee-jerk  and  elbow-jerk  are  absent,  except  in  rare 
cases.  There  is  some  diminution  or  delay  in  temperature  and  pain 
sensibility.  Tactile  anaesthesia  is  present,  often  associated  with 
hyperalgesia.  The  muscular  and  articular  senses  are  usually  im- 
paired. There  is  De  E.  in  the  muscles,  varying  in  degree  in  different 
muscles  and  nerves.  The  sphincters  are  rarely  involved,  the  bladder 
only  being  occasionally  affected  for  a  short  time.  In  alcoholic  cases 
there  may  be  mental  symptoms,  usually  consisting  of  a  low  muttering 
delirium.  An  acute  confusional  insanity  may  develop.  There  is  often 
marked  prostration.  In  diphtheritic  neuritis  some  of  the  throat  and 
eye  muscles  are  involved,  with  few  sensory  symptoms  and  less  involve- 
ment of  the  extremities.  In  the  less  affected  muscles  contracture 
and  shortening  may  occur.     Sensory  symptoms  consist  of  numbness. 


964  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

hyperaesthesia,  severe  pains,  marked  tenderness  and  burning  sensa- 
tions, and  tactile  anassthesia.    They  occur  in  the  hands,  legs,  and  feet. 

(2)  Sensory  or  Pseudo-tahetic  Form. — Diabetes,  and  infectious  and 
metallic  poisons  are  the  causative  factors  in  this  form  more  often 
than  alcohol.  The  course  is  similar  to  that  of  -the  motor  form, 
although  the  paralysis  is  usually  less  marked  and  the  sensory  symp- 
toms are  more  prominent.  The  muscular  and  articular  senses  are 
lost.  Inco-ordination  is  a  prominent  symptom,  hence  the  resemblance 
of  this  form  to  tabes  dorsalis. 

(3)  Epidemic  and  endemic  forms  are  due  to  acute  infection  and 
malaria  (see  Beri-beri,  page  748). 

(4)  The  acute  pernicious  form  comes  on  suddenly.  The  course  is 
rapid,  and  death  follows  in  a  few  weeks.  The  cardiac  and  respiratory 
nerves  are  involved.  The  cause  seems  to  be  some  septic  organism. 
Landry's,  or  acute  ascending,  paralysis  is  another  form  in  which 
acute  pernicious  multiple  neuritis  appears.  In  this  type  there  are 
no  electrical  changes  or  atrophy  and  few  sensory  symptoms. 

Differential  Disignosis  of  Multiple  Neuritis. — The  cardinal  points 
are :  alcoholic  history,  acute  onset,  gradual  paralysis  of  legs  and 
hands  ;  foot-drop  and  wrist-drop  ;  severe  pains  and  tenderness ;  early 
loss  of  faradic  and  change  in  galvanic  excitability ;  the  absence  of 
sphincter  involvement ;  and  loss  of  the  knee-  and  elbow-jerks. 

It  is  distinguished  from  anterior  poliomyelitis  by  the  persistence  of 
pain  and  other  sensory  symptoms,  the  tenderness  of  the  nerve  trunks, 
the  early  loss  of  electrical  excitability,  the  history  of  the  case,  and  the 
age  of  the  patient.  In  anterior  poliomyelitis  the  paralysis  is  not 
symmetrical,  and  the  loss  of  electrical  excitability  occurs  after  weeks 
or  months.  In  myelitis  the  bladder  is  affected,  while  in  multiple 
neuritis  it  is  seldom  disturbed.  The  onset  and  progress  of  myelitis 
are  more  rapid,  the  muscular  atrophy  less,  and  the  knee-jerks  are 
Increased.  It  is  distinguished  from  tabes  by  its  more  rapid  onset, 
the 'presence  of  paralysis,  atrophy,  and  De  E.,  and  the  absence  of 
involvement  of  the  organic  centres  and  pupils.  In  spinal  hemorrhage 
there  is  usually  pain  in  the  back.  Xeuralgia  is  unilateral,  while 
the  pains  of  multiple  neuritis  are  bilateral.  The  persistence  of 
tenderness  and  hyperaesthesia  would  also  indicate  multiple  neuritis. 

The  prognosis  of  multiple  neuritis  is  good  in  all  forms  except  those 
due  to  alcohol  or  toxaemia.  The  majority  of  cases  recover  almost 
entirely.  In  alcoholic  cases  death  is  frequent,  although  often  not 
due  to  the  neuritis,  but  to  alcoholism  or  to  phthisis. 

II.  Symmetrical  Spontaneous  Ulnar  Neuritis. — Probably 
a  degenerative  neuritis  and  due  to  some  infection.  The  exciting 
cause   is   unknown.     A  neuropathic   tendency  is   the  predisposing 


DISEASES  OP  THE  NERVOUS  SYSTEM  965 

cause.  The  onset  is  gradual,  with  pain  and  parsesthesia  along  the 
ulnar  nerve  of  one  side.  There  are  weakness  and  atrophy  of  the 
muscles  supplied  by  the  ulnar.  Anaesthesia  develops  also.  The 
other  hand  then  becomes  affected.  The  disease  is  chronic  and  com- 
plete recovery  is  rare. 

III.  Migrating  Neuritis. — This  is  a  rare  disease,  and  usually 
follows  an  operative  or  other  wound  of  a  nerve,  the  neuritis  extend- 
ing up  the  arm.  Pain,  paralysis,  anaesthesia,  and  atrophy  are  the 
chief  symptoms.  The  course  of  the  disease  is  chronic,  and  it  does 
not  respond  well  to  treatment. 

IV.  Acute  Ascending  Paralysis  {Landry's  Paralysis).— This 
rare  disease  consists  of  a  paralysis  which  develops  rapidly,  involves 
first  the  legs,  and  then  in  turn  the  trunk,  arms,  respiratory  and 
throat  muscles,  and  generally  ends  in  death.  Men  are  affected 
oftener  than  women,  chiefly  between  the  ages  of  20  and  40.  The 
causes  are  exposure,  syphilis,  and  the  acute  infectious  fevers. 

Symptotns. — Slight  prodromal  symptoms  may  be  present  for  a 
few  days,  consisting  of  general  malaise,  slight  fever,  numbness  in  the 
limbs,  and  pain  in  the  back  or  legs.  When  these  are  absent,  weak- 
ness in  the  legs  is  the  first  symptom.  The  paralysis  rapidly  extends 
and  soon  affects  the  arms.  Finally,  the  medulla  is  involved,  respira- 
tion becomes  difficult,  and  the  patient  may  be  unable  to  talk  or  swal- 
low. There  is  almost  no  pain  or  disturbance  of  sensation,  although 
there  may  be  slight  anaesthesia.  Atrophy,  De  R.,  and  secretory  or 
vasomotor  disturbances  are  absent.  The  bladder  and  rectum  are 
rarely  affected,  and  sometimes  there  are  facial  and  eye  palsies.  The 
disease  may  begin  in  the  cervical  region  and  descend. 

Diagnosis. — The  cardinal  points  are :  the  acute  ascending  course  of 
the  paralysis,  the  absence  of  fever,  anaesthesia,  decubitus,  sphincter 
involvement,  and,  especially,  De  R.  Acute  myelitis,  acute  multiple 
neuritis,  and  acute  poliomyelitis  are  the  diseases  from  which  it  must 
be  distinguished.  An  alcoholic  history  and  the  age  of  the  patient 
must  be  taken  into  account.  The  prognosis  is  bad.  The  disease 
usually  runs  its  course  within  7  days  and  ends  in  death.  If  it  does 
Tiot  extend  into  the  medulla,  and  the  patient  is  paralyzed  only  below 
his  neck,  improvement  begins,  and  in  1  or  2  years  a  partial  recovery 
of  muscular  power  may  take  place. 

V.  Paralysis  of  the  Spinal  Part  of  the  Accessory.— 
Causes. — Caries  of  the  vertebrae,  chronic  meningitis,  progressive  mus- 
cular atrophy,  injuries,  and  all  forms  of  spinal  disease  which  extend 
high  up  in  the  cervical  cord. 

Symptoms. — If  one  nerve  is  paralyzed  there  is  inability  to  rotate 
the  head  perfectly,  but  it  can  still  be  held  straight.     There  is  atro- 
63 


966  DIAGNOSIS,    DIRECT  AND   DIFFERENTIAL 

phy  of  the  steruo-mastoid.  If  the  trapezius  is  involved  there  is  a 
depression  in  the  neck,  seen  best  on  deep  inspiration.  It  is  difficult 
to  raise  the  arm.  When  both  nerves  are  paralyzed  there  is  marked 
difficulty  in  rotating  the  head  or  lifting  the  chin.  Paralysis  of  both 
sterno-mastoids  tends  to  cause  the  head  to  fall  backward ;  of  the 
upper  parts  of  both  trapezii,  to  drop  forward.  The  paralysis  is  fol- 
lowed by  atrophy  and  De  R.  When  both  parts  of  the  spinal  acces- 
sory are  affected  there  are  also  dysphonia,  dropping  of  the  palate, 
and  rapid  pulse.     The  characteristic  features  are  marked. 

VI.  Paralysis  of  Phrenic  Nerve. — Due  to  injury  or  disease 
of  the  cervical  cord,  peripheral  disease,  hysteria,  mediastinal  tumours, 
rheumatic  and  toxic  influences,  pleurisy,  and  peritonitis.  The  most 
common  causative  factors  are,  however,  tabes  dorsalis,  acute  ascend- 
ing paralysis,  spinal-cord  disease,  and  surgical  injuries.  In  bilateral 
paralysis  of  the  diaphragm  there  is  no  movement  of  the  abdomen  or 
the  epigastrium,  and  the  hypochondrium  is  drawn  in  (pages  387,  388). 
Dyspnoea  and  rapid  breathing  follow  slight  exertion.  If  the  di- 
aphragm alone  is  affected  the  trouble  is  in  the  trunk  of  the  nerve. 

VII.  Combined  Paralysis  of  the  Brachial  Nerves. — Oc- 
curs oftenest  in  men.  It  is  not  rare  in  infants  as  a  result  of  obstet- 
rical injuries.  Exciting  causes  are  injuries,  tumours,  dislocation  of 
the  shoulder,  neuritis,  and  crutch  and  other  compressions.  There 
are  also  functional  palsies  from  hysteria  and  overwork. 

According  to  the  degree  of  compression  or  injury  to  the  nerve, 
there  are  pain,  tenderness,  paralysis,  atrophy,  electrical  changes  in 
the  muscles,  anaesthesia,  or  trophic,  vasomotor,  and  secretory  dis- 
turbances. If  the  musculo-cutaneous  is  chiefly  affected  the  patient 
can  not  flex  the  forearm.  If  the  musculo-spiral  is  affected  the  pa- 
tient can  not  extend  the  arm.  If  the  circumflex  or  the  lower  cervical 
and  upper  dorsal  nerves  and  the  posterior  thoracic  are  involved  the 
patient  can  not  elevate  the  arm  outward. 

Diagnosis. — Can  be  made  by  ascertaining  the  special  nerves  in- 
volved and  the  nature  and  seat  of  the  lesion.  Distinguish  between 
(1)  a  total-arm  palsy ;  and  (2)  an  upper-arm  type  {Erb's  palsy),  in 
which  the  deltoid,  the  biceps,  brachialis  anticus,  supinator  longus, 
and  sometimes  the  supinator  brevis  are  involved.  The  arm  hangs 
by  the  side  and  the  forearm  can  not  be  flexed.  Erb's  palsy  is  fre- 
quent in  infants  and  is  one  of  the  obstetrical  palsies.  There  is  also 
(3)  a  lower-arm  type,  in  which  the  triceps,  the  flexors  of  the  wrist,  the 
pronators,  the  flexors  and  extensors  of  the  fingers,  and  the  hand  mus- 
cles are  involved.  The  hand  is  useless  and  the  extension  of  the  fore- 
arm is  impossible.  Combined  nerve  palsy  due  to  a  primary  brachial 
neuritis  is  differentiated  from  progressive  muscular  atrophy  by  the^ 


DISEASES  OP  THE  NERVOUS  SYSTEM  967 

pain,  anaesthesia,  and  electrical  reactions.     The  jjrognosis  is  usually 
good.     Nearly  all  cases  recover. 

VIII.  Paralysis  of  Single  Brachial  Plexus  Nerves.— (1) 
Posterior  Thoracic. — Causes  are  sudden  strains  or  injuries  in  the 
neck.  Occurs  rarely,  usually  in  adult  males.  May  be  involved  in 
progressive  muscular  atrophy.  The  nerve  supplies  the  serratus  mag- 
nus.  There  may  be  pain,  and  the  course  of  the  paralysis  is  often 
long.  There  is  difficulty  in  raising  the  arm  above  the  horizontal 
position,  and  the  movements  of  the  shoulder  are  impaired.  The 
posterior  edge  of  the  scapula  recedes  from  the  thorax  when  the  arm 
is  put  forward.  At  the  same  time  the  scapula  is  rotated,  its  lower 
angle  going  inward  and  upward  (Fig.  63,  page  285). 

(2)  Circumflex. — Often  paralyzed.  It  supplies  the  deltoid,  teres 
minor,  third  head  of  the  triceps,  and  shoulder  joint.  It  is  caused  by 
injuries  or  falls,  dislocation,  and  rheumatic  inflammation.  The 
symptoms  are  anaesthesia,  atrophy,  and  occasionally  pain.  The  arm 
can  not  be  rotated  outward  or  elevated. 

(3)  Suprascajnilar. — Rare.  The  teres  minor,  spinati  muscles,  and 
the  shoulder  joint  receive  this  muscle.  There  is  an  impairment  in 
elevation  of  the  shoulder  and  also  in  rotation. 

(4)  Musculo-spiral  ( Wrist-drop). — Frequently  paralyzed.  Pres- 
sure on  the  nerve  during  sleep,  fractures,  wounds,  crutch  pressure, 
tumours,  lead,  arsenic-  and  alcohol-poisoning,  and  multiple  neuritis 
are  common  causes. 

Symptoms. — There  is  an  inability  to  extend  the  wrist  and  fingers, 
and  "  wrist-drop  "  results.  The  first  finger  is  least  affected.  There 
may  be  atrophy  and  De  R.  Numbness  may  be  present,  and  also  some 
anaesthesia  over  the  radial  nerve  distribution  on  the  hand.  The 
course  of  the  disease  is  short  if  due  to  pressure,  but  longer  if  due  to 
lead-poisoning,  neuritis,  or  severe  injury  of  the  nerve.  When  lead- 
poisoning  is  the  cause  the  supinator  longus  is  usually  unaffected,  the 
paralysis  comes  on  more  slowly  and  affects  both  arms,  and  there  is 
seldom  any  pain  or  anaesthesia.  In  paralysis  due  to  compression 
there  is  often  an  involvement  of  the  supinators  and  the  triceps. 

Diagnosis. — Easy.  Differentiate  between  lead  palsy,  neuritic 
palsy,  and  compression  palsy.  Find  out  the  cause  of  the  paralysis. 
Exclude  progressive  muscular  atrophy.     The  prognosis  is  good. 

(5)  Median. — Rarely  affected  alone,  but  may  be  due  to  injuries  or 
neighbouring  lesions.  Abduction  and  flexion  of  the  thumb  and 
flexion  of  1st  and  2d  fingers  are  impaired.  The  grip  is  weakened. 
There  may  be  atrophy  of  the  thenar  eminence.     There  is  anaesthesia. 

(6)  Ulnar. — Frequently  paralyzed.  Early  involved  in  progressive 
muscular  atrophy,  but  rarely  affected  in  lead-poisoning.      Injuries 


968  DIAGNOSIS,    DIRECT  AND   DIFFERENTIAL 

are  the  most  common  cause.     It  may  be  the  seat  of  a  primary  de- 
generative neuritis. 

Symytoms. — The  ring  and  little  fingers  are  especially  weak,  and 
the  hand  can  not  be  closed  tightly.  There  is  a  condition  of  "  main 
en  griffe.''''  There  is  some  anaesthesia  over  the  distribution  of  the 
nerve.     Pain  and  tenderness  may  be  present. 

IX.  Paralyses  of  the  Lumbar  Nerves. — Paralyses  and  spas- 
modic troubles  of  these  nerves  are  usually  symptomatic — e.  g.,  of 
caries  of  the  spine,  psoas  abscess,  impacted,  faeces,  pelvic  tumours  or 
injuries,  hip  disease,  obturator  hernia,  or  pressure  of  the  foetal 
head. 

If  the  2  upper  lumbar  nerves  are  affected  only  sensory  symptoms 
occur.  If  the  next  2  are  affected  there  is  trouble  in  extending  the 
leg  and  flexing  the  hip  on  the  trunk.  If  the  obturator  nerve  is  para- 
lyzed the  thigh  can  not  be  adducted  or  the  leg  crossed,  and  outward 
rotation  of  the  thigh  is  weak.  If  the  anterior  crural  is  paralyzed 
the  anterior  thigh  muscles  are  weak  and  the  leg  can  not  be  extended. 
There  is  anaesthesia  or  pain  over  the  crural  area.  If  the  posterior 
branches  of  the  lumbar  nerves  are  paralyzed  there  is  weakness  or 
paralysis  of  the  erectors  of  the  spine.  This  occurs  in  progressive 
muscular  atrophy. 

X.  Peripheral  Leg  Palsies. — May  be  combined  or  single. 

(I)  Combined  Palsies. — Due  to  dislocation,  injury,  hip  disease, 
tumours,  and  neuritis.  There  may  be  an  hysterical  sacral  palsy. 
The  foot  can  not  be  moved  nor  the  leg  flexed.  The  thigh  can  not  be 
drawn  back  or  rotated  freely.  Pain,  anaesthesia,  atrophy,  and  vaso- 
motor and  secretory  disturbances  are  present.  The  diagnosis  de- 
pends on  the  history,  the  area  of  anaesthesia,  and  the  extent  of 
paralysis.  It  is  differentiated  from  spinal-cord  disease  by  the  uni- 
lateral symptoms,  the  absence  of  sphincter  trouble,  and  the  atrophy 
and  sensory  disturbances. 

(II)  Single  Nerve  Sacral  Palsy. — The  sciatic  is  oftenest  affected, 
especially  its  anterior  tibial  branch.     Symptom. — "  Foot-drop." 

XI.  Facial  Palsies. — The  most  common  variety  is  here  con- 
sidered (see  also  pages  169  to  174). 

Peripheral  Facial  Palsy  {BelVs  Palsy). — Causes. — Infection,  ex- 
posure, and  rheumatism.  Occurs  between  the  ages  of  20  and  40, 
more  frequently  in  males.  A  neuropathic  constitution  predisposes. 
It  may  occur  in  tabes  and  multiple  neuritis,  or  follow  injuries  to  the 
petrous  bone  or  ear  disease. 

Symptoms. — Sudden  onset.  Is  usually  complete  in  a  few  hours. 
There  may  be  some  pain  about  the  ear.  For  a  description  of  pe- 
ripheral paralysis,  see  page  169.     If  the  paralysis  is  not  complete. 


DISEASES  OP  THE  NERVOUS  SYSTEM 


969 


secondary  contractions  ap^jear  after  two  months  or  more,  and  the 
mouth  may  be  drawn  to  the  affected  side. 

The  diagnosis  is  easy.  In  facial  palsy  from  a  cerebral  cause  the 
upper  branch  of  the  nerve  is  not  much  involved,  the  eye  can  be 
closed,  and  there  is  no  De  E.  In  nuclear  palsy  there  is  a  history  of 
diphtheria,  lead  palsy,  or  bulbar  paralysis.  The  prognosis  is  good, 
although  recovery  is  seldom  complete. 

XII.  The  Progressive  Muscular  Dystrophies. — The  fol- 
lowing varieties  are  recognised  (see  also  Fig.  223) : 

(I)  Pseudo  -  Hypertrophic  Muscular  Paralysis  {Pseudo- muscular 
Hypertrophy^  Atro- 
phia Musculorum 
Lipomatosa).  —  Oc- 
curs usually  under 
the  age  of  10  years, 
perhaps  shortly  aft- 
er infancy,  more 
often  in  boys  than 
in  girls.  In  the 
majority  of  cases 
heredity  is  an  im- 
portant factor.  A 
history  of  neuro- 
pathic or  psycho- 
pathic conditions 
in  the  patient's  an- 
cestry is  often  ob- 
tained. Syphilis, 
alcoholism,  neu- 
roses, or  consan- 
guinity do  not  play 
any  part  in  the 
causation.     The  exciting  cause  may  be  an  injury  or  an  acute  disease. 

Symptoms.— There  is  first  noticed  a  "waddling  gait"  and  a  tend- 
ency to  stumble  and  fall,  due  to  weakness  of  the  legs.  After  a  short 
time  the  leg  muscles,  especially  those  of  the  calves  (Fig.  183,  page 
510),  seem  hypertrophied.  The  extensors  of  the  knee  and  the 
gluteal  and  lumbar  muscles  may  become  involved.  The  hypertrophy 
may  be  marked  or  slight.  The  affected  muscles  have  a  peculiar  hard 
and  non-elastic  feeling.  Of  the  muscles  in  the  upper  part  of  the 
body  the  infraspinatus  is  most  often  hypertrophied,  but  the  supra- 
spinatus  and  deltoid  may  be  somewhat  affected.  There  is  usually 
also  atrophy  of  the  lower  parts  of  the  pectoralis  major  and  of  the 


Fig.  223. 


-Points  first  involved  in  the  various  types  of  mus- 
cular dystrophies  and  atropliies. 


970 


DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 


latissimus  dorsi.  Some  atrophy  is  often  present  in  the  muscles  of 
the  upper  arm,  but  those  of  the  face,  neck,  and  forearm  are  rarely 
affected.     There  may  be  hypertrophy  of  the  tongue. 

Together  with  the  pseudo-hypertrophy  there  is  an  atrophy  of  cer- 
tain groups  of  muscles.  After  a  time  the  pseudo-hypertrophy  disap- 
pears and  the  atrophy  increases. 
In  the  lower  limbs  the  atrophy 
affects  chiefly  first  the  flexors  of 
the  hips,  then  the  extensors  of 
the  knee  and  hip.  The  calf 
muscles  become  atrophied,  then 
the  anterior  tibial  groups.  The 
gait  becomes  more  waddling ; 
there  is  great  difficulty  in  going 
upstairs,  and  the  patient  can  not 
get  up  from  the  floor.  This  dis- 
ability is  due  to  the  weakness  of 
the  extensors  of  the  knees  and 
hip  and  the  flexors  of  the  hip. 
For  the  same  reason  there  is  a 
condition  of  lordosis,  which  dis- 
appears when  the  patient  sits. 
There  may  be  also  some  lateral 
curvature  of  the  spine.  As  a 
result  of  the  weakness  and  con- 
tractures of  the  leg  muscles  a 
talipes  equinus  appears  early. 
Later  the  forearms  may  become 
flexed  on  the  arms,  and  the  legs 
on  the  hips.  There  is  no  De  E. 
The  knee-jerks  and  elbow- jerks 
gradually  diminish  and  are  final- 
ly lost.  There  are  no  fibrillary 
twitchings,  pain,  or  sensory  dis- 
turbances. There  is  no  mental 
impairment  or  involvement  of 
the  organic  spinal  centres.  The 
parts  affected  feel  cold  and  have 
a  reddened  appearance. 
Diagnosis. — The  chief  diagnostic  points  are :  the  peculiar  gait, 
and  the  mode  of  rising  from  the  floor  (Fig.  324) ;  the  age  of  the 
patient ;  the  progressive  character  of  the  impairment ;  the  enlarge- 
ment of  the  calf  muscles ;  the  combination  of  enlargement  of  the 


Via.  224. — Mode  of  rising  from  floor  in  pseudo- 
muscular  hypertrophy.  Kead  from  above 
downward. 


DISEASES  OF  THE  NERVOUS  SYSTEM  971 

infraspinatus  with  a  wasting  of  the  latissimus  dorsi  and  lower  part 
of  the  pectoralis.  In  congenital  spastic  paraplegia  the  knee-jerk 
is  exaggerated,  there  are  spasms  of  the  legs,  the  resulting  contrac- 
tures of  which  can  be  overcome,  and  the  patient  does  not  rise  from 
the  floor  in  the  same  way  as  in  pseudo-hypertrophic  paralysis. 

Progtiosis. — The  disease  may  last  for  from  10  to  25  years  or  longer. 
Its  progress  at  first  is  slow,  but  the  prognosis  is  serious,  and  the 
patient  does  not  live  long  after  becoming  bedridden. 

(II)  Juvenile  Dystrophy  of  Erb  {Scapulo-Mmeral  Form  of  Dys- 
trophy).— This  form  of  dystrophy  begins  in  childhood  or  early  youth, 
a  little  later  than  pseudo-hypertrophy.  The  muscles  of  the  shoulder 
girdle  are  first  attacked,  then  those  of  the  arm.  The  legs  and  fore- 
arms are  not  involved  until  late  in  the  disease.  The  muscles  affected 
are  parts  of  the  pectoralis  and  trapezii,  the  latissimus  dorsi,  the 
rhomboid,  upper-arm  muscles,  and  supinators.  The  supraspinati 
and  infraspinati  are  not  usually  involved.  Fibrillary  twitchings  and 
De  E.  are  absent.     False  and  true  hypertrophy  may  occur. 

(III)  Facio-Scapulo-Humeral  Form  {Landouzy-Dejerine  Type,  In- 
fantile Progressive  Muscular  Atrophy  of  Duchenne). — This  occurs 
usually  in  the  3d  or  4th  year  of  childhood.  It  may  develop  later. 
There  is  first  atrophy  of  the  facial  muscles,  causing  the  "  myopathic 
face."  The  oral  muscle  becomes  weak  and  the  lips  protrude  ("  tapir 
mouth  ").  There  may  be  atrophy  of  the  muscles  of  deglutition  and 
mastication,  and  also  of  those  of  the  eye.  The  shoulders  are  next 
attacked,  and  then  the  disease  progresses  as  in  other  dystrophies. 
The  age  of  onset,  the  hereditary  history,  and  the  location  of  the 
initial  atrophies  are  the  cardinal  points  in  diagnosing  this  form.  The 
prognosis  is  bad.     In  some  cases  the  disease  becomes  stationary. 

(IV)  Arthritic  Muscular  Atrophy.— The  most  common  cause  is 
rheumatic  arthritis.  The  muscles  oftenest  affected  are.those  of  the 
shoulder  girdle.  The  extensors  are  always  first  and  most  affected, 
whichever  joint  is  attacked.  Atrophy  is  greater  in  the  muscles 
above  the  joint  than  in  those  below  it.  The  atrophy  advances 
rapidly  at  first,  but  more  slowly  later.  The  whole  length  of  the 
affected  muscles  becomes  wasted.  There  are  no  fibrillary  twitchings, 
no  De  E.,  no  pain,  tenderness,  or  anaesthesia.  The  irritability  of  the 
muscles  may  be  increased,  and  there  may  then  be  exaggerated  re- 
flexes and  perhaps  a  clonus.  The  prognosis  is  good.  The  muscles 
recover  when  the  arthritis  becomes  well. 

(V)  Occupation  Muscular  Atrophies.— Constant  overuse  of  certain 
muscles  is  the  cause  of  this  form  of  atrophy.  The  atrophy  occurs 
most  frequently  in  the  small  muscles  of  the  hand.  Usually  the 
atrophy  disappears  when  the  muscles  are  given  rest,  but  it  may  pass 


972  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

over  into  progressive  muscular  atrophy.     It  is  distinguished  from 
the  latter  by  the  absence  of  pain  and  vasomotor  symptoms. 

III.    DISEASES  OF  THE  SPINAL  CORD  AND  BULB 

I.  Acute  Anterior  Poliomyelitis. — This  is  a  disease  of  the 
anterior  horns  of  the  spinal  cord  (Fig.  169)  with  sudden  paralysis 
of  one  or  more  limbs  followed  by  atrophy  of  muscles,  but  with  no 
sensory  disturbances.  It  occurs  at  all  ages,  but  the  average  age  at 
the  time  of  the  attack  is  2  years.  Occurs  more  often  in  males  and 
in  the  hot  summer  months.  It  may  be  hereditary  and  also  epidemic. 
Infectious  fevers  (especially  measles),  falls,  injuries,  overexercise,  and 
chilling  of  the  body  when  heated  are  the  chief  causes. 

Symptoms. — The  onset  is  sudden,  with  slight  fever  (100°  to  102°) 
lasting  from  1  to  4  days,  sometimes  with  vomiting,  diarrhoea,  delir- 
ium, and  convulsions.  Within  24  hours  in  acute  cases,  or  a  week  in 
the  subacute,  paralysis  appears,  most  commonly  a  paraplegia,  or  in  one 
leg,  or  a  diplegia,  or  simultaneous  monoplegias.  After  the  acute 
symptoms  subside  there  may  be  pain  in  the  back  and  limbs  for  a  few 
days.  Earely  there  may  be  retention  of  urine.  In  infants  the  respir- 
atory, laryngeal,  and  ocular  muscles  are  not  involved.  The  paraly- 
sis increases  for  from  1  to  4  days,  remains  stationary  for  from  1  to  6 
weeks,  and  improves  for  from  6  to  12  months.  Within  2  or  3  weeks 
there  may  be  some  atrophy  in  the  affected  limbs.  The  paralysis 
gradually  disappears  from  the  limbs  least  affected,  but  leaves  one 
or  both  legs,  generally  one  (and  that  the  right)  permanently  para- 
lyzed. The  affected  limb  is  cold,  mottled,  and  reddish  purple  in 
colour ;  the  muscles  are  flaccid,  become  atrophied,  De  E.  is  present, 
reflexes  absent.  In  the  leg  the  anterior  tibial  group  of  muscles  are 
oftenest  affected  and  foot-drop  results.  The  paralyzed  limb  does  not 
grow  as  rapidly  as  the  unaffected  limb,  but  remains  smaller  and 
shorter,  and  may  develop  contractures  and  various  deformities — e.  g., 
in  the  leg,  talipes  equinus,  varus,  and  valgus,  and  contraction  of  the 
plantar  fascia.  Lateral  curvature  of  the  spine  and  a  deformed  knee 
may  ensue.  In  adults  the  facial  nerve  may  be  attacked.  Earely  the 
nuclei  of  the  ocular  muscles  are  involved  (polio-encephalitis  superior) 
or  the  lower  cranial  nerve  nuclei  (polio-encephalitis  inferior). 

Differential  Diagnosis. — The  cardinal  symptoms  are  :  infancy,  sud- 
den onset,  immediate  and  profound  paralysis ;  the  absence  of  spas- 
ticity, pain,  anesthesia,  and  vesical  or  rectal  symptoms ;  the  pres- 
ence of  De  E.,  the  subsequent  improvement,  and  the  arrested  devel- 
opment of  the  permanently  paralyzed  limb.  In  cerebral  palsy  there 
is  spasticity,  the  reflexes  are  exaggerated,  the  paralysis  is  unilateral, 
and  there  is  no  atrophy  or  De  E.     In  myelitis  and  spinal-cord  hem- 


DISEASES  OF  THE  NERVOUS  SYSTEM  973 

orrhage  there  are  disorders  of  sensation,  yesical  symptoms,  and  bed- 
sores. Multiple  neuritis  and  progressive  muscular  atrophy  rarely 
occur  in  children,  and  their  onset  is  not  so  abrupt. 

Prognosis. — Good  as  to  life,  but  recovery  is  rarely  complete,  one 
leg  remaining  undeveloped  and  more  or  less  paralyzed  and  deformed. 

II.  Cliroiiic  Anterior  Poliomyelitis.— This  disease  is  rare. 
Adult  males  are  chiefly  affected.  The  principal  causative  factors  are 
exposure,  syphilis,  and  lead-poisoning.  One  or  more,  sometimes  all, 
the  extremities  gradually  become  paralyzed,  and  atrophy  with  De  E. 
quickly  follows.  There  are  no  vesical  symptoms,  and  only  slight 
pain  and  sensory  troubles.  The  presence  of  pain,  tenderness,  and 
anaesthesia  in  multiple  neuritis  distinguishes  it  from  this  disease. 
The  rapid  onset,  the  paralysis  quickly  followed  by  atrophy,  the  early 
De  K.,  and  the  absence  of  fibrillary  twitchings  distinguish  it  from 
progressive  muscular  atrophy.  It  may  be  impossible  to  differentiate 
a  central  from  a  peripheral  atrophy. 

In  some  cases,  after  the  paralysis  reaches  its  height  an  improve- 
ment sets  in  which  may  be  nearly  complete.  In  others  the  disease 
progresses  until  a  condition  similar  to  progressive  muscular  atrophy 
exists,  and  after  a  short  time,  or  perhaps  1  or  2  years,  death  ensues. 

III.  Progressive  Muscular  Atrophy  {Progressive  Spinal 
Amyotrophy,  Duchenne-Aran'^s  Disease). — May  occur  between  14  and 
70  years  of  age,  usually  between  25  and  45,  and  is  more  frequent  in 
males.  The  chief  causes  are  traumatism,  exposure,  excessive  use  of 
certain  groups  of  muscles,  great  mental  strain,  childbirth,  syphilis, 
acute  infectious  diseases,  especially  typhoid  fever,  cholera,  and 
measles,  acute  rheumatism,  and  lead-poisoning  (frequent)  (Fig.  169). 

Sympto7ns. — The  first  symptoms  are  slight  rheumatoid  pains  in 
the  arm  or  shoulder,  with  some  numbness  and  a  feeling  of  weariness. 
Atrophy  next  appears,  usually  in  one  hand  (Fig.  223),  the  adductor 
longus  poUicis,  the  thenar,  and  the  interossei  muscles  being  the 
earliest  affected.  The  wasting  extends  without  regard  to  the  nerve 
distribution,  although  the  muscles  supplied  by  the  ulnar  nerve  are 
most  affected.  The  different  motions  of  the  fingers  become  impaired 
according  to  the  muscles  involved.  The  wasting  passes  gradually 
up  the  forearm  to  the  arm  and  shoulder.  The  flexors  and  extensors 
are  alike  affected.  The  hand  is  now  flattened  and  thin,  there  is 
inability  to  flex  the  wrist  or  extend  the  fingers,  and  the  characteris- 
tic condition  of  main  en  griffe  or  claw  hand  is  the  result.  The 
other  hand  usually  becomes  affected  within  from  3  to  9  months. 
Occasionally  the  shoulders  and  arms  are  first  affected  ("  upper-arm 
type "),  the  atrophy  appearing  in  the  deltoid,  triceps,  and  biceps, 
and  extending  downward  to  the  hands. 


974  DIAGNOSIS,   DIRECT   AND   DIFFERENTIAL 

The  wasting  usually  progresses,  passing  from  the  shoulder  mus- 
cles to  the  deep  muscles  of  the  back,  thence  down  to  the  hip  and 
thigh  muscles.  In  this  region  the  glutei,  the  crural  abductors  and 
extensors  are  most  often  affected.  The  muscles  of  the  legs  are  not 
usually  involved,  although  they  may  be.  The  wasting  in  the  trunk 
extends  to  the  intercostals.  The  disease  may  ascend  the  neck,  re- 
sulting finally  in  paralysis  of  the  diaphragm,  or  a  bulbar  palsy  may 
begin.     Exceptionally  the  atrophy  may  begin  in  the  legs  and  ascend. 

From  the  beginning  there  are  weakness  and  paralysis  correspond- 
ing to  the  degree  of  wasting.  This  paralysis  follows  and  is  due  to 
the  atrophy.  There  are  fibrillary  twitchings,  and  the  myotatic  irrita- 
bility is  marked.  Occasionally  the  muscles  are  flaccid,  the  deep 
reflexes,  knee-jerk,  and  arm-jerk  are  early  lost,  and  the  condition  is 
one  of  "  atonic  atrophy."  In  the  majority  of  cases  the  tonicity  and 
rigidity  of  the  muscles  are  increased,  the  knee-jerks  exaggerated,  and 
the  condition  is  one  of  "  tonic  atrophy."  If  this  condition  is  marked 
it  resembles  amyotrophic  lateral  sclerosis. 

The  electrical  irritability  of  the  muscles  is  at  first  only  dimin- 
ished, but  later  there  may  be  partial  De  R.  Parsesthesias  and  rheu- 
matoid pains  may  occur.  There  is  no  anaesthesia  in  uncomplicated 
cases.  Often  there  are  vasomotor  disturbances,  excessive  sweating, 
and  congestion  in  the  parts  involved.  One  or  both  sides  of  the  face 
may  be  affected.  The  pupils  may  be  unequal  in  size.  The  optic 
nerve  is  never  involved.  The  sphincters  are  not  affected.  The  sex- 
ual power  may  be  impaired. 

Diagnosis. — The  disease  must  be  distinguished  from  the  pro- 
gressive muscular  dystrophies,  syringomyelia,  neuritis,  neuritic  fam- 
ily atrophy,  and  chronic  anterior  poliomyelitis.  The  muscular  dys- 
trophies offer  a  history  of  heredity ;  the  disease  begins  in  childhood ; 
the  progress  is  slower ;  there  is  a  more  frequent  involvement  of  the 
lower  limbs ;  and  an  absence  of  De  R.  and  of  fibrillary  twitchings. 
In  syringomyelia  there  are  peculiar  trophic  and  sensory  disturbances. 
In  neuritis  there  is  the  history  of  the  case,  the  involvement  of  the 
extensors  of  the  forearms  chiefly,  and  no  progressive  tendency.  Oc- 
casionally lead  palsy  develops  into  a  true  progressive  muscular  atro- 
phy. The  onset  of  multiple  neuritis  is  rapid,  and  pain  is  a  promi- 
nent symptom.  The  onset  of  chronic  anterior  poliomyelitis  is  sud- 
den, and  the  disease  does  not  progress  after  it  has  reached  its  height. 
The  wasting  follows  the  paralysis.  The  muscles  affected  are  physio- 
logically related,  not  merely  anatomically,  as  in  progressive  muscular 
atrophy.  In  the  hereditary  or  "  leg  type  "  of  progressive  muscular 
atrophy  the  legs  are  first  affected,  there  are  marked  sensory  disturb- 
ances, a  hereditary  or  family  history,  and  typical  De  R. 


DISEASES  OF  THE  NERVOUS  SYSTEM  975 

Prognosis. — The  disease  usually  progresses  with  remissions  until 
it  is  well  developed  and  then  remains  stationary.  Its  duration  is 
from  3  to  30  years,  with  an  average  of  10  years.  Death  is  usually 
caused  by  lung  disease  due  to  paralysis  of  the  respiratory  muscles, 
sometimes  by  involvement  of  the  deglutitory  and  laryngeal  muscles. 

IV.  Progressive  Hereditary  Muscular  Atrophy  of  Leg 
Type  {Charcot- Marie-Tooth  Type). — Occurs  in  males  somewhat 
oftener  than  in  females,  usually  before  the  age  of  20.  It  is  a  family 
or  hereditary  muscular  atrophy  of  a  central  or  neuritic  origin. 

Symptoms. — The  muscles  of  the  leg,  not  the  foot,  are  primarily 
affected,  the  order  of  involvement  being  first  the  peronei,  then  the 
extensors  of  the  toes,  then  the  calcaneal  muscles.  The  thighs  are 
not  affected  until  later.  The  small  hand  muscles  and  those  of  the 
upper  extremities  become  involved  after  some  years ;  still  later  the 
arm  muscles,  except  the  supinator  longus.  The  trunk,  neck,  and 
shoulder  muscles  are  not  affected.  There  may  be  some  fibrillary 
twitchings.  De  R.,  varying  in  degree,  is  always  present.  There  is 
no  anaesthesia,  but  there  may  be  some  pain  and  numbness.  Occa- 
sionally there  may  be  spasmodic  contractions,  especially  of  the  thigh 
muscles.  The  course  of  the  disease  is  long,  and  there  may  be  remis- 
sions, but  it  is  incurable. 

V.  Glosso-Labio-Laryngeal  Paralysis  (Progressive  Bulbar 
Paralysis). — Occurs  usually  between  the  ages  of  40  and  70,  more  fre- 
quently in  men.  A  neuropathic  heredity  is  occasionally  found.  The 
chief  causes  are  sjrphilis,  lead-poisoning,  exposure,  excessive  use  of 
the  muscles  in  talking,  debilitating  influences,  and  mental  strain. 

Symptoms. — The  disease  first  affects  the  tongue,  which  can  not 
be  elevated  or  protruded,  and  appears  wrinkled  and  scarred.  The 
patient  does  not  talk  distinctly  (see  (2),  page  246),  and  is  unable  to 
pronounce  the  lingual  consonants,  I,  n,  r,  and  t.  Xext,  the  lips  be- 
come weak,  and  there  is  inability  to  articulate  the  consonants  m,  p, 
b,  or  the  vowel  0,  or  to  whistle.  Difficulty  in  swallowing,  and  drib- 
bling of  saliva  from  the  mouth  soon  begin.  Hard  solids,  and  later 
fluids,  are  the  most  difficult  to  manage,  semi-solids  being  taken  more 
easily.  The  lips  finally  become  so  paralyzed  that  the  patient  can  not 
shut  the  mouth,  and  the  lower  part  of  the  face  becomes  motionless 
and  expressionless,  while  the  upper  part  manifests  great  suffering 
and  anxiety.  Sometimes  the  facial  nerve  becomes  a  little  involved. 
Articulation  is  at  last  almost  entirely  impossible.  Paralysis  of  the 
palate  gives  the  voice  a  rasal  twang. 

The  patient's  throat  feels  tired  with  a  sense  of  dr}Tiess  and  stiff- 
ness. There  may  be  some  impairment  in  the  sense  of  taste.  Pain 
and  anaesthesia  are  absent.     In  the  latter  part  of  the  disease  there  is 


976  DIAGNOSIS,   DIRECT   AND   DIFFERENTIAL 

partial  De  E.,  but  at  first  the  electrical  reaction  is  normal.  There  is 
a  weakness  of  the  laryngeal  reflex,  and  of  the  adductors,  but  abductor 
paralysis  is  uncommon.  There  is  no  mental  disturbance,  but  often 
there  is  some  emotional  weakness.  The  disease  may  be  the  final 
stage  of  spinal  muscular  atrophy,  or  it  may  be  associated  with  the 
latter,  or  with  ophthalmoplegia,  or  amyotrophic  lateral  sclerosis. 

Diagnosis. — The  cardinal  points  are :  slow  onset ;  progressive 
course;  the  bilateral  character;  absence  of  involvement  of  sensory 
nerves  and  De  E.  This  disease  must  be  discriminated  from  polio- 
encephalitis inferior,  tumours,  bulbar  apoplexy,  softening,  multiple 
sclerosis,  chronic  lesion  of  the  cerebral  hemispheres  causing  pseudo- 
bulbar paralysis,  and  asthenic  bulbar  paralysis.  There  is  marked 
paralysis  in  asthenic  bulbar  paralysis,  but  no  typical  atrophy. 

The  course  of  the  disease  is  progressive,  often  with  remissions  of 
a  few  weeks  or  months.  The  duration  of  the  disease  is  from  3  to 
4  years.     Death  results  from  inanition,  or  pulmonary  disease. 

VI.  Asthenic  Bulbar  Paralysis  and  Asthenic  Bulbo- 
spinal Paralysis. — Occurs  usually  under  the  age  of  30  years,  but 
may  occur  later.  Sometimes  profound  anaemia  is  a  causative  factor, 
also  overwork  and  mental  strain. 

Symptoms. — The  onset  is  gradual.  The  muscles  of  the  throat, 
face,  and  eyes  are  oftenest  affected.  Ptosis  of  one  or  both  eyes  is  a 
common  symptom.  Weakness  of  the  muscles  of  mastication,  defect- 
ive articulation,  and  difficulty  in  swallowing  follow.  The  voice  is 
nasal.  The  condition  resembles  that  of  glosso-labio-laryngeal  paraly- 
sis. Some  ophthalmoplegia  develops  with  great  exhaustion  and 
marked  weakness  of  the  extremities.  The  patient  becomes  almost 
helpless,  perhaps  unable  to  lift  his  arms  or  legs. 

Diagnosis. — This  disease  is  distinguished  clinically  from  true  bul- 
bar paralysis  and  progressive  muscular  atrophy  by  the  fact  that  there 
is  no  true  atrophy  of  the  muscles  of  the  face,  tongue,  or  extremities, 
and  no  fibrillary  twitchings,  and  that  its  course  is  irregular,  with  remis- 
sions. The  disease  is  of  long  duration^  and  its  rate  of  progress  varies. 
The  patient  may  be  almost  moribund,  then  pick  up,  become  worse 
again,  and  so  on  for  years.  He  may  die  within  6  months,  or  after  a 
number  of  years,  or  may  recover.     The  cause  of  death  is  exhaustion. 

VII.  Amyotrophic  Lateral  Sclerosis  (Spastic  Form  of 
Progressive  Muscular  Atrophy.,  or  Charcofs  Disease). — Occurs  usually 
between  the  ages  of  35  and  50,  more  often  in  women.  It  is  not 
caused  by  lead-poisoning,  syphilis,  or  acute  infectious  diseases,  and 
is  considered  to  be  a  disease  of  involution — that  is,  due  to  an  in- 
herently deficient  vitality.  Cold,  trauma,  and  shock  seem  to  be  pre- 
cursors in  some  cases.     (See  also  Fig.  169,  page  490). 


DISEASES  OF  THE  NERVOUS  SYSTEM  977 

Symptoms. — The  disease  in  its  typical  form  combines  the  symp- 
tom complexes  of  anterior  poliomyelitis,  spastic  spinal  paralysis,  and 
bulbar  palsy.  Usually  the  initial  symptoms  are  referable  to  the 
medulla,  but  the  arms  may  be  primarily  affected,  less  often  the  legs. 
There  is  first  a  difficulty  in  swallowing  or  speaking.  There  may  be 
an  occasional  spasm  of  the  tongue,  and  the  lips  or  cheek  may  feel 
stiff.  Then  the  legs  and  arms  become  weak  and  stiff.  The  progress 
of  the  symptoms  is  slow.  There  are  disturbances  of  speech,  and 
swallowing  is  difficult.  The  arms  atrophy  and  become  stiff  and  rigid, 
producing  characteristic  deformities.  The  reflexes  are  markedly  ex- 
aggerated ;  there  is  ankle  clonus ;  the  arm  reflexes  are  increased,  and 
there  is  an  active  Jaw-jerk.  The  jaw  is  stiff.  Slight  pain  may  be 
present.  Ansesthesia  and  sphincter  involvement  do  not  appear  until 
late  in  the  disease.  The  patient  may  become  quite  helpless  and  be 
confined  to  bed  within  a  year,  because  of  the  rigidity  and  con- 
tractures in  both  arms  and  legs.  In  some  cases  the  bulbar  symptoms 
are  prominent,  and  the  atrophies  and  contractures  not  marked. 

Diagnosis. — The  disease  must  be  distinguished  from  multiple 
sclerosis,  transverse  myelitis,  and  the  other  forms  of  progressive  mus- 
cular atrophy.  The  chief  points  of  diagnosis  are :  the  marked  and 
progressive  wasting ;  the  rigidity  and  contractures ;  the  exaggerated 
reflexes ;  and  the  absence  of  sphincter  or  sensory  disturbances.  The 
disease  differs  from  ordinary  bulbar  paralysis  in  that  there  are  stiff- 
ness, cramps,  increased  reflexes,  and  rigidity  in  the  muscles  supplied 
by  the  facial,  trigeminal,  glosso-pharyngeal,  10th,  11th,  and  12th 
nerves.  The  prognosis  is  always  bad.  The  duration  of  the  disease 
is  rarely  longer  than  2  or  3  years.  It  is  shortest  when  the  medulla 
is  most  involved. 

YIII.  Progressive  Ophthalmoplegia  {Progressive  Upper  Bnl- 
hor  Palsy). — This  is  a  degenerative  disease  of  the  nuclei  of  the  motor 
nerves  of  the  eye,  occurring  between  the  ages  of  15  and  40.  Onset 
slow.  Lead,  diphtheria,  syphilis,  and  traumatism  are  the  causes.  It 
occurs  in  locomotor  ataxia,  and  progressive  muscular  atrophy. 

Symptoms.— Often  not  noticed  until  the  condition  is  well  ad- 
vanced. The  mobility  of  the  eyeball  gradually  becomes  limited. 
Then  there  is  a  slight  strabismus,  usually  divergent,  and  drooping 
of  the  eyelids.  The  eye  can  not  follow  the  finger  beyond  a  certain 
limit.  The  peculiar  expression  of  the  face  is  known  as  the  "  Hutch- 
inson face."  Reactions  of  the  pupil  to  light  and  accommodation  are 
not  usually  impaired.  There  may  be  diplopia.  The  coitrse  of  the 
disease  is  slow,  sometimes  almost  stationary,  except  when  complicated 
with  progressive  muscular  atrophy,  in  which  case  it  is  more  rapid, 
and  death  results  in  2  to  3  years,  from  the  latter  disease. 


978  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

IX.  Myelitis  {Injiammation  of  the  Spinal  Cord). — Maybe  acute, 
subacute,  or  chronic.  When  both  white  and  gray  matter  are  affected 
it  is  called  diffuse  myelitis  and  transverse  myelitis.  (See  Fig.  169, 
page  490.)  If  the  periphery  is  involved  the  condition  is  called  mar- 
ginal or  annular  myelitis.  If  the  inflammation  occurs  in  isolated 
parts  of  the  cord  it  is  called  disseminated  myelitis,  and  when  it  sur- 
rounds the  central  canal,  periependymal  myelitis. 

(I)  Acute  Transverse  Myelitis. — This  is  usually  an  acute  softening 
of  certain  parts  of  the  cord  followed  by  secondary  inflammation.  The 
lesion  commonly  involves  1  or  2  inches  of  the  length  of  the  cord, 
and  as  it  affects  both  white  and  gray  matter  it  is  often  called  diffuse 
myelitis.     Disseminated  myelitis  sometimes  occurs  in  an  acute  form. 

Causes. — It  occurs  in  early  adult  life,  chiefly  in  males.  The  pre- 
disposing causes  are  a  neuropathic  tendency,  occupations  necessitat- 
ing exposure,  and  muscular  strain.  The  exciting  causes  are  injuries 
of  all  kinds  to  the  cord,  muscular  strains,  exposure  to  cold,  exten- 
sion of  inflammation  from  surrounding  parts,  alcoholism,  syphilis, 
septic  infections,  and  infective  fevers.  Injury  and  syphilis  are  the 
commonest  causes. 

Symptoms. — Very  rarely  there  are  paraesthesias  or  pain  in  the  back 
and  limbs,  or  a  chill,  as  prodromal  symptoms.  At  flrst  the  feet  and 
legs  feel  heavy,  weak,  and  numb,  occasionally  with  some  pain  in  the 
back.  Spasmodic  twitchings  in  the  limbs  or  even  a  general  convul- 
sion may  occur.  Walking  soon  becomes  difficult,  and  the  legs  begin 
to  feel  stiff.  A  paraplegia  develops  in  a  day  or  so,  perhaps  within  a 
few  hours.  There  is  some  anaesthesia.  The  arms  are  also  paralyzed, 
sometimes  before  the  legs,  if  the  lesion  is  in  the  cervical  cord,  and 
the  intercostal  muscles  may  be  affected.  There  may  be  a  febrile 
movement.  The  sphincters  are  disturbed,  and  very  early  there  is  re- 
tention or  incontinence  of  urine,  and  constipation.  At  the  height  of 
the  disease  the  legs  can  be  moved  slightly,  but  the  patient  is  unable 
to  walk  or  stand.  The  flexors  of  the  feet  are  more  affected  than  the 
extensors.  There  is  no  pain  or  tenderness  in  the  legs,  but  they  feel 
numb  and  heavy.  There  is  often  a  girdle  sensation  at  the  level  of 
the  spinal  lesion.  Upon  the  limbs  and  as  high  up  on  the  body  as  the 
level  of  the  lesion  there  is  anaesthesia  to  touch,  pain,  and  tempera^ 
ture  in  varying  degrees.  At  the  level  of  the  lesion  there  is  usually  a 
zone  of  hyperaesthesia.  When  the  anaesthesia  is  not  total,  the  loss  of 
tactile  sensibility  is  most  complete,  that  of  tenderness  next,  and  that 
of  pain  least.  There  is  an  anaesthesia  of  the  bladder,  with  retention 
of  urine ;  also  anaesthesia  of  the  rectum  and  constipation,  and  the 
patient  does  not  feel  the  faeces  when  his  bowels  move.  The  sexual 
power  is  abolished  when  the  lesion  is  in  the  lumbar  cord,  but  there 


DISEASES  OF  THE  NERVOUS  SYSTEM  979 

may  be  strong  erections  without  the  patient's  knowledge  if  the 
lesion  is  in  the  dorsal  or  cervical  region.  The  bladder  may  also  con- 
tract automatically  and  forcibly  expel  the  urine  when  the  lesion  is 
above  the  lumbar  region.  The  temperature  of  the  limbs  is  at  first 
slightly  elevated,  but  later  it  is  subnormal.  In  a  few  cases  there  may 
be  a  body  temperature  of  102°  to  104°,  under  which  circumstances  the 
prognosis  is  bad.  On  the  buttocks  and  heels  bedsores  may  appear 
early  in  the  disease.  They  are  due  to  trophic  disturbances  and  pres- 
sure. The  skin  may  be  dry,  or  there  may  be  hyperidrosis.  When  the 
lesion  is  in  the  lumbar  cord  the  skin  and  tendon  reflexes  are  dimin- 
ished, the  paralysis  is  flaccid,  the  muscles  tend  to  atrophy,  and  there 
is  De  E.  More  commonly  it  is  dorsal,  and  the  reflexes  become  exag- 
gerated ;  spasms  and  contractions  appear,  and  deformities  result. 

The  reflexes  will  be  absent  if  the  lesion  extends  entirely  across 
the  cord,  although  there  may  be  still  some  excessive  muscular  ten- 
sion. The  arms  are  generally  affected  to  a  greater  extent  than  the 
legs  when  the  lesion  is  in  the  cervical  cord.  The  pupils  may  be 
dilated  and  unequal  because  of  the  involvement  of  the  cilio-spinal 
centre.  If  the  cervical  lesion  is  extensive,  paralysis  of  the  intercostal 
muscles  and  disturbance  of  the  action  of  the  heart  may  ensue. 

The  disease  reaches  its  height  in  a  few  days,  or  at  the  most  within 
2  weeks,  remains  stationary  for  some  weeks,  and  then,  in  non-fatal 
cases,  a  gradual  improvement  begins.  Within  the  first  6  months 
there  is  a  return  of  sensation,  and  within  18  months  some  return 
of  motion  accompanied  by  spasms  and  contractures  due  to  a  descend- 
ing degeneration.  If  the  patient  has  enough  strength  to  walk,  there 
is  apt  to  be  some  ataxia  and  also  a  little  anaesthesia  left,  which  will 
leave  him  in  a  condition  similar  to  "  ataxic  paraplegia." 

Differential  Diagnosis. — This  must  be  made  from  hemorrhage, 
acute  embolic  or  thrombotic  softening,  multiple  neuritis,  meningitis, 
acute  ascending  paralysis,  meningeal  hemorrhage,  and  hysterical 
paralysis.  Spinal  hemorrhage  is  sudden  in  its  onset  and  usually 
there  is  no  fever.  Acute  softening  is  the  initial  lesion  in  many  cases 
of  acute  myelitis  and  therefore  can  not  be  differentiated  from  it.  The 
onset  of  multiple  neuritis  is  slower ;  pain,  local  tenderness,  and  sen- 
sory disturbances  are  more  severe,  and  the  sphincters  are  rarely 
involved.  Acute  ascending  paralysis  is  progressive,  and  disturbances 
of  sensation,  atrophy,  and  changes  in  electrical  irritability  are  absent 
or  slight.  Pain  and  tenderness  in  the  back  and  limbs  are  present  in 
meningitis,  and  there  are  rigidity,  cramps,  and  slight  paralysis,  but 
the  bladder  is  not  affected.  In  hysterical  paraplegia  there  are  the 
various  signs  of  hysteria,  little  spasm  or  rigidity,  and  no  marked 
atrophic  or  electrical  changes.     There  may  be  some  characteristic 


980  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

changes  in  sensation,  and  if  the  knee-jerks  are  exaggerated  it  is 
but  slightly.  The  diagnosis  of  the  location  of  the  lesion  is  made  by 
studying  the  various  symptoms  presented.  When  the  disease  goes 
entirely  through  the  cord  the  reliexes  are  absent. 

Prognosis. — Depends  on  the  extent  and  severity  of  the  motor 
paralysis.  If  there  is  no  improvement  in  6  months,  the  outlook  is 
unfavourable  ;  so  is  the  presence  of  bedsores  and  fever. 

(II)  Subacute  Myelitis  is  that  form  in  which  the  onset  lasts  from 
2  to  6  weeks.  The  course  and  symptoms  are  otherwise  identical 
with  the  acute  form. 

(III)  Chronic  Myelitis. — Usually  occurs  as  a  transverse  myelitis, 
perhaps  as  a  disseminated  or  a  diffuse  myelitis.  Occurs  commonly  in 
early  and  middle  adult  life,  and  is  more  often  secondary  than  primary. 
It  is  really  only  the  later  stage  of  acute  myelitis,  softening,  injury,  or 
hemorrhage.  Chief  causes  are  shock,  alcoholism,  exposure,  infectious 
fevers,  lead-poisoning,  syphilis,  and  the  gouty  diathesis. 

Symptoms. — In  chronic primari/ mi/elitis  the  legs  feel  heavy  and 
tire  easily ;  there  are  numbness  and  prickling  in  the  feet ;  perhaps  a 
feeling  of  constriction  around  the  waist.  The  reflexes  are  exagger- 
ated. The  legs  stiffen,  but  atrophy  is  slight.  There  are  retention  of 
urine  and  constipation.  After  a  few  months  the  condition  is  one  of 
partial  paraplegia  with  exaggerated  reflexes,  rigidity  of  the  legs,  anges- 
thesia,  and  sometimes  slight  pain,  chiefly  in  the  back.  The  muscles 
show  little  change  in  electrical  excitability,  but  become  somewhat  atro- 
phied. Eetention  of  urine  becomes  marked.  The  gait  is  stiff  and  shuf- 
fling. When  the  paraplegia  becomes  complete  the  patient  is  bedridden, 
the  atrophy  increases,  contractures  occur,  the  rigidity  and  anaesthesia 
increase,  and  cystitis  and  nephritis  develop.  If  the  arms  are  involved, 
weakness,  stiffness,  some  atrophy,  anaesthesia,  and  pain  appear. 

Chronic  secondary  myelitis  (most  common)  presents  the  same 
symptoms  as  the  primary  form,  but  they  are  worse  at  first,  then  im- 
prove, or  remain  stationary  for  some  time  before  finally  growing 
worse.  The  dorso-lumbar  regions  of  the  cord  are  usually  affected. 
In  lumbar  lesions,  the  paraplegia,  atrophy,  and  involvement  of  or- 
ganic centres  are  more  marked. 

Compression  myelitis  is  due  to  compression  of  the  cord,  usually 
from  caries  of  the  vertebrae,  tumours,  or  aneurism.  The  onset  is  slow, 
and  the  initial  symptoms  are  those  of  spinal  irritation.  The  final 
condition  is  one  of  spastic  paraplegia  following  weakness,  spasms, 
and  contractures. 

Differential  Diagnosis  of  Chronic  Myelitis. — Must  be  differenti- 
ated from  tabes  dorsalis,  pachymeningitis,  spinal  tumours,  mul- 
tiple sclerosis,  brain  palsies,  amyotrophic  lateral  sclerosis,  and  pro- 


DISEASES  OF  THE  NERVOUS  SYSTEM  981 

gressive  muscular  atrophy.  In  tabes  dorsalis  there  are  ataxia  and 
sensory  disturbances,  with  little  motor  paralysis.  In  pachymenin- 
gitis there  is  a  history  of  injury ;  the  cervical  region  is  usually  the 
seat  of  the  lesion ;  the  pain  and  anaesthesia  are  marked,  and  the 
sphincters  are  not  involved.  The  symptoms  of  spinal  tumours  come 
on  more  slowly,  are  more  localized,  and  there  is  usually  much  more 
pain.  In  multiple  sclerosis  there  are  speech  disturbances,  tremor, 
and  eye  symptoms.  In  brain  palsies  the  paralysis  is  unilateral, 
spastic,  and  without  pain  or  disturbances  of  the  visceral  centres. 
Progressice  muscular  atrophy  presents  atrophy  with  no  sensory  or 
sphincter  disturbance.  The  prognosis  is  not  favourable,  although 
patients  may  live  for  20  years  or  longer. 

X.  Spina  BijQ.da  {Rhacliischisis  Posterior). — Congenital  hernia 
of  the  spinal  membranes,  sometimes  the  cord,  through  a  cleft  due 
to  the  absence  of  some  of  the  vertebral  arches.  Occurs  in  1  child 
out  of  every  1,200,  oftener  in  females.  Hydrocephalus  and  other 
developmental  defects  are  often  associated. 

Forms. — (1)  Spinal  meningocele — the  spinal  membranes  alone 
protrude  into  the  sac.  (2)  Spinal  meningo-myelocele — the  cord  and 
membranes  both  protrude.  (3)  Syringo-myelocele — the  fluid  is  in 
the  central  canal,  and  the  inner  lining  of  the  sac  is  formed  by  the 
meninges  and  thinned-out  spinal  cord. 

Symptoms. — Because  the  lumbar  and  sacral  laminae  are  the  last 
to  solidify,  spina  bifida  almost  always  occurs  in  these  regions.  Two 
or  three  vertebrae  are  usually  involved.  The  skin  is  often  glossy, 
tough,  thickened,  or  ulcerated.  The  tumour  may  be  pedunculated 
or  sessile,  and  varies  in  diameter  from  1  to  6  inches.  The  subjects 
are  feeble,  badly  nourished,  and  poorly  developed  mentally.  Para- 
plegia occurs  in  a  great  number.  In  some  there  is  sphincter  trouble 
and  anaesthesia.  Talipes  is  frequent.  The  diagnosis  is  easy.  Con- 
genital tumours  must  be  excluded.  Important  to  determine  whether 
the  cord  is  in  the  sac  or  not.  Marked  paraplegia,  sphincter  troubles, 
or  anaesthesia  indicate  its  presence.  Most  of  the  cases  die,  but  the 
prognosis  is  best  for  meningocele. 

XI.  Spinal  Hemorrhage.— (I)  Spinal  Meningeal  Hemorrliage. 
—ffcematorrhachis  (hemorrhage  into  the  membranes  of  the  cord, 
usually  outside  the  dura)  is  the  most  common  form.  Occurs  in  the 
newborn  and  in  adults,  in  men  rather  than  women.  Injuries,  frac- 
tures of  the  spine,  and  falls  are  the  most  common  exciting  causes ; 
also  severe  convulsions  from  strychnine  poisoning,  epilepsy,  tetanus, 
chorea,  eclampsia,  or  severe  muscular  exertion.  More  rarely  the 
bursting  of  an  aortic  or  vertebral  aneurism,  cerebro-spinal  meningitis, 
or  malignant  infectious  fevers  are  responsible. 

64 


982  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

Symptoms. — Slight  hemorrhages  may  be  latent.  In  larger  hemor- 
rhages there  are  sudden  severe  pains  in  the  back  and  limbs  corre- 
sponding to  the  seat  of  the  lesion,  with  numbness,  tingling,  hyper- 
aesthesia,  and  muscular  spasms,  chiefly  of  the  back  muscles.  Very 
shortly  weakness  or  paralysis,  anaesthesia,  and  disturbance  of  the 
visceral  centres  may  follow.  The  symptoms  reach  their  height  in  a 
few  hours,  followed  by  slow  recovery,  or  by  chronic  meningitis. 

Diagnosis. — The  cardinal  points  are  :  a  history  of  injury  or  child- 
birth ;  sudden  pain,  and  symptoms  of  irritation,  which  rapidly  sub- 
side. There  is  less  pain  in  haematomyelia  (see  (II),  following)  and 
injury  of  the  cord,  but  more  paralysis  and  anaesthesia.  In  tetanus 
the  symptoms  develop  more  slowly,  and  trismus  is  present. 

Prognosis. — In  severe  cases,  bad,  but  if  the  patient  lives  3  or  4 
days  the  prospect  is  good  for  a  partial  or  nearly  complete  recovery. 

(II)  Hemorrhage  into  the  Substance  of  the  Cord  {Hcemato- 
myelia). — Xot  very  infrequent.  Occurs  as  a  primary  condition,  usu- 
ally in  males  between  20  and  40,  sometimes  in  infants,  from  vascular 
disease  or  purpura  haemorrhagica ;  or,  secondarily,  after  myelitis  and 
tumours.  Overexertion,  exposure,  injuries,  excessive  coitus,  vascu- 
lar syphilis,  convulsions,  old  age,  and  senile  arteries  are  causes. 

Symptoms. — Onset  rapid.  For  1  or  2  hours  there  may  be  numbness 
or  weakness,  followed  by  a  sudden  paraplegia  with  ataxia  or  anaesthe- 
sia, or  both,  perhaps  with  transient  loss  of  consciousness.  The  sphinc- 
ters may  be  paralyzed.  At  first  the  reflexes  may  be  absent,  but  they 
soon  return  and  become  exaggerated.  There  is  often  much  pain  in 
the  back.  If  the  lesion  is  high  up,  the  thorax  and  arms  are  involved. 
In  about  10  days  the  symptoms  subside,  and  a  condition  similar  to- 
chronic  myelitis  ensues ;  otherwise  acute  myelitis  and  death  follow. 

Diagnosis. — Meningeal  hemorrhage  is  more  painful,  with  less 
paralysis,  more  spasm,  and  a  better  recovery.  Sudden  onset,  absence 
of  fever,  and  gradual  recovery  are  points  of  use  in  the  diagnosis. 
Initial  fever  suggests  myelitis. 

Prognosis. — Often  serious  as  to  life,  always  as  to  health,  depend- 
ing on  the  location  and  extent  of  the  lesion ;  better  in  dorsal  than  in 
cervical  hemorrhages. 

XII.  Tumours  of  the  Spinal  Cord. — Comparatively  rare,  and 
occur  usually  between  30  and  50  years,  more  often  in  males.  Tu- 
bercle appears  between  15  and  35  years  ;  lipoma  is  congenital.  Pre- 
disposing causes  are  syphilis,  tuberculosis,  and  cancer.  Exciting 
causes  are  injuries  and  exposure. 

Symptoms. — Depend  upon  the  location,  character,  size,  and  rate 
of  growth  of  the  tumour.  Pain  is  early  and  constant,  usually  con- 
tinuous and  severe,  and  ordinarily  referred  to  nerves  originating  in. 


DISEASES  OP  THE  NERVOUS  SYSTEM  983 

the  region  of  the  tumour.  Girdle  sensation,  numbness,  hyperaesthe- 
sia,  and,  after  a  time,  ansesthesia  may  follow,  with  spinal  tenderness 
and  rigidity.  The  sensory  symptoms  are  generally  more  marked  on 
one  side.  Subsequently  there  are  spasm,  contractures,  and  exagger- 
ated reflexes  involving  one  leg,  or  both,  or  an  arm  and  a  leg.  Para- 
plegia, sphincter  disturbance,  atrophy,  bedsores,  and  death  from 
exhaustion  follow.  With  cervical  tumours  there  may  be  a  gradual 
involvement  of  all  the  extremities  and  the  trunk,  cervical  rigidity, 
and  optic  neuritis.  When  lower  down  a  hemiparaplegia,  or  a  para- 
plegia with  increased  reflexes,  occurs.  If  in  the  lumbar  region  the 
sphincters  are  early  involved  and  the  reflexes  are  sooner  abolished. 

Broicn-Sequard  paralysis  is  a  hemiparaplegia  with  paralysis  of 
motion  and  muscle  sense  on  the  side  of  the  lesion,  and  paralysis  of 
cutaneous  sensation,  especially  of  pain  and  temperature,  on  the  oppo- 
site side.  The  reflexes  are  exaggerated.  There  is  frequently  hyper- 
aesthesia  on  the  side  of  the  lesion,  with  a  band  of  anaesthesia  at  the 
level  of  the  tumour.  The  growth  may  be  outside  or  inside  the  dura 
and  the  symptoms  vary  accordingly.  Cancer,  lipoma,  sarcoma,  and 
gumma  are  the  most  common  extradural  tumours.  In  these  the  sen- 
sory and  motor  irritation  is  more  marked;  there  is  usually  some 
malignant  tumour  elsewhere ;  there  may  be  some  symptoms  of  dis- 
ease of  the  vertebrae,  and  the  paralysis  does  not  usually  take  the 
form  of  hemiparaplegia.  Tubercle  and  glioma  are  the  common  forms 
of  medullary  or  intradural  tumours.  In  these  hemiparaplegia  is 
more  common,  while  early  in  the  disease  spasm,  rigidity,  and  pain 
are  less  common.  There  may  be  a  secondary  myelitis.  Spinal 
tumours  occur  most  frequently  just  below  the  mid-cervical,  and  in 
the  upper  and  the  lower  dorsal  regions.  Hemorrhages,  softening, 
secondary  degenerations,  and  inflammatory  reactions  may  result. 

Diagnosis. — Transverse  myelitis,  caries  of  the  vertebrae,  and  hyper- 
trophic pachymeningitis  must  be  eliminated.  The  points  in  which 
tumour  differs  from  caries  are  the  absence  of  any  external  swelling 
or  kyphosis,  or  of  a  tuberculous  diathesis,  the  slight  amount  of 
rigidity  and  tenderness,  and  the  age  of  the  patient.  Hypertrophic 
pachymeningitis  frequently  can  not  be  distinguished  from  spinal 
tumour.  From  myelitis  the  disease  can  be  differentiated  by  the  his- 
tory of  early  pain,  followed  by  motor  and  then  sensory  paralysis,  by 
the  localization  of  the  symptoms,  and  by  the  progressive  course  of 
the  disease.  In  middle  life  the  tumour  is  probably  a  sarcoma  or  a 
glioma.  Tubercle  is  rare.  The  average  duration  of  the  disease  is 
from  2  to  3  years,  but  it  may  last  for  5  years.  The  prognosis  is  bad. 
Tubercle  may  become  stationary,  and  syphiloma  may  be  amenable 
to  treatment.     Surgery  occasionally  saves  life. 


984  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

XIII.  Syringomyelia.— A  disease  of  the  spinal  cord  in  which 
there  is  a  development  of  gliomatous  tissue  in  the  central  parts  with 
the  formation  of  cavities  (Fig.  169,  page  490).  It  is  comparatively 
rare ;  occurs  in  men  more  often  than  in  women,  and  develops  between 
the  ages  of  15  and  25.  Hand  workers  are  especially  affected.  Preg- 
nancy, trauma,  and  infectious  diseases  seem  causative,  but  it  is  not 
due  to  alcoholism,  heredity,  or  syphilis. 

Symptoms. — Onset  gradual,  with  paraesthesias  in  the  hands  and 
some  aching  pains  in  the  neck  and  arms,  followed  by  muscular  wast- 
ing of  both  hands,  which  increases  and  extends  gradually  toward  the 
trunk.  There  may  be  fibrillary  twitchings  and  a  partial  De  E.  There 
is  usually  a  marked  anaesthesia  of  the  hands  and  arms  to  temperature 
and  pain,  but  not  to  touch.  When  the  legs  are  involved  (late  in  the 
disease)  there  is  generally  spastic  paraplegia.  There  is  a  scoliosis  of 
the  spine,  as  a  rule,  in  the  dorso-lumbar  region.  Earely  the  throat 
and  face  are  involved.  Vasomotor,  secretory,  and  trophic  symptoms 
are  marked — e.  g.,  sweating  or  dryness  of  the  skin  ;  red,  congested,  or 
edematous  hands ;  skin  eruptions,  such  as  herpes,  eczema,  and  bullae ; 
painless  whitlows,  erosions,  and  ulcerations  of  the  terminal  phalanges, 
and  the  nails  may  become  dry  and  brittle  and  drop  off ;  and  arthrop- 
athies or  spontaneous  fractures.  The  pupils  may  be  unequal.  In 
the  late  stages  of  the  disease  the  bladder,  rectum,  and  genital  centres 
are  affected,  and  the  medulla  becomes  involved. 

There  are  5  types  of  the  disease  (Dana)  :  (1)  The  disease  may 
be  latent,  with  few  or  non-characteristic  symptoms  ;  (2)  there  may  be 
a  period  of  irritation  and  pain  in  the  extremities  followed  by  para- 
plegia, with  few  sensory  troubles,  the  course  suggesting  a  chronic 
transverse  myelitis  or  a  Brown-Sequard  paralysis  ;  (3)  a  type  in  which 
bulbar  symptoms  develop  early,  but  differing  from  ordinary  bulbar 
paralysis  in  the  involvement  of  the  trigeminus  and  other  cranial  nerves 
not  commonly  attacked ;  (4)  a  form  characterized  by  a  rather  rapid 
ascending  paralysis;  and  (5)  a  type  characterized  by  the  symptoms 
of  muscular  atrophy  with  analgesia  and  felons  (Morvan's  disease). 
In  this  there  is  probably  a  complicating  neuritis. 

Diagnosis. — The  distinguishing  points  are :  its  beginning  dur- 
ing adolescence,  the  progressive  muscular  atrophy  combined  with 
the  peculiar  dissociated  disturbances  of  sensibility,  and  the  scoliosis 
and  trophic  disturbances.  It  must  be  distinguished  from  progressive 
muscular  atrophy  and  dystrophy,  hypertrophic  cervical  pachymenin- 
gitis, amyotrophic  lateral  sclerosis,  chronic  transverse  myelitis,  anaes- 
thetic leprosy,  and  Morvan's  disease.  In  progressive  muscular  atro- 
phy there  are  no  sensory  or  trophic  disturbances,  or  scoliosis.  The 
disease  can  not  often  be  differentiated  from  Morvan's  disease,  al- 


DISEASES  OF  THE  NERVOUS  SYSTEM  985 

though  whitlows  are  rare  in  the  ordinary  forms  of  syringomyelia. 
Morvan's  disease  begins  in  one  hand  and  slowly  extends  to  the  other, 
and  there  is  generally  loss  of  tactile  as  well  as  thermic  and  pain  sense. 
Dissociation  of  the  sensory  symptoms  is  not  present  in  leprosy,  and 
the  anaesthesia  is  found  along  the  course  of  the  nerves  or  in  sharply 
defined  patches.  The  prognosi,s  is  bad.  The  duration  of  the  disease 
is,  however,  from  5  to  20  years,  with  periods  of  remission. 

IV.    SYSTEMIC  CORD  DISEASES 

Locomotor  Ataxia  {Posterior  Spinal  Sclerosis,  Tabes  Dorsalis). — 
A  chronic  progressive  disease  in  which  primarily  the  posterior  spinal 
ganglia  or  analogous  neurones  are  involved,  later  the  spinal  cord 
and  peripheral  nerves  (Figs.  169,  page  490;  and  197,  page  540). 

There  is  a  common,  a  paralytic,  and  a  neuralgic  form,  and  one  in 
which  optic  atrophy  is  one  of  the  first  symptoms.  The  disease  may 
also  be  complicated  with  muscular  atrophy,  general  paralysis,  and 
other  scleroses. 

Causes. — Occurs  between  the  ages  of  30  and  50,  oftenest  between 
30  and  40,  perhaps  as  early  as  10  or  as  late  as  60,  more  often  in 
males.  Exposure  to  cold  and  wet,  combined  with  muscular  exertion 
and  excessive  railroad  travelling,  dancing  with  exposure,  or  sexual 
intercourse,  are  important  causes.  Heredity  is  indirect  only,  and 
very  unimportant.  The  most  important  single  factor  is  syphilis, 
which  does  not  act  directly,  but  if  followed  by  excesses  and  exposure 
tends  to  produce  the  disease.  A  syphilitic  history  is  found  in  from 
60  to  90  per  cent  of  all  cases.  Acute  infectious  diseases,  depressing 
emotions,  prolonged  lactation,  difficult  labour  with  hemorrhage,  ex- 
cessive smoking,  and  injuries  with  shock  are  also  influential. 

Symptoms. — Locomotor  ataxia  may  be  divided  into  3  stages  :  the 
initial  or  pre-ataxic,  the  ataxic,  and  the  paralytic. 

(1)  The  initial  stage  may  last  for  a  few  months  or  several  years. 
First  noticed  are  slight  uncertainty  in  walking  (especially  in  the 
dark),  occasional  darting  pains  in  the  legs  or  rectum,  sensations  of 
numbness  in  the  feet,  and  attacks  of  double  vision  and  vertigo. 
Vesical  control  is  impaired  and  sexual  power  diminished.  The  knee- 
jerk  is  lost.  The  patient  feels  profoundly  fatigued  without  exer- 
tion.    Areas  of  tactile  anaesthesia  may  be  discovered  on  the  trunk. 

(2)  The  ataxic  stage  lasts  for  several  years.  The  patient's  un- 
steadiness increases,  so  that,  when  walking,  he  uses  a  cane  and 
watches  the  ground  and  his  feet.  He  can  not  stand  with  eyes 
closed  without  swaying  or  perhaps  falling.  The  numbness  in  his 
feet  is  such  that  he  feels  as  if  walking  on  a  thick  carpet.  There  are 
areas  of  anaesthesia  on  the  legs  or  the  feet  and  toes.    The  leg  pains  are 


986  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

lightning-like  and  occur  in  paroxysms.  Sexual  power  may  be  lost. 
Vesical  control  is  impaired,  and  there  are  constipation,  girdle  sensa- 
tion, attacks  of  epigastric  pain  with  vomiting,  and  perhaps  a  cause- 
less diarrhoea.  The  pupils  become  small  and  react  to  accommoda- 
tion, but  not  to  light.  Later  the  ataxia,  pain,  and  anaesthesia  may 
affect  the  arms. 

(3)  The  paralytic  stage.  The  power  of  walking  is  entirely  lost, 
although  the  muscular  strength  of  the  legs  is  fairly  good.  With 
closed  eyes  the  patient  does  not  know  where  his  legs  are,  the  ataxia 
and  anaesthesia  are  marked,  and  he  does  not  feel  a  touch  or  the  prick 
of  a  pin.  The  ataxia,  anaesthesia,  and  pains  in  his  arms  have  in- 
creased, but  never  become  as  bad  as  in  the  legs.  The  pains,  although 
present,  are  not  as  severe.  The  bladder  is  paretic,  anaesthetic,  and 
has  to  be  catheterized.     There  is  usually  no  mental  involvement. 

Description  of  Symptoms. — Ataxia,  both  static  and  motor,  is  pres- 
ent very  early  in  a  moderate  degree,  due  to  a  beginning  anaesthesia  of 
the  joints  and  tendons.  The  knee-jerk  is  early  lost — an  important 
diagnostic  sign.  The  station  (III,  page  32)  and  gait  ((1),  page  33) 
are  characteristic ;  so  also  are  pains  of  a  lightning  or  lancinating 
type,  usually  in  the  legs,  along  the  course  of  the  nerves,  or  in  small 
areas  on  the  leg,  foot,  or  thigh,  so  sudden  and  severe  that  the  pa- 
tient involuntarily  jumps  or  jerks  the  limb.  An  early  symptom 
may  be  a  severe  rectal  neuralgia.  The  pains  may  be  nearly  continu- 
ous, or  may  occur  every  few  days  or  only  once  or  twice  a  month. 
Sometimes  they  are  entirely  absent  for  several  months,  only  to  return 
with  renewed  vigour,  but  usually  persist  throughout  the  disease. 
There  may  be  some  trigeminal  neuralgia. 

Areas  of  tactile  anaesthesia  on  one  or  both  sides  of  the  chest,  and 
in  the  back  at  the  same  level,  are  early  and  diagnostic  symptoms. 
Anaesthesia  affects  first  the  feet,  then  the  legs  and  thighs,  fingers  and 
hands,  later  extending  from  the  thighs  to  the  trunk.  The  anaesthesia 
is  greatest  to  pain,  but  also  affects  the  tactile  and  temperature  senses. 
There  are  often  delayed  sensation  and  polygesthesia.  In  the  hands 
the  anaesthesia  appears  first  over  the  ulnar  distribution. 

Optic  atrophy  (6  per  cent  of  all  cases,  more  often  in  left  eye) 
appears  in  the  pre-ataxic  stage,  and  if  the  patient  has  reached  the 
second  stage  without  it  he  will  probably  escape  it  altogether  (Dana). 
It  begins  with  flashes  of  light,  muscce  volitantes,  and  increased  sen- 
sitiveness to  light.  Vision  fails,  and  there  is  often  a  disturbance  of 
colour  sense,  and  always  an  irregular  contraction  of  the  field  of  vision. 
The  atrophy  progresses  until  in  about  3  years  blindness  results. 
Disorders  of  hearing  are  frequent,  usually  due  to  middle-ear  disease. 

The  eye  muscles  are  nearly  always  implicated.     The  pupils  are 


DISEASES  OF  THE  NERVOUS  SYSTEM  987 

small,  sometimes  uneven,  and  react  to  accommodation  but  not  to 
light  (Argyll-Robertson  pupil).  At  the  beginning  the  light  reaction 
may  be  merely  sluggish.  The  ocular  skin  reflex  is  early  abolished. 
Sometimes  light  and  accommodation  reflexes  are  both  lost,  more  fre- 
quently in  exudative  brain  syphilis. 

Xot  infrequently  there  is  early  a  slight  drooping  of  one  or  both 
lids — sympathetic  nerve  ptosis.  Of  the  external  eye  muscles  those 
most  often  affected  are  the  external  rectus,  levator  palpebrae  and 
internal  rectus,  one  or  several.  These  paralyses  occur  most  often  in 
syphilitic  cases,  and  may  be  transitory  or  permanent.  Early  paraly- 
ses are  usually  transitory. 

Arthropathies  (especially)  and  spontaneous  fractures  of  bones 
occur  in  from  5  to  10  per  cent  of  all  cases.  The  knees,  ankles,  and 
hips  are  most  often  affected,  but  the  shoulder,  elbow,  wrist,  and  fin- 
ger joints  may  be  involved.  Fractures  occur  oftenest  in  the  shaft 
and  neck  of  the  femur.  In  arthropathies  a  sudden  painless  swelling 
of  the  joint  develops  in  from  24  to  48  hours.  An  osseous  hyper- 
plasia of  the  joint  occurs  and  it  becomes  much  enlarged.  If  the 
swelling  is  due  simply  to  synovial  distention  and  enlargement  of 
bones,  as  in  some  mild  cases,  it  soon  goes  down  and  the  joint  returns 
to  nearly  its  natural  size.  In  more  severe  cases  the  disturbance  pro- 
gresses, the  ligaments  become  relaxed,  the  bones  of  the  joint  are 
freely  movable,  luxations  are  easily  produced,  and  the  limb  is  almost 
or  quite  useless.  Arthropathies  may  occur  in  the  early  stages  and 
often  are  not  recognised. 

Spontaneous  fractures  are  usually  due  to  a  slight  fall  or  injury, 
but  violent  muscular  efforts  may  cause  them.  They  are  painless, 
and  heal  well,  sometimes  with  unusual  rapidity. 

Trophic  disturbances  of  the  skin  are  numerous  and  usually 
appear  late.  Herpes  and  lichen  are  the  most  common.  A  round 
perforating  ulcer  may  form  on  the  sole  of  the  foot,  sometimes  follow- 
ing the  cutting  of  a  corn.  Teeth  and  nails  may  fall  out  in  rare 
cases. 

"  Crises  "  of  various  kinds  occur  in  tabes.  Gastric  crises  are  the 
most  common.  They  consist  of  attacks  of  severe  epigastric  pain 
with  vomiting,  sometimes  diarrhoea,  and  may  last  for  2  or  3  days. 
Laryngeal  crises  are  sudden  attacks  of  spasm  of  the  adductors  or 
paralysis  of  abductors,  with  noisy,  croupy  respirations,  cough,  and 
struggling  for  breath.  Vertigo  may  be  present  and  cause  the  pa- 
tient to  fall.  The  pulse  may  be  very  rapid.  The  attack  lasts  from 
a  few  minutes  to  several  hours,  and  is  distressing  but  not  dangerous. 
Simple  aphonia  may  be  present.  Cardiac  crises  consist  of  a  sudden 
dyspnoea  with  rapid  heart  action  and  a  sense  of  suffocation.     Great 


988  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

weariness  and  heaviness  in  the  limbs  is  an  early,  characteristic,  and 
constant  symptom. 

Muscular  atrophies  sometimes  occur.  There  may  be  a  true  pro- 
gressive muscular  atrophy,  with  ophthalmoplegia,  bulbar  paralysis, 
and  spinal  amyotrophy ;  localized  muscular  atrophies,  with  wasting 
of  certain  groups  of  muscles  in  arms  or  legs ;  or  general  wasting. 
Hemiplegia  and  acute  paraplegia  are  found  rarely.  Cerebral  symp- 
toms sometimes  occur  in  tabes,  mainly  insomnia  and  vertigo. 

The  course  of  the  disease  is  not  always  progressive.  Its  duration 
varies  from  1  to  30  years.  The  1st  and  2d  stages  may  last  between 
5  and  20  years  each. 

Diagnosis. — The  cardinal  points  are :  loss  of  knee-jerks ;  light- 
ning pains ;  Eomberg  symptom  and  ataxic  gait ;  Argyll-Eobertson 
pupil ;  numbness  of  the  feet ;  a  history  of  syphilis ;  and  the  slow  on- 
set of  the  disease.  Lightning  pains,  loss  of  knee-jerks,  and  Argyll- 
Eobertson  pupils  are  usually  sufficient  to  assure  a  diagnosis.  The 
disease  in  the  first  stage  must  be  distinguished  from  multiple  neu- 
ritis, hereditary  ataxia,  spinal  syphilis,  spinal  tumour,  chronic  mye- 
litis, neurasthenia,  and  general  paresis. 

Prognosis. — In  a  few  cases  the  disease  may  be  stopped  in  the  1st 
stage  and  the  patient  may  get  practically  well.  After  the  2d  stage 
a  cure  is  impossible,  but  the  patient  may  be  made  comfortable  and 
his  condition  somewhat  improved.  Death  is  rarely  due  to  the  dis- 
ease or  its  "  crises." 

II.  Spastic  Spinal  Paralysis  {Lateral  Spinal  Sclerosis). — A  con- 
genital form,  known  as  Little's  disease,  is  here  considered. 

Little's  Disease. — A  spastic  spinal  paralysis.  Always  congenital, 
presumably  due  to  developmental  defects  in  the  pyramidal  tracts  of 
the  cord  (Fig.  169,  page  490).     It  may  be  hereditary. 

In  family  types  the  disease  may  not  appear  until  the  5th  year  or 
even  later,  but  is  usually  manifested  within  the  1st  year.  The  symp- 
toms are  those  of  ordinary  cerebral  diplegia  or  birth  palsy,  except 
that  there  are  no  marked  mental  defects ;  the  child  is  not  micro- 
cephalic and  idiotic ;  there  are  no  hydrocephalus,  cranial  nerve  pal- 
sies, or  epilepsy.  Children  suffering  from  this  disease  walk  "cross- 
legged,"  the  legs  crossing  one  in  front  of  the  other.  The  legs  are 
more  affected  than  the  arms.  The  facial  and  throat  muscles  may  be 
involved.  Pain  is  absent.  Occasionally  the  disability  increases  as 
the  child  grows  older,  rigidity  and  contractures  occurring  in  the 
legs  and  arms.  At  puberty  mental  impairment  and  epilepsy  may 
appear. 

The  absence  of  epilepsy,  microcephalus,  and  mental  defects  dis- 
tinguishes the  disorder  from  cerebral  diplegia.     The  involvement  of 


DISEASES  OF  THE  NERVOUS  SYSTEM  989 

the  arms  and  the  absence  of  pain  and  sphincter  disturbance  are  the 
points  in  which  it  differs  from  myelitis  due  to  compression.  He- 
reditary spastic  paraplegia  makes  its  appearance  at  about  the  5th 
year,  is  found  in  succeeding  generations  of  a  family,  and  involves 
chiefly  the  legs.  In  mild  cases  the  patient  may  learn  to  walk  and 
use  his  hands,  and  may  slowly  improve  and  live  to  a  good  age. 

III.  The  Combined  Scleroses. — Involvement  of  both  posterior  and 
lateral  columns  of  the  spinal  cord  (Fig.  169,  page  490). 

(1)  The  Combined  Scleroses  of  Pernicious  Ancemia  and  Cachectic 
States  {Putnam's  Type). — Occurs  more  often  in  women  between  the 
ages  of  45  and  65.  A  neuropathic  constitution  predisposes.  Active 
causes  are  severe  malarial  toxaemia,  pernicious  anaemia  and  its  fac- 
tors, disease  of  the  suprarenal  capsule,  and  perhaps  lead-poisoning. 

Symptoms. — The  initial  symptom  is  usually  numbness  in  the  ex- 
tremities, followed  by  increasing  weakness,  and,  finally,  paraplegia. 
Emaciation  and  anaemia  are  marked,  and  obstinate  diarrlwBa  may 
be  present.  There  is  no  paralysis  until  the  paraplegia  appears. 
The  common  symptoms  are  spasticity,  exaggerated  knee-jerk,  ankle 
clonus,  perhaps  ataxia  and  some  anaesthesia.  Girdle  sensation  and 
lightning  pains  are  rare.  The  arms  are  involved,  but  not  so  much  as 
the  legs.  Speech,  vision,  and  other  special  senses  are  not  affected. 
The  sphincters  are  not  involved  until  late.  Finally  there  may  be 
some  mental  disturbance.  In  diagnosis  the  cardinal  points  are  :  the 
age ;  the  presence  of  profound  anaemia  and  perhaps  of  a  malarial 
history;  paraesthesia ;  slight  ataxia;  marked  and  progressive  weak- 
ness and  emaciation;  obstinate  diarrhoea  and  rather  sudden  para- 
plegia.    The  prognosis  is  not  good. 

(2)  Hereditary  Spinal  Ataxia  {Friedreich'' s  Ataxia).— The  chief 
predisposing  cause  is  an  inherited  lack  of  development  of  the  cord^ 
more  especially  of  its  posterior  columns  and  pyramidal  tracts  (Fig. 
169,  page  490).  Other  predisposing  causes  are  neuroses,  syphilis, 
and  habitual  intemperance  in  the  parents.  The  disease  develops  be- 
tween 6  and  15  years  of  age,  sometimes  earlier  or  later,  usually  about 
the  12th  year,  more  often  in  males,  in  children  of  the  labouring  and 
farming  classes,  and  seems  to  follow  the  infectious  fevers. 

Symptoms.— There  is  at  first  some  ataxia  and  weakness  in  the 
legs,  which  gradually  increases  and  after  5  or  6  years  extends  to  the 
arms.  Walking  is  seriously  interfered  with,  and  movements  of  the 
arms  are  impaired.  Within  the  first  year  the  knee-jerks  are  abol- 
ished. There  may  be  bulbar  symptoms,  such  as  thick  or  scanning 
speech,  and  frequently  nystagmus.  Headache  and  vertigo  are  often 
present.  There  are  no  vesical  or  rectal  disturbances.  Talipes  varus, 
dorsal  flexion  of  the  toes,  or  some  other  deformity  of  the  foot,  and 


990  DIAGNOSIS,   DIRECT   AND   DIFFERENTIAL 

lateral  curvature  of  the  spine  often  appear.  The  legs  become  weaker, 
until  finally  paraplegia,  with  contractures  and  atrophy,  begins.  Os- 
cillation of  the  head  and  choreiform  or  inco-ordinate  movements  of 
the  extremities  may  appear.  The  progress  of  the  disease  is  slow. 
Less  common  symptoms  are :  tremors,  spasms,  decreased  elec- 
trical irritability,  vasomotor  paresis,  polyuria,  muscular  atrophy, 
glycosuria,  fibrillary  tremor,  attacks  of  choking,  anaesthesia,  ptya- 
lism,  diplopia,  strabismus,  blepharospasm,  ptosis,  sluggish  pupils,  im- 
potence, tachycardia,  incontinence  of  urine,  fragilitas  ossium,  and 
profuse  sweats. 

Differential  Diagnosis. — The  cardinal  points  are  :  Ataxia,  begin- 
ning in  legs  and  extending  to  arms  and  tongue;  peculiar  rolling, 
ataxic  gait ;  disturbance  of  speech ;  spinal  curvatures  and  talipes ; 
gradual  development  of  paraplegia ;  loss  of  knee-jerk ;  absence  of 
cutaneous  anaesthesia,  bladder  disturbance,  severe  pains,  and  eye 
troubles,  except  nystagmus ;  and  the  development  of  the  symptoms 
at  about  puberty. 

Prognosis. — Although  progressive,  the  disease  may  be  stationary 
for  a  long  time.     Its  average  duration  is  between  15  and  20  years. 

(3)  Hereditary  Ataxic  Paraplegia. — Occurs  in  females  between 
the  ages  of  12  and  16  (Dana).  The  predisposing  cause  is  a  neurotic 
heredity.  Xo  exciting  cause  is  known.  The  symptoms  are  weak- 
ness and  stiffness  of  the  legs  with  marked  ataxia,  occasionally  more 
cerebellar  than  spinal.  The  reflexes  are  much  exaggerated,  with 
ankle  clonus,  and  some  parsesthesia,  but  no  pains,  painful  spasms,  or 
anaesthesia.  The  arms  may  be  slightly,  but  the  legs  are  chiefly,  in- 
volved. The  face,  cranial  nerves,  and  sphincters  escape.  The  health 
is  otherwise  good.  The  diagnosis  must  be  made  from  the  gradual 
onset  and  slow  progress  of  the  disease,  the  age  at  the  onset,  the 
hereditary  and  family  history,  the  ataxia,  and  the  paraplegia.  The 
course  is  slow  and  long,  and,  as  far  as  life  is  concerned,  favourable. 

V.    INFLAMMATION  OP  THE  SPINAL  MENINGES 

(I)  External  Meningitis  {Pachymeningitis  Externa).— Mtecimg 
outer  surface  of  dura  mater.  Eare  and  nearly  always  secondary  to 
tuberculosis,  caries  of  spine,  psoas  abscess,  sacral  bedsores,  perito- 
nitis, pyaemia,  or  purulent  pleurisy. 

Symptoms. — Local  pain  in  back,  radiating  pains,  tenderness, 
hyperaesthesia,  paresis,  twitching,  paraplegia,  exaggeration  of  re- 
flexes, sphincter  involvement,  and  sometimes  anaesthesia. 

Diagnosis. — Eadiating  pains,  tenderness,  kyphosis,  and  the  pres- 
ence of  the  local  disease,  with  the  motor  and  sensory  irritation  and 
paralysis,  are  the  diagnostic  points.     Prognosis  usually  bad. 


DISEASES  OF  THE  NERVOUS  SYSTEM  991 

(II)  Internal  Spinal  Meningitis  {Pachymeningitis  Interna). — 
Affecting  inner  surface  of  dura  mater.  Two  varieties  are  recognised, 
hemorrhagic  and  hypertrophic.  Usually  occurs  in  adults,  sometimes 
in  children,  more  often  in  males.  Exciting  causes  are  alcoholism, 
exposure,  syphilis,  and  trauma  (most  important). 

Symjitoms. — Pain  (shooting  to  occiput  and  back)  and  stiffness  in 
the  neck,  with  numbness,  prickling,  pain,  and  perhaps  stiffness  and 
cramps,  in  the  arms,  generally  more  in  one  than  the  other,  and  worse 
&t  night.  There  may  be  nausea  and  vomiting.  After  6  months  par- 
-alysis  begins,  with  weakness,  atrophy,  rigidity,  and  contractures  in 
the  arms.  Anaesthesia,  hyperaesthesia,  and  trophic  changes  occur. 
Paraplegia  follows,  with  rigidity  and  increased  reflexes,  and  the 
patient  finally  dies  of  exhaustion.  Diagnosis  must  be  made  from 
tumour.  Pott's  disease,  myelitis,  wryneck,  and  progressive  muscular 
atrophy.  The  important  points  are :  history  of  injury ;  slow  pro- 
gressive course ;  the  localization  of  the  symptoms  and  their  bilateral 
character ;  and  pain.  The  majority  of  cases  die.  Some  are  cured, 
others  remain  stationary  for  long  periods. 

(III)  Acute  Spinal  Leptomeningitis  {Inflainmation  of  the  Pia  Mater 
of  the  Spinal  Cord). — Frequently  occurs  in  connection  with  disease 
of  the  cerebral  pia  mater,  seldom  alone.  Children  are  most  often 
affected,  and  among  adults,  men.  Alcohol  predisposes.  Always  sec- 
ondary to  an  infection,  with  or  without  traumatism.  Exciting  causes 
are  tuberculosis,  syphilis,  typhoid  fever,  rheumatism,  insolation,  ex- 
posure, and  surgical  operations. 

Symptoms. — Pain  in  the  back  and  along  the  nerves,  with  some 
fever  and  an  initial  chill.  The  pain  increases,  and  there  is  dorsal 
tenderness,  and  rigidity  of  the  muscles  of  the  back,  sometimes 
amounting  to  opisthotonus.  There  is  constipation,  occasional  re- 
tention of  urine,  and  hyperaesthesia  of  the  skin.  The  reflexes  at  first 
are  increased.  Paralysis  comes  on  after  a  time,  and  there  are  reten- 
tion of  urine,  ansesthesia,  and  atrophy.  The  weakness  increases,  bed- 
sores may  occur,  and  death  from  exhaustion  ensue.  The  symptoms 
come  on  more  slowly  in  the  tuberculous  form,  and  with  greater 
severity  in  the  septic  form. 

Differential  Diagnosis.— This  must  be  made  from  myelitis,  rabies, 
tetanus,  gonorrhceal  rheumatism,  rheumatism  of  the  dorsal  muscles, 
and  strychnine  poisoning.  In  myelitis  there  is  not  much  pain  and  a 
great  deal  of  paralysis.  In  tetanus  there  is  trismus,  no  fever,  and  a 
Tiistory  of  trauma. 

Prog)iosis.—yot  good,  especially  in  cases  with  high  fever,  severe 
pains,  and  early  paralysis,  and  in  tuberculous  meningitis.  The  acute 
form  mav  subside  and  become  chronic. 


992  DIAGNOSIS,    DIRECT  AND   DIFFERENTIAL 

(IV)  Chronic  Spinal  Leptomeningitis  and  Meningo-Myelitis.— Eare^ 
always  secondary,  generally  to  cerebro- spinal  meningitis,  syphilis,  or 
chronic  alcoholism.     Occurs  oftenest  in  male  adults. 

The  symptoms  are  the  same  as  those  of  the  disease  to  which  it  is 
secondary.  Pain  in  back,  radiating  to  trunk  and  limbs,  tenderness 
and  stiffness  of  spine,  twitching  and  spasms  in  limbs  with  weakness, 
and  later,  paralysis,  atrophy,  anassthesia,  and  weakness  of  the  bladder, 
are  the  usual  symptoms.     The  course  of  the  disease  is  irregular. 

The  differential  diagnosis  must  be  made  from  tabes  dorsalis,  my- 
elitis, spinal  irritation,  vertebral  caries,  and  tetanus.  In  tabes  dorsalis 
the  knee-jerk  is  absent  and  there  is  ataxia,  but  no  paralysis  and  no 
tenderness  along  the  spine.  In  vertebral  caries  there  is  deformity, 
the  pain  and  tenderness  is  more  localized,  and  there  is  spasmodic 
fixation  of  the  trunk.  In  spinal  irritation  there  is  neurasthenia  or 
hysteria,  and  no  rigidity,  radiating  pains,  twitching,  atrophy,  or 
paralysis.     The  disease  is  seldom  fatal. 

VI.    INFLAMMATION  OF  THE  MEMBRANES  OF  THE   BRAIN 

(I)  Serous  Meningitis  {Alcoholic  Meningitis^  "  Wet  Brain  "). — An 
acute  toxaemia  of  the  brain  rather  than  a  true  meningitis.  Occurs 
most  frequently  in  males,  usually  after  8  or  10  years  of  drinking,  and 
between  the  ages  of  30  and  40.  The  persistent  use  of  chloral,  co- 
caine, or  morphine  may  lead  to  the  same  condition.  The  exciting 
cause  is  usually  a  continuous  drinking  spell  of  2  or  3  weeks,  ending 
perhaps  in  delirium  tremens. 

Symptoms. — If  the  patient  has  had  delirium  tremens,  he  sinks,. 
after  2  or  3  days,  into  a  semi-coma  with  muttering  delirium,  delu- 
sions, and  hallucinations.  The  temperature  is  normal,  or  slightly 
above,  with  rapid  pulse.  There  is  hyperaesthesia  of  the  skin,  and 
pain  upon  pressure  on  the  muscles  of  the  arms,  legs,  or  abdomen. 
The  pupils  are  small.  In  a  few  days  the  stupor  becomes  more  com- 
plete and  the  patient  hardly  can  be  aroused.  Arms,  legs,  and  neck 
are  stiff,  and  the  latter  is  somewhat  retracted,  and  painful  if  moved. 
The  reflexes  are  exaggerated,  and  the  abdominal  walls  retracted. 
The  eyelids  are  closed,  the  pupils  small  and  do  not  react  well 
to  light.  The  tongue  is  dry  and  coated.  There  may  be  invol- 
untary evacuations  of  the  rectum  and  bladder.  The  extremities 
become  cold  and  stiff,  the  pulse  fast  and  weak.  The  coma  deepens, 
and  the  fever  may  rise  to  104°.  Pneumonia  may  be  present  near 
the  end.  Some  cases  do  not  go  into  this  last  stage,  but  improve  and 
recover. 

Diagnosis. — Must  be  distinguished  from  acute  encephalitis,  ordi- 
nary suppurative  meningitis,  and  acute  serous  meningitis  caused  by 


DISEASES  OP  THE  NERVOUS  SYSTEM  993 

infection,  but,  as  the  symptoms  of  all  these  are  very  similar,  the 
alcoholic  history  usually  decides  the  diagnosis.  Prognosis  bad  after 
marked  rigidity  and  coma  have  begun.  In  most  cases  when  the 
neck  is  stiff  the  patient  dies;  if  not,  the  prognosis  is  better. 

(II)  Inflammation  of  the  Dura  Mater  {Pachymeningitis  Externa). 
— Common  causes  are  injuries,  caries  of  the  petrous  bone  in  mas- 
toid disease,  or  the  ethmoid  bone  in  ozena,  necrosis,  erysipelas,  and 
syphilis.  The  disease  may  be  acute  or  subacute.  The  symptoms  are 
fever,  local  headache,  delirium,  and  occasionally  convulsions  and 
paralysis.     The  diagnosis  is  made  by  finding  the  local  cause. 

(III)  Inflammation  of  the  Pia  Mater  {Leptomeningitis). — The  fol- 
lowing varieties  are  recognised : 

(1)  Acute  Simple  Leptomeningitis. — Occurs  more  frequently  in 
males,  especially  in  the  young.  Trauma  and  acute  alcoholism  pre- 
dispose. The  disease  is  always  the  result  of  an  infection,  reaching 
the  membranes  usually  from  without,  sometimes  through  the  blood. 
Disease  of  the  middle  ear  and  mastoid  cells  is  the  most  frequent 
cause.  Others  are  operations  upon  or  disease  of  the  frontal  sinuses 
and  upper  nasal  passages ;  disease,  injuries,  and  fractures  of  the  cra- 
nial bones ;  pneumonia,  septicaemia,  pyaemia,  scarlet  fever,  variola, 
rheumatism,  empyema,  typhoid  fever,  mumps,  measles,  and,  more 
rarely,  endocarditis  and  brain  abscess.  Sunstroke  alone  does  not 
seem  to  be  a  potent  factor. 

Symptoms. — Prodromal  symptoms  are  languor,  malaise,  headache 
(most  prominent),  irritability,  vertigo,  loss  of  appetite,  and  vomiting. 
In  the  second  or  irritative  stage,  headache,  delirium,  rigidity  of  the 
neck,  hyperaesthesia  of  the  skin,  vomiting,  retraction  of  the  abdo- 
men, irregular  fever,  contracted  and  often  unequal  pupils,  and  occa- 
sionally optic  neuritis  or  retinitis  are  the  chief  symptoms.  Headache 
is  persistent  with  severe  exacerbations.  There  is  an  early  muttering 
delirium,  with  perhaps  alternating  stupor  and  violence.  Vomiting, 
when  present,  is  of  an  explosive  (projectile)  character.  The  neck  is 
retracted  and  rigid.  General  rigidity,  resembling  catalepsy,  may 
appear.  If  the  skin  is  scratched  a  red  line  appears  {tache  ccrehrale). 
The  abdomen  is  "  boat-shaped."  There  is  photophobia,  usually  with 
contracted  and  uneven  pupils.  Convulsions  and  cranial-nerve  pa- 
ralysis (ptosis,  strabismus,  facial  palsy)  may  ensue.  Eespiration  is 
rapid  and  uneven;  the  pulse  usually  arrhythmic  or  intermittent 
(50  to  70).  There  is  irregular  fever  (101°  to  103°),  with  constipation 
and  oliguria  (sometimes  albuminuria). 

In  the  paralytic  stage  there  is  stupor  or  coma.  Some  rigidity 
persists,  so  also  the  scaphoid  abdomen.  The  pupils  may  become 
dilated,  the  skin  is  moist,  and  urine  and  stools  may  be  passed  invol- 


994  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

untarily.  Usually  death  occurs  within  a  day  or  so  after  this.  The 
disease  generally  lasts  from  1  to  2  weeks,  but  it  may  begin  suddenly 
with  coma  and  the  patient  die  within  1  or  2  days. 

Diagnosis. — The  symptoms  and  the  history  of  the  exciting  cause 
usually  make  the  diagnosis  easy.  The  chief  difficulty  is  to  distin- 
guish it  from  cerebro-spinal  fever  or  tuberculous  meningitis.  The 
prognosis  is  bad,  not  so  serious  as  in  tuberculous  meningitis,  more 
80  than  in  cerebro-spinal  meningitis. 

(2)  Epidemic  Cerebro-spinal  Meningitis  {Spotted  Fever,  Cerebro- 
spinal Fever). — See  page  674. 

(3)  Tuberculous  Meningitis. — See  page  724. 

VII.    DISEASES  OF  THE  CEREBRAL  SUBSTANCE 

I.  Apoplexy  from  Intracranial  Hemorrhage  ( Cerebral  HemorrhagCy 
Hemiplegia). — There  may  be  :  dural  or  pachymeningeal ;  pial  or  sub- 
arachnoid ;  or  central  hemorrhages ;  and  hemorrhage  into  the  me- 
dulla, pons,  and  cerebellum  (Daxa). 

(1)  Central  Hemorrhage. — Most  common,  and  due  to  rupture  of 
the  blood  vessels  supplying  the  internal  capsule,  the  great  basal 
ganglia,  and  the  white  matter.  Occurs  somewhat  more  frequently 
in  males,  and,  in  four  fifths  of  all  cases,  after  the  age  of  40.  The 
predisposition  increases  yearly  from  40  to  80. 

Heredity,  marasmic  conditions,  infective  fevers,  chronic  alco- 
holism, chronic  kidney  disease,  gout,  rheumatism,  and  syphilis  pre- 
dispose. Heart  and  arterial  disease  and  miliary  aneurisms  are  deter- 
mining causes.  Other  factors  are  scurvy,  purpura,  leucocytliasmia, 
and  the  apoplectic  habit.  Exciting  causes  are  sudden  physical  exer- 
tion, coitus,  passion  or  excitement,  excessive  eating  and  drinking, 
straining  at  stool,  or  a  cold  bath. 

Symptoms. — The  discussion  of  the  symptoms  of  apoplexy  involves 
a  complicated  series  of  anatomical  data.  Only  the  more  ordinary 
classical  types  are  here  touched.  Very  rarely,  except  in  syphilitic 
cases,  there  are  prodromal  symptoms,  vertigo,  "  full  "  feelings  or  pain 
in  the  head,  numbness  of  one  hand  and  foot,  loss  of  memory  for 
words,  and  bad  dreams.  The  heart  action  may  be  irregular  and  nose- 
bleed may  occur.  The  attack  is  sudden  with  convulsions  and  coma  ; 
coma  alone  ;  or  no  loss  of  consciousness  at  all.  Convulsions  rarely 
occur  with  the  attack  ;  are  unilateral  or  partial,  but  may  be  general 
(due  to  meningeal  hemorrhage). 

The  attack  usually  begins  with  sudden  vertigo  and  unconscious- 
ness (see  Coma  from  Apoplexy,  page  69).  Retention  or  incontinence 
of  urine  and  faeces  may  occur.  The  sp.  g.  of  the  urine  is  high,  and  it 
may  contain  albumin.     In  severe  cases  the  temperature  may  be  sub- 


DISEASES  OF  THE  NERVOUS  SYSTEM  995 

normal  during  the  first  12  hours.  Usually  the  temperature  of  the 
paralyzed  side  exceeds  that  of  the  other  by  1°  or  2°.  In  rapidly 
fatal  cases  the  coma  persists,  the  pulse  increases  in  rapidity,  there  is 
Cheyne-Stokes  breathing,  the  temperature  rises  to  102°  or  103°  until 
shortly  before  death,  when  it  may  fall  again,  speech  and  swallowing 
become  difficult,  hypostatic  pneumonia  develops,  and  the  patient 
dies  in  from  2  to  4  days.  There  are  fatal  cases  which  run  a  slower 
course  of  2  to  3  weeks ;  in  these  consciousness  is  partially  regained, 
and  the  patient  is  stuporous  or  mildly  delirious,  with  restlessness 
and  headaches.  The  temperature  remains  normal,  until  after  2  or 
3  weeks,  when  it  rises,  pneumonia  sets  in,  the  patient  becomes  uncon- 
scious and  dies. 

The  majority  of  cases  are  not  fatal.  In  these  the  coma  disap- 
pears within  5  or  6  hours,  the  patient  is  weak  and  may  be  mentally 
confused,  with  some  disturbances  of  speech.  The  condition  is  now 
one  of  hemiplegia,  the  arm  and  leg  being  affected  most,  the  face 
least.  Of  the  facial  nerve  only  the  lower  2  branches  are  involved 
and  the  eyes  can  be  closed.  The  tongue  protrudes  toward  the  affected 
side.  Anaesthesia  is  sometimes  present  on  the  paralyzed  side,  and 
occasionally  there  may  be  hemianopia  and  disturbances  of  hearing. 
According  to  the  site  of  the  lesion  there  may  be  motor  or  sensory 
aphasia  (page  252).  The  paralyzed  limbs  are  at  first  usually  flaccid^ 
but  rigidity  may  begin  early.  The  temperature  usually  rises  to  100* 
or  102°  on  the  2d  or  3d  day,  and  then  gradually  falls  to  the  normal 
about  the  10th  day.  A  continued  rise  of  temperature  after  the  4th 
or  5th  day  indicates  an  inflammatory  reaction  or  more  hemorrhage. 

The  chronic  stage  begins  when  the  fever  and  signs  of  cerebral 
irritation  have  disappeared,  usually  in  about  4  weeks.  The  leg  and 
arm  can  be  moved  somewhat,  the  sensory  symptoms  are  less  marked,, 
the  mind  is  clear,  and  there  is  no  headache.  The  face  is  least 
affected,  the  leg  next,  and  the  arm  most. 

The  rigidity,  beginning  about  the  2d  week,  gradually  increases^ 
until  there  are'  contractures  of  the  affected  limbs,  involving,  in  the 
foot,  the  extensors  more  than  the  flexors.  For  the  gait,  see  (4),  page 
34.  The  shoulder  is  adducted  and  the  forearm  flexed,  and  the  fingers 
are  flexed  into  the  palm.  The  face  muscles  are  slightly  contracted 
and  draw  to  the  affected  side.     There  is  no  muscular  atrophy. 

The  reflexes,  at  first  diminished  or  absent,  reappear,  the  knee, 
elbow,  and  wrist  jerks  are  much  exaggerated,  and  there  is  ankle 
clonus.  Electrical  irritability  is  never  much  altered.  In  the  par- 
alyzed limbs  there  may  be  tremor,  ataxia,  associated,  continuous  or 
athetoid,  choreic,  and  spastic  movements;  also  burning,  cramping 
pains,  joint  affections,  vasomotor  disturbances,  sweating,  and  skin 


996  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

eruptions.  Parassthesias  are  common.  The  patient  cries  easily,  is 
irritable,  and,  in  general,  emotional,  and  his  memory  and  power  of 
attention  are  affected.     Epilepsy  and  insanity  may  develop. 

(2)  Meningeal  Apoplexy. — Due  to  rupture  of  the  middle  menin- 
geal artery,  or  vein,  or  their  branches.  Obstetrical  and  other  injuries 
to  the  head,  insanity,  and  alcoholism  are  causes.  Distinct  cerebral 
symptoms  usually  appear  within  a  few  hours  after  the  accident,  but 
may  be  delayed  for  periods  of  a  few  hours  to  2  months.  Partial  or 
complete  hemiplegia  appears  on  the  side  opposite  the  clot,  with 
increased  reflexes,  some  rigidity,  and  irregular  spasmodic  movements 
of  the  muscles  of  the  affected  side.  The  pupils  are  contracted  and 
unequal.  The  eyes  usually  look  toward  the  affected  side,  i.  e.,  away 
from  the  lesion.  Stertorous  breathing  is  rare,  the  pulse  is  full  and 
glow,  and  there  may  be  aphasia.  The  temperature  may  be  normal  or 
several  degrees  above.  The  breathing  becomes  stertorous,  the  pulse 
rapid  and  feeble,  and  death  ensues. 

(3)  Pial  Apoplexy. — Rare,  and  usually  caused  by  trauma,  associ- 
ated with  alcoholism  and  syphilis.  There  is  a  sudden  incomplete 
hemiplegia  with  spasmodic  movements. 

(4)  Pons  Apoplexy. — There  is  a  sudden  loss  of  consciousness, 
occasionally  with  spasmodic  movements  of  the  limbs.  There  is 
rigidity  on  both  sides  of  the  body,  and  both  pupils  are  minutely  con- 
tracted. Temperature  always  rises,  perhaps  to  104°.  The  facial  or 
ocular  nerves  may  be  involved,  with  some  hemiplegia. 

(5)  Cerebellar  Apoplexy. — There  may  be  a  headache  for  several 
days,  or  a  sudden  coma  may  occur  with  stertorous  breathing,  perhaps 
vomiting,  and  hemiplegia.  The  hemiplegia  is  on  the  side  of  the 
lesion.     The  respiration  is  especially  affected.     Death  is  inevitable. 

Diagnosis  of  Hemorrhagic  Apoplexy. — To  be  distinguished  from 
uraemic  (page  69),  opium  (page  68),  or  alcoholic  (page  68)  coma,  epi- 
lepsy (page  70),  hysteria  (page  70),  and  acute  softening  from  embolus 
and  thrombus.  Following  are  the  distinguishing  points  between 
hemorrhage  and  acute  softening  (Daxa)  : 

Hemorrhage — Age,  30  to  50  Acute  Softening — Earlier  (in  embolism) 

History  of  arterial  disease  in  family.  or  later  age  (in  thrombus) 

Sudden  onset,  with  coma  and  paralysis  History  of  syphilis. 

occurring  together,  the  coma  deepen-  Premonitory  symptoms  and  more  grad- 
^^S-  ual  onset  (in  thrombus),  more  transi- 

Initial  and  early  rigidity.  tory  coma  or  absence  of  coma. 

Very  unequal  pupils.  Initial  convulsive  movements. 

Stertorous breathingandhard,slowpulse.  Presence  of  weak  heart  (in  thi*ombus). 

Peculiar  alternating  conjugate  deviation.  Presence  of  endocarditis  (in  embolism). 

Early  rigidity.  Slight  hemiplegia  with  anaesthesia. 

Peculiar  disturbances  of  temperature.  The  puerperal  state  (in  embolism). 


DISEASES  OF  THE  NERVOUS  SYSTEM  997 

Prognosis  of  Hemorrhagic  Apoplexy. — Most  cases  recover,  seldom 
completely,  from  the  1st  attack.  A  2d  attack  is  liable  to  occur  within 
6  years,  from  which  the  minority  recover.    A  3d  attack  is  often  fatal. 

II.  Acute  Softening  of  the  Brain  {Embolism,  Thrombosis). — 
Thrombosis  is  more  frequent  in  men,  embolism  in  women.  Em- 
bolism usually  occurs  between  the  ages  of  20  and  50,  rarely  in  chil- 
dren ;  thrombosis  between  50  and  70.  The  predisposing  causes  in 
embolism  are  infectious  fevers,  acute  or  recurrent  endocarditis,  blood 
dyscrasias,  pregnancy,  and  profound  anaemia ;  in  thrombosis,  fatty 
heart,  blood  dyscrasias,  and  syphilitic,  lead,  or  gouty  arteritis. 

Symptoms. — In  embolism  the  onset  is  sudden,  with  convulsive 
twitchings,  then  hemiplegia,  and  a  temporary  loss  of  consciousness. 
Fever  develops  after  a  few  days. 

In  thrombosis  prodromal  symptoms  are  frequent.  There  may  be 
cranial-nerve  paralyses  and  headaches  when  syphilis  is  present ;  in 
other  cases  drowsiness,  numbness  in  the  hand  and  foot,  transient 
hemiplegia,  vertigo,  and  temporary  aphasia.  The  onset  is  slow,  the 
hemiplegia  taking  hours  to  become  complete,  during  which  time  the 
patient  gradually  becomes  comatose ;  sometimes  more  sudden,  with- 
out loss  of  consciousness ;  or  it  may  come  on  during  sleep.  There 
may  be  an  initial  fall  in  temperature  followed  by  a  rise. 

The  hemiplegia  due  to  embolus  or  thrombosis  is  apt  to  improve 
rapidly  within  a  few  days  or  weeks,  but  the  chronic  stage  resembles 
that  of  hemorrhage.  There  is  usually  more  mental  impairment  in 
thrombosis  than  in  embolus. 

Diagnosis. — Distinguished  from  hemorrhage  by  a  syphilitic  his- 
tory, and  the  earlier  or  later  age  of  its  occurrence ;  by  the  presence 
(in  thrombosis)  of  a  more  gradual  onset,  premonitory  symptoms,  and 
a  weak  heart,  and  (in  embolism)  of  endocarditis,  the  puerperal  state, 
initial  convulsive  movements,  and  slight  hemiplegia  with  anaesthesia. 
The  prognosis  is  better  than  in  hemorrhage,  and  the  recovery  is  more 
complete. 

III.  Polio-enceplialitls  {Acute  Exudative  Encephalitis  of  the  Gray 
Matter).— The  symptoms  are  those  of  acute  glosso-labio-laryngeal  palsy 
(page  975),  or  of  ophthalmoplegia  (pages  198,  201,  and  977),  accord- 
ing as  the  disease  is  inferior  or  superior. 

IV.  HEemorrhaglc  Encephalitis  {Acute  Exudative  Encephalitis  with 
ffemorrhage).— Occurs  most  frequently  in  females,  and,  when  due  to 
infection,  usually  under  the  age  of  20.  Exciting  causes  are  infec- 
tious fevers,  such  as  cerebro-spinal  meningitis,  typhus,  and  typhoid, 
influenza,  and  malignant  endocarditis ;  the  puerperal  state,  sunstroke, 
and  acute  alcoholism. 

Symptoms.— Onset  sudden,  with  severe  headache,  and  fever  (per- 
65 


998  DIAGNOSIS,    DIRECT  AND   DIFFERENTIAL 

haps  to  105°).  Vomiting,  vertigo,  photophobia,  and  delirium  may- 
be present,  followed  by  semi-coma  or  stupor.  The  pulse  is  rapid 
and  weak,  breathing  shallow  and  frequent,  deep  reflexes  diminished, 
the  sphincters  perhaps  involved.  After  a  few  days  or  2  or  3  weeks 
the  coma  may  change  to  restlessness  and  irritation,  or  the  patient  may 
gradually  improve  and  eventually  recover.  In  the  early  stage  there 
may  be  epileptoid  convulsions,  hemiplegia,  paralysis  of  an  arm  or  leg^ 
aphasia,  hemiataxia,  hemianopia,  impairment  of  speech  and  degluti- 
tion, eye  palsy,  nystagmus,  or  optic  neuritis. 

Diagnosis. — Must  be  distinguished  from  meningitis  by  the 
sudden  onset  with  coma ;  the  absence  of  stiff  neck,  pinhole  pupils, 
rigidity  of  the  limbs,  projectile  vomiting,  and  hyperaesthesia ;  and 
the  presence  of  local  paralysis  or  hemiplegia,  or  the  occurrence  of  an 
epileptic  attack. 

Prognosis. — Serious,  but  patients  often  recover.  Mild  cases  run 
a  course  of  2  to  3  weeks ;  in  severe  cases  the  patient  soon  dies  of  ex- 
haustion, but  the  disease  may  last  for  weeks  or  months. 

V.  Abscess  of  the  Brain  {Acute  Supimrative  Ejiceplialitis). — Oc- 
curs between  the  ages  of  1  ajid  50,  especially  between  10  and  30. 
More  frequent  in  males.  Due  primarily  to  microbic  infection, 
although  the  microbe  and  mode  of  entrance  vary.  Chief  exciting 
causes  are  disease  of  the  nose,  ear,  or  cranial  bones,  suppurative  pro- 
cesses in  general,  injuries,  tumours,  and  infectious  fevers.  The 
most  common  cause  is  chronic  disease  of  the  middle  and  internal 
ear,  especially  when  the  mastoid  cells  and  tympanum  are  affected  ^ 
next  are  injuries  or  chronic  disease  of  the  cranial  bones,  empyema, 
tuberculosis  of  the  lungs,  fetid  bronchitis,  pyaemia,  typhus  and 
typhoid  fevers,  smallpox,  diphtheria,  influenza,  and  erysipelas. 

Symptoms. — In  acute  cases  the  onset  is  rapid,  and  the  symptoms 
may  be  divided  into  3  groups  :  1.  Those  due  to  pressure  :  vomiting, 
persistent  and  severe  headache,  vertigo,  mental  dulness,  perhaps  de- 
lirium, and  finally  coma.  The  temperature  and  pulse  vary,  but  are 
both  usually  normal  or  subnormal.  The  pupils  may  be  irregular,  and 
optic  neuritis  may  occur.  2.  Toxic  symptoms,  as  in  any  septic  poi- 
soning, i.  e.,  anorexia,  emaciation,  prostration,  irregular  fever,  and 
mental  and  sensory  disturbances.  3.  Those  due  to  local  irritation 
or  destruction :  paralysis,  usually  hemiplegia ;  epileptoid  convulsions 
(rarely) ;  aphasia,  and  some  cranial-nerve  disorders.  The  final  stage 
is  coma  and  death  from  exhaustion. 

In  chronic  cases  the  onset  is  exceedingly  slow ;  perhaps  with  no 
active  symptoms  for  months  or  even  years,  during  which  there  may 
be  depression,  mental  irritability,  headaches,  vertigo,  and  convul- 
sions.    The  symptoms  may  at  times  be  greatly  increased  in  severity, 


DISEASES  OF  THE  NERVOUS  SYSTEM  999 

with  vomiting,  intense  pain,  and  perhaps  delirium  or  convulsions, 
which  subside  and  leave  the  patient  in  fairly  good  health.  The 
final  stage  may  begin  with  symptoms  like  those  in  the  acute  form. 
In  other  cases  sudden  coma,  or  epileptic  or  apoplectic  attacks  may 
occur,  which  are  rapidly  fatal.  The  disease  (especially  if  traumatic) 
is  frequently  complicated  by  meningitis,  or,  when  caused  by  ear 
disease,  by  phlebitis  of  the  superior  and  lateral  sinuses. 

Brain  abscesses  occur  more  frequently  in  the  cerebrum  (right 
side,  frontal  and  temporal  lobes  especially)  than  in  the  cerebellum, 
and  are  rare  in  the  medulla  and  pons,  depending  upon  the  anatom- 
ical relation  of  the  cause  of  the  abscess  to  the  temporal  lobe  and  the 
cerebellum.  The  course  of  an  acute  brain  abscess  is  from  0  to  14 
days,  in  rare  cases  a  month.  In  chronic  brain  abscess  the  latent 
period  may  last  from  a  few  weeks  to  months,  or  even  1  or  2  years, 
the  terminal  symptoms  only  a  few  days. 

Diagnosis. — The  cardinal  points  are :  a  history  of  ear  or  nose 
disease,  injury,  or  remote  suppuration  ;  the  presence  of  septic  symp- 
toms, headache,  vomiting,  local  tenderness  and  increased  tempera- 
ture of  the  scalp,  normal,  subnormal,  or  irregular  temperature,  slow 
pulse,  stupor,  optic  neuritis,  lessened  urinary  chlorides,  rapid  emaci- 
ation, and  delirium.  The  diagnosis  of  the  location  of  the  lesion 
must  be  made  from  a  history  of  the  cause,  the  presence  of  tender- 
ness and  increased  temperature  over  a  local  area  of  the  scalp,  local 
convulsions,  and  hemiplegia.  Brain  abscess  must  be  distinguished 
from  meningitis,  brain  tumours,  and  phlebitis  of  the  sinuses.  The 
prognosis  is  always  bad  without  surgical  interference. 

VI.  Chronic  Hydrocephalus.— Usually  (80  per  cent)  begins  at  birth 
or  within  the  first  6  months.  Predisposing  causes  are  lead-poison- 
ing, tuberculosis,  alcoholism,  or  syphilis  in  the  parents,  rachitis,  and 
some  unknown  family  taint.  Late  childhood  or  adult  cases  are  usu- 
ally due  to  tumour  or  infiammation  obstructing  the  venae  Galeni  and 
the  Sylvian  aqueduct. 

*S'^m;;/owA'.— Usually  the  child's  head  (see  page  154)  begins  to  in- 
crease in  size  (Fig.  18,  page  155)  soon  after  birth,  or  may  be  much 
enlarged  at  birth.  The  infant  becomes  irritable  and  restless ;  its  gen- 
eral nutrition  is  impaired ;  it  does  not  grow  as  do  normal  children, 
although  the  appetite  may  be  good ;  does  not  develop  mentally;  and 
generally  does  not  learn  to  walk.  Strabismus,  and  occasionally 
optic  atrophy,  are  present.  Within  2  or  3  years  vomiting,  coma,  and 
convulsions  appear,  and  death  from  exhaustion  occurs. 

Diagnosis.— The  disease  must  be  distinguished  from  rickets  by  the 
shape  of  the  head  (see  page  155)  and  the  presence  of  bone  changes 
in  the  latter  {q.  v.).     Cases  which  develop  after  birth  may  live  for 


1000  DIAGNOSIS,   DIRECT   AND  DIFFERENTIAL 

about  5  years.  If  mild,  the  process  may  stop  and  the  patient  live  a 
fairly  healthy  life.  Congenital  cases  may  live  from  2  to  3  years,  but 
usually  die  within  a  few  months. 

YII.  Infantile  Cerebral  Palsies. — (1)  Infantile  Hemiplegia. — Oc- 
curs slightly  oftener  in  males,  and  in  the  great  majority  during  the 
first  3  years  of  life.  In  congenital  cases  due  to  emotional  disturb- 
ances, injuries,  and  perhaps  diseases,  affecting  the  mother  during 
pregnancy ;  in  cases  occurring  at  birth,  the  use  of  forceps,  tedious 
labour,  or  other  conditions  involving  injury  to  the  child ;  in  cases 
occurring  after  birth,  injuries,  infectious  fevers  (especially  pertussis, 
measles,  pneumonia,  scarlet  fever),  epileptic  convulsions,  cerebro-spinal 
meningitis,  and  rarely  syphilis. 

Symptoms. — A  general,  perhaps  unilateral,  convulsion,  which  may 
last  for  hours,  initiates  about  one  quarter  of  the  cases,  and  is  accom- 
panied by  fever  which  persists  for  several  days.  During  this  period, 
or  after  the  acute  symptoms  have  disappeared,  the  arm,  leg,  and  face 
of  one  side,  or  of  both  sides,  are  found  to  be  paralyzed.  This  paraly- 
sis gradually  improves,  the  face  first  and  most,  then  the  leg,  and  the 
arm  last  and  least.  The  growth  of  the  affected  side  is  retarded,  and 
eventually  the  leg  or  arm  maybe  1  or  2  inches  shorter  than  the  other. 
The  paralyzed  limbs  are  cold,  there  are  vasomotor  disturbances,  and 
rigidity,  with  contractures  of  the  flexors  and  adductors.  The  most 
common  contractures  are  of  the  heel,  causing  talipes  equino-varus,  or 
equino-valgus ;  and  of  the  forearm,  wrist,  fingers,  and  the  adductors 
of  the  thigh.  Various  motor  spasms  develop,  e.  g.,  ataxic,  choreic, 
and  athetoid  (most  common)  movements,  also  associated  movements 
and  tremors.  The  reflexes  are  exaggerated  and  clonus  is  usually 
present.  The  mental  development  suffers.  Feeble-mindedness,  im- 
becility, and  complete  idiocy  each  claim  an  equal  number.  About 
one  fourth  of  all  cases  preserve  fair  intelligence.  Xearly  one  half  of 
the  cases  have  epilepsy ;  and  a  microcephalic  or  macrocephalic  skull, 
asymmetry  of  the  skull  and  face,  imperfectly  developed  teeth,  a  high 
palatal  arch,  and  prognathism  are  common.  As  a  rule  the  skull  on 
the  side  of  the  lesion  is  flattened.  The  special  senses  are  sometimes 
defective.  The  chronic  stage  begins  a  few  months  after  the  attack. 
After  the  first  amelioration  there  is  little  change  until  after  puberty, 
when  the  general  physical  condition  usually  improves. 

(2)  Diplegias  or  Birth  Palsies. — Due  to  injuries  received  at  birth, 
or  (more  commonly)  to  intra-uterine  disorders.  At  birth  there 
may  be  prolonged  asphyxia  or  convulsions.  Some  weeks  later  it  is 
noticed  that  the  child  does  not  use  its  arms  or  legs.  More  convul- 
sions occur,  and  a  double  hemiplegia  becomes  distinctly  evident,  with 
marked  mental  impairment.     Epilepsy  is  common. 


DISEASES  OP  THE  NERVOUS  SYSTEM  IQOl 

(3)  Spastic  Cerebral  Paraplegia  {Little's  Disease). — See  page  988. 

Diagnosis  of  Cerebral  Palsies. — Must  be  distinguished  from  spinal 
palsies,  in  which  there  is  an  absence  of  rigidity,  the  reflexes  are  not 
exaggerated,  there  is  marked  atrophy  and  shortening  of  the  limbs, 
and  De  E.  is  present.  The  mode  of  onset  and  the  distribution  of  the 
paralyses  in  cerebral  palsies  are  characteristic.  In  mild  cases  the 
hemiplegia  may  almost  disappear ;  with  marked  epilepsy  and  mental 
impairment  they  rarely  reach  adult  life,  otherwise  they  may  improve 
and  live  long. 

VIII.  Tumours  of  the  Brain. — The  commonest  forms  are  the 
sarcomatous  type,  tubercle,  gumma,  and  infectious  granulomata. 
Occur  at  all  ages  up  to  50,  one  third  under  the  age  of  20,  more  often 
in  males.  Predisposing  cause  is  perhaps  heredity ;  occasional  excit- 
ing causes  are  injuries  to  the  head.  In  childhood,  tubercle  is  the  most 
common  form,  next  glioma  and  sarcoma ;  after  20  years,  gumma, 
glioma,  and  sarcoma ;  in  middle  age  and  late  life,  sarcoma,  gumma, 
and  cancer. 

Symptoms. — The  general  symptoms  are :  persistent  intense  head- 
ache with  marked  exacerbations ;  vomiting,  convulsions,  general  or 
local ;  paraesthesias ;  vertigo,  impaired  eyesight,  and  perhaps  mental 
dulness  or  slowness.  Weakness  and  emaciation  follow  the  vomiting 
and  intense  pain.  Paralyses  and  blindness  ensue,  convulsions  occur 
more  frequently,  the  patient  becomes  bedridden,  and  after  from  1  to 
5  years  dies  of  exhaustion. 

Head  pain  occurs  in  over  one  half  of  all  cases,  is  very  severe 
(lancinating,  boring),  and  may  be  in  the  forehead,  occiput,  or  the 
whole  head.  It  may  be  periodic,  quotidian,  or  tertian,  as  if  of 
malarial  origin.  Pain  occurs  most  frequently  with  tumours  of  the 
cerebellum  or  the  cerebral  hemispheres  and  midbrain  ;  less  often  if 
in  the  peduncles  and  at  the  base.  There  may  be  tenderness  of  the 
scalp  and  cranium,  especially  over  the  tumour.  Vertigo  is  present 
in  nearly  one  half  of  the  cases,  either  severe  (especially  with  cere- 
bellar tumours)  and  accompanied  by  forced  movements,  or  slight. 
Vomiting,  frequently  "  projectile  "  and  with  little  or  no  nausea,  oc- 
curs about  as  often  as  headache,  with  rapidly  growing  or  cerebellar 
tumours.  Optic  neuritis  (four  fifths  of  all  cases,  usually  in  both 
eyes)  is  most  frequent  in  tumours  of  the  cerebellum,  midbrain,  and 
great  basal  ganglia ;  rare  in  tumours  of  the  medulla,  infrequent  in 
slow-growing  tumours ;  and  usually  ends  in  optic-nerve  atrophy. 

In  about  one  fourth  of  the  cases  general  convulsions  occur,  more 
frequently  when  the  tumour  is  in  the  cerebral  hemispheres  and  cor- 
tex. Apoplectiform  attacks,  more  rarely  true  apoplexy,  may  occur. 
There  is  almost  always  some  mental  impairment,  e.  g.,  attacks  of 


1002  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

somnolence,  mental  slowness,  weakened  memory  and  power  of  atten- 
tion, and  sometimes  silliness,  childishness,  or  peculiar  mental  irri- 
tability. In  tumours  affecting  the  pons  and  medulla  and  the  origin 
of  the  cranial  nerves,  there  is  frequently  a  speech  disturbance  con- 
sisting of  a  running  together  of  the  syllables  of  words.  The  cranial 
temperature  is  somewhat  higher  than  under  normal  circumstances. 

Tumours  cause,  besides  general  symptoms,  focal  symptoms^  which 
depend  upon  the  site  of  the  tumours.  For  convenience  the  brain  is 
divided  into  12  parts  or  areas,  as  follows  (Daxa)  : 

1.  Prefrontal  Area. — Often  cause  no  distinct  localizing  symptoms.  In  a 
goodly  number  of  cases  there  are  peculiar  mental  disturbances  consisting  of 
childishness,  silliness,  mental  hebetude,  and  a  tendency  to  laugh  or  cry  or  get 
angry  at  slight  causes.  There  may  be  optic  neuritis,  hemianopia,  and  anosmia. 
Involvement  of  the  orbit  results  in  ocular  paralyses  and  exophthalmos.  Back- 
ward growth  causes  irritation  of  the  motor  centres,  with  convulsions,  spasms, 
and  paralyses.  2.  Cerebral  Region. — Tumours  here  first  irritate  the  motor 
centres,  causing  Jacksonian  epilepsy  (page  516).  Sensory  symptoms  often  pre- 
cede or  accompany  the  spasms,  i.  e.,  prickling,  numbness,  or  slight  hemianaes- 
thesia.  As  the  tumour  grows  the  convulsions  become  general,  and  hemiplegia 
may  appear.  There  may  be  some  impairment  of  the  muscular  sense.  Agraphia 
and  motor  aphasia  may  also  be  present.  3.  Parietal  Area. — The  most  charac- 
teristic symptoms,  which  may  be  slight,  are  disorders  of  muscular  sense  and 
word-blindness.  When  the  tumour  is  near  the  longitudinal  fissure  the  leg 
muscles  may  be  involved.  4.  Occipital  Lobes. — Tumours,  situated  in  the  cuneus 
and  first  occipital  convolution,  cause  homonymous  hemianopia  (page  205). 
Mind- blindness  (page  265)  may  result  if  the  other  parts  of  the  occipital  lobe  are 
involved  and  without  serious  injury  of  the  cuneus.  There  may  be  word-blind- 
ness, with  some  hemianopia,  if  the  tumour  grows  toward  the  angular  gyrus. 
HemianiEsthesia  and  perhaps  hemiplegia  may  occur  when  the  tumour  encroaches 
forward  upon  the  parietal  area.  5.  Temporal  Area. — Tumours  on  the  right  side 
produce  few  symptoms  ;  on  the  left  side  word-deafness,  and  attacks  of  vertigo 
or  forced  movements.  There  may  be  disturbances  of  taste  and  smell  if  the 
hippocampal  convolution  and  the  uncus  are  involved.  6.  Conpus  Callosum. — 
Tumours  are  rarely  found  here.  The  focal  symptoms  are  a  gradual  hemiplegia 
followed  by  paraplegia,  with  drowsiness,  mental  dulness,  and  stupidity.  The 
cranial  nerves  are  not  affected.  7.  The  Great  Basal  Ganglia  and  the  Capsule. — 
The  symptoms  are  similar  to  those  of  tumours  in  the  corpus  callosum.  There 
may  be  less  stupidity.  There  is  a  progressive  hemiplegia,  sometimes  with 
anaesthesia  or  choreic  movements.  Involvement  of  the  posterior  part  of  the  optic 
thalamus  will  cause  hemianopia  with  hemiopic  pupillary  inaction  (page  205). 
8.  Corpora  Quadrigemina,  Deep  Marrow,  and  Pineal  Gland. — Inco-ordination, 
forced  movements,  and  oculo-motor  palsies  are  characteristic.  There  may  also 
be  blindness  or  hemianopia.  9.  Crura  Cerebri. — Tumours  here  are  very  rare, 
and  cause  a  crossed  paralysis.  10.  Pons  and  Medulla. — The  symptoms  vary 
according  to  the  size  and  location  of  the  tumour.  If  high  up  in  the  pons  there 
will  be  3d-nerve   paralysis  on  one   side,   hemiplegia  on  the  other  ;    if  lower 


DISEASES  OF  THE  NERVOUS  SYSTEM  1003 

down,  5th-nerve  paralysis  on  one  side,  hemiplegia  on  the  opposite  side.  When 
large,  hemiansesthesia  may  exist  with  the  hemiplegia.  A  tumour  in  the 
medulla  causes  hemiplegia  and  hemianaBsthesia,  with  paralysis  of  the  hypo- 
glossal, or  some  other  cranial  nerve  on  the  same  side.  If  both  sides  of  the 
medulla  are  involved  the  symptoms  of  progressive  bulbar  paralysis  may  appear. 
Pous  tumours  sometimes  cause  a  conjugate  deviation  of  the  eyes  toward  the  side 
opposite  to  the  lesion.  11.  Cerebellum.— If  the  tumour  is  in  the  middle  lobe 
there  is  cerebellar  ataxia  (see  page  530),  and  there  may  be  severe  forced  move- 
ments. There  are  often  secondary  symptoms  from  pressure  on  the  medulla 
when  the  tumour  is  in  the  middle  lobe.  Cranial-nerve  disturbances  and  gly- 
cosuria are  usual.  In  the  lateral  lobes  there  are  no  localizing  symptoms  until 
the  tumour  presses  upon  the  adjacent  parts.  Late  in  the  disease  hemiplegia, 
paraplegia,  bulbar  symptoms,  and  perhaps  hydrocephalus,  may  develop.  12, 
Base  of  the  Brain. — The  symptoms  of  tumours  in  the  anterior  fossa  are  very 
similar  to  those  caused  by  tumours  in  the  prefrontal  area.  There  are,  however, 
anosmia,  and  perliaps  involvement  of  the  optic  and  oculo-motor  nerves.  Tumours 
of  the  middle  fossa  may  involve  the  hypophysis.  The  symptoms  of  tumours  of 
this  region  and  of  the  interpeduncular  space  are  those  of  pressure  on  the  optic 
chiasm,  viz.,  early  optic  neuritis  and  hemianopia. 

It  must  be  borne  in  mind  in  localizing  brain  tumours  that  a  certain  propor- 
tion of  them  are  multiple. 

Diagnosis. — The  cardinal  symptoms  of  brain  tumour  are  :  vomit- 
ing, headache,  vertigo,  optic  neuritis,  mental  disturbances,  and  the 
progressive  course.  Other  points  are  the  history  of  an  injury,  local 
tenderness,  or  tuberculous  or  syphilitic  disease.  Brain  tumour  must 
be  distinguished  from  brain  abscess  (page  998),  meningitis  (page 
992),  hysteria  (page  994),  paretic  dementia,  and  lead-poisoning. 

Prognosis. — Serious,  The  disease  may  last  for  from  1  to  18  years ; 
usually  death  occurs  within  3  years ;  rarely  it  may  remain  stationary. 

IX.  Multiple  Sclerosis. — Occurs  usually  between  the  ages  of  20 
and  30,  more  often  in  males,  also,  rarely,  in  infants  and  children. 
There  is  often  an  inherited  neuropathic  tendency.  The  most  impor- 
tant causative  factor  is  infection — e.  g.,  malaria,  typhoid  fever,  the 
exanthemata,  pneumonia,  rheumatism,  pertussis,  diphtheria,  dysen- 
tery, cholera,  and  erysipelas,  especially  typhoid  and  malarial  fevers. 
Slow  poisoning  by  some  of  the  metals,  and  exposure  to  cold,  more 
rarely  sunstroke,  fright,  shock,  and  trauma,  are  causes. 

Symptoms. — Onset  slow  and  gradual.  First  noticed  are  rigidity 
and  weakness  in  the  legs,  perhaps  with  some  numbness ;  or  a  tremor 
in  the  hands.  Soon  follows  ataxia  of  the  legs,  which,  with  the  weak- 
ness and  rigidity,  increases  the  difficulty  of  walking.  There  may  be 
some  incontinence  of  urine.  The  tremor  in  the  hands,  which  may 
not  have  appeared  until  now,  is  "  intentional,"  The  speech  is  slow, 
syllabic,  and  scanning  in  character.     Deglutition  may  be  impaired. 


1004  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

Occasional  pains  may  occur  in  the  joints  and  extremities,  with  some 
numbness  or  slight  tactile  anaesthesia  in  the  limbs.  The  gait  is 
awkward  and  stiff,  and  there  is,  perhaps,  slight  hemiplegia.  There  is 
marked  atrophy  of  the  limbs,  without  De  K.  The  ataxia  is  due 
mainly  to  the  inability  to  co-ordinate  and  control  the  movements, 
weight  and  pressure  senses  being  unimpaired.  The  Jerky  tremor  of 
the  hands  may  be  so  marked  that  the  patient  finds  it  difficult  to  dress 
himself,  or  to  carry  a  glass  of  water  to  his  mouth  without  spilling  it. 
There  may  be  tremor  in  the  muscles  of  the  neck,  causing  a  constant 
movement  of  the  head,  or  in  those  of  the  face.  The  tongue  is  pro- 
truded in  a  jerky  manner,  and  the  thick,  slow  speech  may  be  nearly 
unintelligible.  There  are  exaggerated  knee-jerks  and  ankle  clonus, 
Nystagmus  is  present,  perhaps  only  to  be  seen  when  the  eyes  are 
turned  far  to  one  side,  but  may  be  manifest  when  looking  directly  at 
an  object,  perhaps  with  diplopia.  The  pupils  react  normally.  Optic 
atrophy  may  be  present,  chiefly  in  the  temporal  half  of  the  disc, 
which  may  become  complete  later  in  the  disease,  followed,  as  results, 
by  weakness  of  vision,  contraction  of  the  visual  fields,  and  scintil- 
lating scotomata.  Occasionally  there  may  be  attacks  of  vertigo,  and 
apoplectiform  and  epileptiform  seizures.  There  may  be  mental 
slowness,  perhaps  slight  melancholia,  or  impulsive  laughing  or  cry- 
ing. The  course  of  the  disease  is  irregular,  usually  lasting  about  5 
years,  occasionally  3  times  as  long. 

Diagnosis. — The  cardinal  points  are :  intention  tremor,  nystag- 
mus, scanning  speech,  exaggerated  knee-jerks,  ankle  clonus,  ataxia, 
and  rigidity  in  the  legs,  attacks  of  vertigo,  and  apoplectiform  and 
epileptiform  seizures.  Must  be  differentiated  from  spastic  spinal 
paralysis,  tabes  dorsalis,  Friedreich's  ataxia,  bulbar  paralysis,  paral- 
ysis agitans,  dementia  paralytica,  hysteria,  and  chronic  meningitis. 

Prognosis. — Good  as  to  life.  The  symptoms  may  disappear  and 
the  patient  apparently  recover,  but  after  some  years  may  reappear ;. 
or  the  disease  may  reach  a  certain  state  and  remain  stationary. 

VIII.    SYPHILIS   OF  THE   NERVOUS   SYSTEM 

Occurs  most  often  between  the  ages  of  20  and  40,  but  may  be 
met  with  at  any  age,  more  often  in  men.  Predisposing  causes  are  a 
neuropathic  constitution,  excessive  physical  exercise,  alcohol,  in- 
juries, mental  strain,  and  overwork.  Usually  appears  in  the  3d  year, 
though  it  may  develop  at  any  time  within  30  years,  after  infection. 
Symptoms. — The  following  divisions  are  made  (Dana)  : 
(1)  Syphilis  of  the  Brain. — The  chief  symptoms  are  intense 
headaches,  cranial-nerve  palsies,  optic  neuritis,  attacks  of  somnolence, 
coma,  and  hemiplegia.     Other  symptoms  are  nausea,  vomiting,  ver- 


DISEASES  OP  NERVOUS  SYSTEM— AND  MUSCLES         1005 

tigo,  mental  irritability  and  dulness,  epileptic  convulsions,  polyuria, 
and  polydipsia.  The  headache  (persistent  and  intense)  comes  on 
gradually.  Hemiplegia  occurs  a  variable  time  after  the  headache, 
and  with  it  there  are  some  cranial-nerve  (especially  ocular)  palsies. 

(2)  Cerebro-spinal  Syphilis. — Xearly  the  same  as  are  present  in 
(1),  but  there  are  in  addition  symptoms  due  to  the  cord  lesions — 
i.  e.,  spastic  paraplegia,  spinal  pains,  and  sphincter  involvement. 

(3)  Spinal  Syphilis. — Usually  those  of  a  transverse  myelitis, 
coming  on  slowly  and  developing  into  spastic  paraplegia  with  much 
pain.     There  is  Brown-Sequard  paralysis,  with  some  ataxia. 

(4)  Syphilis  of  the  Xerves. — The  peripheral  nerves  are  rarely 
affected,  but  deposits  of  syphilitic  exudate  sometimes  cause  symp- 
toms of  irritation.     There  are  symptoms  due  to  cranial-nerve  palsies. 

(5)  Post-syphilitic  Degenerative  Processes. — These  are  general 
paresis  and  locomotor  ataxia,  to  which  syphilis  may  predispose. 

(6)  Hereditary  Syphilis. — May  present  all  or  any  of  the  symptoms 
of  acquired  syphilis.  Usually  develops  under  5  years  of  age,  but 
may  occur  up  to  18  years. 

Diagnosis  of  Syphilis  of  the  Nervous  System. — The  cardinal 
points  are :  History  of  infection,  age  of  the  patient,  severe  head- 
aches, irregular  and  fleeting  character  of  the  symptoms,  presence  of 
optic  neuritis,  and  therapeutic  results.  The  headache  of  syphilis  is 
worse  at  night,  very  intense,  irregular  in  regard  to  the  part  of  the 
head  affected,  and  may  be  periodical.  Hemiplegia,  or  paralyses  of 
one  or  more  cranial  nerves,  occurring  after  a  headache  of  the  above 
character,  suggest  syphilis.  Prognosis. — Marked  improvement,  per- 
haps recovery,  may  be  brought  about,  but  if  nerve  tissue  is  de- 
stroyed the  effect  is  permanent. 


SECTION   vin 

DISEASES   OF  THE  MUSCLES 

Peepared  by  Henry  Goodwin  Webster,  M.D. 

I.  Myositis.— Dujardin-Beaumetz  recognises  three  varieties  : 
Symptoms.— (1)  Simple  Acute  i^orm.— Characterized  by  lassitude 
and  mild  constitutional  disturbance,  with  pain  and  tenderness  in  one 
or  several  muscles,  coming  on  after  unusual  exertion  and  exposure. 
After  a  few  days  it  resolves  or  passes  into  (2)  or  (3). 

(2)  Acute  Primary  Infectious  i^orm.— Ushered  in  like  (1),  or  suc- 
ceeds it.     There  are  lassitude,  prostration,  and  muscular  pain.     The 


1006  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

affected  muscle  is  prominent,  sensitive  to  pressure,  and  either  of  a 
wooden  hardness  or  soft  and  doughy.  The  overlying  skin  may  he 
reddened  or  edematous.  The  patient  is  apt  to  assume  a  position 
which  will  relax  the  affected  muscles.  AYhen  deep  muscles  only  are 
involved,  the  local  signs  fail,  and  the  diagnosis  rests  upon  the  posi- 
tion, together  with  the  constitutional  disturbance.  When  suppura- 
tion occurs  fluctuation  often  appears.  There  are  fever  (even  to 
104°  F.),  dry,  coated  tongue,  free  sweating,  dyspnoea,  loss  of  appetite, 
and  perhaps  a  vesicular  eruption  over  the  affected  part.  Fatal  cases 
develop  diarrhoea  and  the  typhoid  state. 

(3)  Primary  Acute  Infectious  Polymyositis  differs  from  (2)  in 
its  long  prodromal  period — 3  to  5  weeks  of  lassitude  and  wandering 
pains — its  extensive  distribution,  and  the  absence  of  suppuration. 
There  are  distinct  chills,  oedema  of  face  and  extremities,  pain  (gen- 
eral), and  redness,  the  latter  a  fine  macular  eruption  on  the  extremi- 
ties, face,  and  abdomen.  Gastric  disturbances  supervene,  the  oedema 
becomes  hard,  the  patient  rigid,  and  the  muscular  reactions  and  re- 
flexes disappear.  There  are  profuse  sweats,  intense  thirst,  coated 
tongue,  constipation,  scanty  and  albuminous  urine.  The  entire 
muscular  system  becomes  involved  and  death  ensues. 

Course  and  Prognosis. — Form  (2)  lasts,  in  severe  cases,  from  5  to 
6  days ;  in  less  severe  ones  from  10  to  20  days.  A  number  recover 
after  a  convalescence  extending  over  months.  Muscular  stiffness 
and  disability  are  likely  to  be  permanent.  The  course  of  form  (3)  is 
longer — 3  or  4  months — and  few  cases  recover.  Eecovery  from  form 
(1)  is  the  rule,  but  it  may  run  into  the  infectious  variety. 

Diagnosis. — Acute  articular  rheumatism,  typhoid  fever,  suppura- 
tive arthritis,  pyaemia,  osteomyelitis,  and  other  acute  suppurative  con- 
ditions may  simulate  the  acute  infectious  variety,  but  the  peculiar 
condition  of  the  muscle  should  make  the  diagnosis  clear.  A  localized 
cellulitis  may  be  distinguished  by  being  more  superficial,  and  by  the 
involvement  of  the  neighbouring  lymphatics.  The  distinction  be- 
tween polymyositis  and  trichinosis  is  difficult,  and  microscopic  exam- 
ination of  a  section  of  the  muscle  may  be  required.  The  former  at- 
tacks extremities  and  extensor  muscles  first,  the  latter  selects  the 
tongue  and  flexor  groups.     Glanders  is  not  likely  to  be  mistaken. 

II.  Myositis  Ossificans  Progressiva. — This  rare  disease 
appears  as  a  tumefaction  of  the  muscles  at  the  back  of  the  neck. 
The  overlying  skin  is  somewhat  reddened,  and  there  is  slight  fever. 
After  the  swelling  subsides  the  muscle  is  found  to  be  permanently 
hardened,  and  a  progressive  substitution  of  bony  for  muscular  ele- 
ments takes  place.  Muscle  after  muscle  is  invaded  until  the  entire 
system  is  involved.     After  a  year  or  more  death  ensues. 


DISEASES  OF  MUSCLES— CONSTITUTIONAL  DISEASES     1007 

III.  Myotonia  {TJiomsen's  Disease). — (a)  Symptoms. — Thisaffec- 
-tion  is  met  with  in  Norway,  Sweden,  and  Germany,  but  is  rare  in 
America.  It  is  hereditary ;  appears  in  childhood ;  often  attacks  sev- 
eral members  of  a  family ;  and  is  characterized  by  tonic  contraction 
of  the  voluntary  muscles,  especially  those  of  locomotion,  prehension, 
and  speech.  It  is  noticed  that  the  child  is  clumsy,  that  it  can  not 
perform  the  nicer  movements,  but  that  after  a  time  the  spasm  re- 
laxes and  these  motions  may  be  perfect.  This  is  also  true  for  relax- 
ation, the  patient  being  unable  to  relinquish  his  grasp  until  some 
seconds  after  he  has  willed  the  action.  The  arms  and  legs  suffer 
most,  the  eyes,  face,  and  vocal  organs  least,  while  sensation  and  the 
reflexes  are  undisturbed.  There  is  occasional  mental  hebetude.  Cold 
and  excitement  increase  the  disorder.  Although  the  muscles  are 
unusually  large,  they  lack  power,  and  present  "  Erb's  myotonic  reac- 
tion." Either  current  causes  a  normal  contraction,  which,  however, 
develops  and  relaxes  very  slowly,  while  during  the  interval  slow, 
wavelike  contractions  occur,  passing  from  cathode  to  anode.  The 
disease  pursues  a  chronic  course,  with  remissions,  and  is  incurable. 

Diagnosis. — May  be  made  from  pseudo-hypertrophic  paralysis  by 
the  gait,  the  absence  of  paralysis,  and  the  myotonic  reaction. 

IV.  Paramyoclonus  Multiplex  (J/yoc/owia).— Friedreich's 
disease  must  not  be  confused  with  the  hereditary  ataxia  of  the  same 
authority.  It  occurs  most  commonly  in  young  men ;  affects  the 
muscles,  especially  of  the  hands  and  feet,  and  is  marked  by  clonic 
contractions,  continuous  or  paroxysmal.  It  may  follow  severe  men- 
tal or  physical  strain.  The  muscles  are  subject  to  rapid  symmetrical, 
usually  rhythmical,  clonic  spasms.  Sensation  is  undisturbed,  and 
auring  sleep  the  movements  cease.  The  affection'  may  be  general, 
and  the  rapid  contraction  cause  the  body  to  be  thrown  to  and  fro 
with  great  violence.  Voluntary  efforts  at  control  often  serve  to  in- 
tensify the  spasms.  Fere  reports  cases  of  improvement  under  treat- 
ment as  well  as  a  few  of  spontaneous  cure. 


SECTION  IX 

CONSTITUTIONAL  DISEASES 

Peepared  by  Henry  Goodwin  Webster,  M.  D. 

I.  Chronic  Rheumatism.— Cold,  dampness,  and  exposure 
commonly  predispose,  although  it  may  follow  an  acute  attack. 
Usually  there  is  little  but  pain  and  stiffness  of  the  joints  (page  93), 


1008  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

although  there  may  be  tenderness,  redness,  and  swelling.  All  symp- 
toms are  aggravated  in  the  morning,  gradually  wearing  off  during 
the  day.  The  disease  attacks  many  joints,  passing  from  one  to 
another,  with  alternating  periods  of  quiescence  and  exacerbation, 
which  are  often  dependent  upon  changes  in  the  weather.  One  joint 
only  may  be  attacked.  Ultimately  marked  changes  in  and  about 
the  joint  with  muscular  atrophy  and  great  deformity  may  occur.  In 
severe  cases  there  may  be  constitutional  disturbances,  especially 
gastric  disorders  and  anaemia.  As  a  rule  the  disease  grows  steadily 
worse  in  spite  of  treatment. 

II.  Muscular  Rheumatism. — Pain  in  the  muscles  and  their 
attachments  coming  on  suddenly  after  exposure  and  cold,  and  known, 
when  occurring  in  definite  locations,  as  lumbago,  torticollis,  pleuro- 
dynia, etc.  Fever  is  usually  absent.  Generally  the  pain  is  aching, 
sometimes  severe,  cutting,  or  cramping,  and  may  be  constant  or 
occur  only  upon  use  of  the  affected  muscles.  As  lumbago  it  attacks 
the  muscles  of  the  lumbar  regions  and  lower  back ;  as  torticollis  it 
affects  the  neck,  usually  the  trapezius  and  sterno-mastoid  with  their 
immediate  neighbours,  generally  on  one  side  only ;  as  pleurodynia  the 
intercostals  suffer.  The  latter  is  particularly  distressing,  as  respira- 
tory movements  and  coughing  aggravate  it.  The  back,  shoulder, 
arm,  or  abdominal  muscles  may  be  involved.  Pleurodynia  is  differ- 
entiated from  pleurisy  by  the  lack  of  physical  signs  ;  from  intercostal 
neuralgia  by  the  more  general  and  constant  pain  and  the  presence  of 
tender  nerve  points. 

III.  Diabetes  Insipidus.  —  The  diagnosis  depends  upon  the 
persistent  polyuria  and  the  urinalysis  ((15),  page  647).  Xervous  or 
physical  shock,  violent  exertion,  or  excess,  may  predispose.  The 
onset  may  be  acute,  more  often  gradual.  The  patient  usually  enjoys 
good  health,  but  notices  a  decidedly  increased  output  of  urine  and 
corresponding  thirst,  usually  without  bulimia.  The  condition  may 
persist  for  years,  the  patient  passing  from  6  to  12  times  the  normal 
daily  quantity  of  urine.  -While  polyuria  may  depend  on  a  number 
of  definite  conditions,  such  as  cerebral  or  medullary  disease,  menin- 
gitis, and  disorders  of  the  abdominal  viscera,  including  tuberculous 
peritonitis  and  tumours,  true  diabetes  insipidus  occurs  as  a  well- 
marked  disease,  probably  of  nervous  origin,  possibly  referable  to  the 
sympathetic  system. 

Differential  Diagnosis. — From  diabetes  mellitus  by  the  low  spe- 
cific gravity  and  absence  of  glucose ;  and  from  chronic  interstitial 
nephritis  by  the  presence  of  albumin  and  casts,  arteriosclerosis,  and 
cardiac  hypertrophy,  with  high-tension  pulse.  Hysterical  subjects 
occasionally  pass  large  quantities  of  pale  clear  urine  {urina  spastica) f. 


CONSTITUTIONAL  DISEASES  1009 

and  nervous  excitement  not  infrequently  produces  similar  phenomena. 
The  brief  duration,  with  the  history  and  characteristics  of  the 
patient,  should  make  the  diagnosis  clear. 

Prognosis. — Patients  may  live  to  the  normal  age  limit  without 
particular  discomfort,  or  may  fall  victims  to  intercurrent  disease, 
while  occasionally  cases  of  spontaneous  cure  occur.  The  prognosis 
of  symptomatic  polyuria  is  necessarily  dependent  on  the  nature  of 
the  causative  lesion. 

IV.  Diabetes  Mellitus. — Types  and  Symptoms. — This  disease 
may  manifest  itself  in  a  variety  of  ways.  The  uri7iary  characters 
are  given  in  (16),  page  647. 

(1)  A  small  number  of  cases  are  acute  in  onset  and  course. 
Many  of  these  patients  have  suffered  severe  nervous  shock  or  injury, 
and  nearly  all  are  young  adults  with  a  family  history  of  diabetes, 
rheumatism,  or  syphilis.  The  symptoms  are  those  typical  of  the  dis- 
ease— increased  urine,  glycosuria,  ravenous  hunger  and  thirst,  rapid 
failure  of  flesh  and  strength,  general  itching,  irritability  of  temper, 
and  sleeplessness.     Such  cases,  as  a  rule,  prove  rapidly  fatal. 

(2)  More  often  the  severe  type  of  diabetes  begins  insidiously,  and 
even  after  a  year  or  more  the  nervous  symptoms,  debility,  and  loss  of 
flesh  may  be  attributed  to  neurasthenia.  Loss  of  sexual  power, 
impaired  vision,  pulmonary  troubles,  eczema,  and  other  complications 
gradually  develop,  while  the  urine,  although  containing  immense 
amounts  of  sugar,  is  not  sufiiciently  increased  in  quantity  to  attract 
attention.  Finally,  the  characteristic  symptoms  appear,  and  the 
patient  either  enters  upon  a  chronic  remitting  course,  lasting  for  a 
few  years,  with  mental,  pulmonary,  or  digestive  disorders,  and  is 
oarried  off  by  intercurrent  disease ;  or  progresses  rapidly  to  a  fatal 
termination.  Toward  the  end  carbuncle,  gangrene,  myocarditis,  or 
tuberculosis  are  common,  and  diabetic  coma  ends  the  scene. 

(3)  Possibly  the  most  frequent  form  is  that  appearing  in  fat  or 
lithaemic  patients.  The  train  of  symptoms  is  much  the  same  as  in 
(2),  but  the  patients  respond  more  readily  to  treatment,  and  live  in 
comparative  comfort  for  many  years,  the  sugar  in  some  cases  disap- 
pearing entirely.     Chronic  interstitial  nephritis  often  succeeds. 

All  degrees  between  these  types  may  be  met  with. 

Complications.— Many  and  important.  In  the  kidneys  there  may 
be  a  diffuse  or  chronic  interstitial  nephritis.  Albuminuria  is  fre- 
quent ;  uraemia  less  common.  In  the  liver  there  is  often  hypertrophy, 
sometimes  gallstones.  In  the  lungs  tuberculous  disease  is  common  ; 
acute  lobar  pneumonia,  infarction,  and  gangrene  occur.  Dilatation 
of  the  stomach  is  met  with,  as  well  as  bulimia  and  polyphagia. 
Stomatitis,  gingivitis,  caries,  and  loss  of  teeth  are  frequent,  and  the 


1010  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

tongue  is  often  dry  and  red.  The  pancreas  is  not  uncommonly  dis- 
eased. 

In  the  nervous  system,  melancholia  and  insanity  are  referable  to 
the  higher  functions ;  neuritis  and  the  various  forms  of  paralysis  are 
frequent ;  trophic  changes,  such  as  onychia  and  glazing  of  the  skin, 
occur;  and  most  important  of  all,  diabetic  coma  (see  8,  page  71), 
often  heralded  for  a  day  or  two  by  the  sudden  appearance  of  a  large 
number  of  tube  casts  in  the  urine.  Death  usually  follows  after  36 
hours.  Of  the  special  senses,  ocular  symptoms  are  most  frequent, 
including  retinitis,  optic  neuritis,  cataract,  amaurosis,  iritis,  and 
opacities  of  the  vitreous  humour. 

Intense  itching,  especially  about  the  external  genitals,  is  the  most 
annoying  skin  manifestation  ;  next  furunculosis,  carbuncle,  and  gan- 
grene. Arteriosclerosis  is  apparently  responsible  for  certain  compli- 
cations, especially  gangrene  of  the  extremities.  The  endocardium 
and  myocardium  are  frequently  the  seat  of  extensive  changes  leading 
to  valvular  disease  and  fatty  degeneration.  Sexual  disorders,  espe- 
cially impotence,  usually  appear  early. 

Prognosis. — It  is  essential  that  the  family  and  personal  history 
should  be  thoroughly  sifted  to  determine  the  presence  of  syphilis, 
gout,  or  other  constitutional  disease,  the  outlook  being  more  hopeful 
foT  those  in  whom  such  diseases  can  be  detected.  Favourable  signs 
are  late  onset,  obesity,  and  long-continued  disease  with  but  slight 
loss  of  flesh  and  strength.  If  the  sugar  •  diminishes  rapidly  under 
treatment  the  outlook  is  hopeful.  In  children  an  early  fatal 
termination  is  the  rule.     Coma  is  of  the  gravest  import. 

V.  Gout. — Three  forms:  acute,  chronic,  and  irregular. 

Symptoms  — (1)  Acute  Gout. — The  attack  usually  occurs  between 
the  hours  of  12  to  2  a.  m.,  often  without  warning,  in  a  person  whose 
family  history  shows  the  lithaemic  diathesis,  or  who  has  acquired  it 
by  constant  overindulgence  in  nitrogenous  food,  wines  (especially 
champagne),  or  malt  liquors;  by  sedentary  habits;  by  saturnism;  or 
by  privation  (poor  man's  gout).  The  attack  is  usually  precipitated 
by  unusual  dietetic  indulgence,  exposure,  or  injury. 

The  onset  is  sudden,  with  excruciating,  vicelike  pain  in  the  first 
great-toe  joint,  chill,  fever  (rarely  over  102"),  marked  restlessness, 
and  insomnia.  By  morning  the  pain  lessens,  the  joint  is  swollen, 
and  the  skin  red,  tense,  and  shining.  During  the  day  the  pain  may 
disappear,  returning  at  night.  An  attack  may  last  from  5  to  8  days, 
or  longer,  with  gradual  amelioration  of  all  symptoms.  During  the- 
attack  the  urine  is  scanty,  high-coloured,  and  acid,  although  the  total 
uric-acid  excretion  is  diminished.  As  the  symptoms  subside  the 
uric  acid  increases. 


CONSTITUTIONAL  DISEASES  1011 

While  the  ankle,  mid  tarsal,  and  knee  joints,  and  outer  side  of 
the  foot  are  frequently  involved,  in  the  order  named,  the  first  joint 
of  the  great  toe  is  by  far  the  most  often  affected.  In  some  cases 
polyarthritis,  usually  unilateral,  may  be  present.  The  affected  joint 
may  be  left  somewhat  stiffened.  The  severity  of  the  constitutional 
disturbance  varies  with  the  intensity  of  the  arthritis. 

Premonitory  symptoms,  especially  in  patients  who  have  suffered 
repeated  attacks,  include  constipation,  palpitation,  irritability  of 
temper,  dyspepsia,  bronchitis,  and  the  urinary  changes  already 
noted.  In  a  certain  number  of  cases  the  joint  symptoms  are 
slight,  or,  beginning  severely,  will  rapidly  subside,  with  correspond- 
ing alarming  internal  symptoms,  so-called  "  retrocedent "  or  "  sup- 
pressed "  gout.  The  symptoms  may  l)e  gastro-intestinal,  pulmonary, 
cardiac,  or  cerebral.  If  the  first,  there  is  nausea  and  vomiting,  much 
severe  pain,  usually  diarrhoea  and  great  prostration.  The  pulmonary 
variety  appears  as  asthma.  If  the  heart  is  affected  there  may  be 
dyspnoea,  pain,  and  arrhythmia,  even  syncope.  Rapidly  developing 
fatal  pericarditis  has  been  reported.  Headache  and  delirium  are  the 
most  common  cerebral  symptoms. 

(2)  Chronic  Gout. — Acute  attacks,  previously  described,  recur 
more  or  less  regularly,  the  patient  in  the  interim  being  in  poor 
health.  The  gradual  deposit  of  sodium  urate  in  the  articular  surface 
of  the  joints,  and  later  in  the  surrounding  tissues,  with  the  continued 
inflammation,  produces  first  disability,  later  deformity.  This  con- 
dition spreads  from  the  feet  to  the  hands,  the  knees  and  elbows 
being  involved  in  severe  cases,  the  deposits  even  extending  up  and 
down  the  tendon  sheaths  and  into  the  neighbouring  burste.  Lastly, 
deposits  occur  in  the  cartilages  of  the  ear  and  throughout  the  skin. 
These  deposits  ("tophi,"  "chalk  stones")  in  long-standing  cases 
may  be  exposed  by  ulceration,  especially  about  the  finger  joints. 

With  these  local  symptoms  gastric  and  bronchial  irritation  are 
associated,  and  arteriosclerosis  appears,  the  vascular  disturbances 
inducing  cardiac  hypertrophy,  and  chronic  interstitial  nephritis.  In 
the  later  stages  the  gouty  symptoms  are  associated  with  those  of 
eczema,  endarteritis,  diabetes,  bronchitis,  endocarditis,  or  nephritis, 
the  last  usually  being  the  direct  cause  of  death. 

(3)  Irregular  (7ow^— Lithsmia  (gouty  diathesis)  comprises  an  ill- 
defined  group  of  symptoms  occurring  in  members  of  gouty  famihes, 
or  in  the  gastronomically  overindulgent.  The  symptoms  are  varied. 
The  manifestations  in  the  gastro-intestinal  tract  are  catarrhal  gas- 
tritis, or  simply  functional  disturbance  with  constipation,  foul 
breath,  coated  tongue,  deficient  biliary  secretion,  a  "bilious  attack." 
In  the  vascular  system  there  is  arteriosclerosis,  with  increased  ten- 


1012  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

sion,  leading  to  cardiac  and  renal  changes,  either  of  which  may  pre- 
dominate ;  or  the  sclerotic  process  in  the  aorta  or  the  cerebral  vessels 
may  favour  the  growth  of  aneurisms,  and  death  from  apoplexy  may 
result ;  or  myocarditis  or  pericarditis  may  determine  a  fatal  issue. 
As  mentioned,  chronic  interstitial  nephritis  supervenes.  In  the 
lungs  bronchitis  is  usual — sometimes  emphysema  or  pleurisy.  The 
skin  lesions  are  pronounced,  eczema  in  particular ;  next  acne,  psori- 
asis, and  urticaria.  In  the  eye,  iritis  is  most  common,  though  reti- 
nitis is  not  infrequent.  Of  nervous  symptoms  headache  is  common  ; 
next  neuralgias  and  sciatica ;  lastly  peripheral  disturbances,  itching 
eyeballs,  burning  and  itching  feet,  and  cramps  in  the  legs.  Sugar 
and  oxalates  are  found  in  gouty  urine,  so  also  small  quantities  of 
albumin.     Spontaneous  urethritis  has  been  reported. 

Differential  Diagnosis. — Acute  polyarticular  attacks  may  be  dis- 
tinguished from  rheumatic  fever  by  the  history,  frequently  obtain- 
able, of  previous  typical  monarticular  attacks.  Eheumatism  selects 
the  larger  joints,  is  less  painful,  causes  less  superficial  inflammation, 
and  never  shows  the  marked  venous  engorgement  peculiar  to  gout. 
The  temperature  runs  higher,  there  may  be  delirium,  even  convul- 
sions, which  seldom  accompany  gout.  Arthritis  deformans,  however, 
is  often  differentiated  with  great  difficulty  from  chronic  gout.  In 
these  cases  careful  inquiry  may  demonstrate  a  gouty  family  history, 
which,  coupled  with  the  patient's  previous  manner  of  life  and  the 
:finding  of  tophi,  may  serve  to  separate  the  conditions.  So,  too,  the 
gouty  origin  of  the  various  disorders  referable  to  the  special  organs 
may  be  distinguished  from  malarial  or  syphilitic  taints.  It  must  be 
borne  in  mind  that  either  of  the  latter  may  be  present  in  a  gouty 
person. 

Prognosis. — In  vigorous  patients,  with  single  attacks,  the  outlook 
is  favourable,  providing  the  prescribed  regimen  be  strictly  followed. 
The  sudden  subsidence  of  articular  and  the  appearance  of  internal 
symptoms  is  of  serious  import.  The  pronounced  tendency  to  endar- 
teritis, endocarditis,  and  nephritis  should  always  be  considered,  and 
the  grave  consequences  of  neglect  impressed  upon  the  patient. 

VI.  Arthritis  Deformans.— Varieties  and  Symptoms. — Char- 
cot recognises  the  following  forms  :  general  progressive  form,  monar- 
ticular form,  and  Heherden's  nodosities.  Of  the  first  named  acitte  and 
chronic  varieties  exist,  the  latter  being  much  the  more  frequent  and 
differing  in  intensity  and  rapidity  of  onset. 

(1)  Acnte  Fo?'m. — The  onset  of  the  acute  form  closely  simulates 
acute  articular  rheumatism.  Many  joints  are  involved  at  once. 
There  are  pain  and  swelling  of  the  joints,  the  former  out  of  all  pro- 
portion to  the  latter ;  but  the  temperature  does  not  run  high  and 


CONSTITUTIONAL   DISEASES  1013 

hyperaemia  is  seldom  marked.  Such  cases  are  most  often  noted  in 
young  women,  especially  after  childbed.  A  subacute  form  appears 
in  children,  girls  particularly,  subsequent  to  exposure,  privation,  and 
injury,  occasionally  with  a  rheumatic  family  history  (Garrod).  They 
have  reasonable  hope  of  recovery,  though  subsequent  childbearing 
determines  fresh  attacks. 

(2)  Chronic  Form. — In  this  there  is  a  symmetrical  progressive 
involvement  of  the  peripheral  joints.  Swelling  in  or  about  the  joint, 
with  moderate  pain,  signalizes  the  invasion  of  the  disease.  In 
extreme  cases  it  tends  to  involve  all  the  articulations.  There  are 
frequent  remissions,  and  the  pain  is  variable.  Many  severe  cases  suf- 
fer little  or  no  pain.  The  ultimate  result  is  locking  of  the  joints, 
due  to  the  bony  outgrowths  (osteophytes),  with  deformity  due  to 
muscular  atrophy  and  contracture.  Garrod  enumerates  the  follow- 
ing symptoms :  symmetrical  distribution  (not  invariable) ;  enlarge- 
ment, due  to  osteophytes,  or  gradual  infiltration  of  entire  joints, 
or  serous  effusion,  alone  or  combined  ;  muscular  atrophy,  frequently 
with  exaggerated  reflexes,  leading  to  deformities ;  pigmentation  and 
glossiness  of  the  skin  about  the  joints ;  subcutaneous  nodules ;  pain, 
exceedingly  variable  in  degree,  numbness,  and  tingling ;  undue 
rapidity  of  the  pulse,  and  frequent  palpitation.  The  deformity  in 
the  hand  and  wrists  is  striking.  Osteophytes,  infiltration,  and 
effusion  cover  up  the  natural  tapering  at  the  wrist,  the  carpus  is 
pushed  toward  the  radial  and  the  fingers  toward  the  ulnar  side 
they  are  flexed  on  the  hand,  and  all  the  small  joints  are  enlarged  and 
deformed  (Fig.  55,  page  276). 

(3)  Monarticular  i^orw.— Identical  with  the  other  types  of  the 
disease  in  its  anatomical  and  histological  features,  it  is  peculiar  in 
that  it  rarely  attacks  any  but  the  aged,  and  selects  the  hip,  knee, 
shoulder,  or  vertebral  articulations.  A  history  of  traumatism  is  more 
frequently  obtainable,  and  men  seem  more  often  affected.  The  con- 
ditions known  as  "  morbus  coxae  senilis  "  and  "  spondylitis  "  are  the 
most  frequent  varieties  of  the  monarticular  form. 

(4)  Heberden's  Nodosities.— Vf omen  are  the  chief  sufferers.  The 
condition  is  limited  to  the  fingers,  and  appears  in  middle  life.  A 
history  of  heredity,  gout,  and  rheumatism  may  be  elicited.  The 
characteristic  deformity  is  a  symmetrical  bony  outgrowth  on  the 
dorsal  aspect  of  the  distal  phalanges  (Fig.  56,  page  277).  With  these 
are  often  associated  little  translucent  cysts,  possibly  pouches  of  the 
synovial  membrane.  Pain  may  accompany  the  growth,  and  there 
may  be  redness  and  swelling.  Tenderness  is  often,  but  by  no  means 
always,  present.     The  thumb  frequently  escapes. 

Diagnosis.— The  acute  form  is  hardly  distinguishable  from  acute 
66 


1014  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

articular  rheumatism.  Pain  out  of  proportion  to  the  signs  of  local 
inflammation  and  the  presence  of  deforming  changes  should  exclude 
the  latter.  Arthropathies,  while  anatomically  the  same,  are  asso- 
ciated with  the  other  symptoms  of  locomotor  ataxia.  Gonorrhceal 
and  scarlatinal  arthritis,  cerebro-spinal  meningitis,  pyasmia,  etc.,  can 
scarcely  be  confused  with  arthritis  deformans  because  of  their  acute 
character  and  previous  history.  From  chronic  gout  the  distinction 
has  been  made  (page  1012).  Osier  describes  a  localized  arthritis  of 
the  shoulder  joint  which  closely  simulates  arthritis  deformans  by  the 
pain,  thickening  of  the  ligaments,  muscular  atrophy,  and  occasional 
neuritis.     The  bones  are  unaffected.     (See  also  pages  93  to  95.) 

VII.  Rickets. — Symptoms. — Beginning  between  the  sixth  and 
twenty-fourth  months,  the  disease  usually  manifests  itself  by  irritabil- 
ity, restlessness,  and  slight  fever,  most  marked  toward  night.  The 
child  resents  handling,  wakes  frequently,  cries  out,  and  is  subject  to 
drenching  sweats,  especially  about  the  face  and  head.  In  a  pre- 
viously quiet  sleeper  this  restlessness  and  intolerance  of  the  bed- 
clothing  is  always  suggestive.  Increasing  hypersensitiveness  of  the 
entire  surface,  with  anaemia  and  disturbed  digestion,  as  evidenced  by 
diarrhoea,  with  flatus  and  foul  passages,  follow,  and  enlargement  of 
the  liver  and  spleen  is  recognisable.  Dentition  is  delayed,  the  fon- 
tanels do  not  close,  and  skeletal  changes  become  manifest. 

The  course  of  the  disease  up  to  this  point  is  estimated  at  from 
eight  to  ten  months.  There  is  progressive  pallor,  and  the  flesh  has 
become  soft,  flabby,  and  doughy.  Various  nervous  phenomena  are 
present.  The  loss  of  muscular  tone,  taken  with  the  soreness  and 
pain,  may  simulate  paralysis. 

Of  skeletal  changes,  possibly  the  first  noticed  are  those  in  the 
thorax  (see  page  300).  The  abdominal  walls  are  relaxed  and  pro- 
trude unduly.  These  changes  may  appear  as  early  as  the  third  month 
of  the  disease.  The  skull  is  subject  to  marked  deformities.  Xutri- 
tional  changes  allow  softening  and  absorption  of  the  bony  tables, 
which  become  in  spots  thin  as  parchment,  are  compressible,  crackle 
under  the  touch,  and  permit  the  internal  pressure  to  materially  alter 
the  shape  of  the  cranium.  This  condition,  "  craniotabes,"  is  most 
frequent  in  the  parieto-occipital  regions.  Coincidently  flat,  bony 
plates  form  over  the  frontal  and  parietal  prominences,  producing  the 
deformity  known  as  "  caput  quadratum."  A  distinct  furrow  may 
mark  the  sagittal  and  coronal  sutures.  This  cranial  enlargement, 
with  flattening  of  the  malar  prominences,  makes  the  face  seem  small 
and  out  of  proportion  (Fig.  19,  page  155).  A  systolic  murmur  over 
the  anterior  fontanel  is  by  no  means  peculiar  to  rickets  (Osler). 

All  the  long  bones  show  changes;  in  the  shaft  from  muscular 


CONSTITUTIONAL  DISEASES  '  ioi5 

tension,  in  the  ends  from  epiphyseal  proliferation.  Knock-knee, 
bowleg,  and,  in  bad  cases,  talipes  result,  while  even  the  clavicles  and 
scapulae  may  be  deformed.  Pelvic  deformities  in  girls  are  impor- 
tant from  their  influence  on  parturition.  Of  nervous  symptoms  there 
may  be,  aside  from  those  already  noted,  laryngismus  stridulus, 
tetany,  and  convulsions,  and  occasionally  hydrocephalus  and  ocular 
symptoms.  Particularly  susceptible  children  may  develop  maniacal 
symptoms.  Taylor  and  Wells  describe  a  form  of  "pressure  palsy" 
due  to  inflammatory  change  in  the  vertebrae. 

Prognosis.— The  disease  is  not  in  itself  fatal,  but  its  resulting 
deformities  are  to  be  remembered  and  guarded  against.  Death  may 
occur  from  intercurrent  disease. 

VIII.  Obesity. — Two  forms  are  recognised :  the  plethoric  and 
the  ancemic,  which  later  merge  into  the  JiydrcBmic  (Oertel). 

The  pletlioric  form  appears  in  adolescents  and  young  adults,  be- 
ginning as  a  rounding  out  of  the  entire  frame,  at  first  symmetrical, 
later  becoming  extreme,  and  producing  the  characteristic  appearance 
of  obesity.  The  mucous  membranes  and  skin  become  congested, 
there  is  gradual  loss  of  muscular  tone  and  increasing  laziness,  all 
this  in  hearty  subjects,  large  eaters,  and  drinkers.  The  pulse,  at  first 
strong,  gradually  slows  and  weakens,  the  area  of  cardiac  dulness 
increases,  and  the  apex  beat  becomes  diffuse.  The  belly  grows  pen- 
dulous, the  abdominal  and  thoracic  organs  enlarge,  their  pressure 
induces  dyspnoea  at  night,  and  the  overerect  posture  in  walking 
causes  backache.     This  condition  merges  into  the  hydraemie  fonn. 

The  anwmic  type  begins  in  patients  who  are  already  anaemic  or 
chlorotic.  Fat  is  present  in  doughy,  flabby,  shapeless  masses,  the 
muscular  tone  is  gone,  the  skin  cool,  the  body  temperature  sub- 
normal, the  heart  weak,  the  patients  complain  of  dyspnoea  and 
palpitation,  and  sleep  much.  They  are  seldom  great  eaters,  but  take 
large  quantities  of  sweets  and  water.  A  majority  of  these  patients 
are  women,  commonly  with  menstrual  irregularities.  The  condition 
may  appear  post  partum,  or  after  prolonged  lactation.  In  men  it 
frequently  follows  typhoid,  secondary  syphilis,  and  chronic  alcohol- 
ism.    The  urine  is  scanty  and  irregular,  and  oedema  is  coriimon. 

The  hydremic  form  is  merely  an  aggravated  condition,  in  which 
the  anaemia  is  profound  and  all  the  symptoms  intensified.  As  the 
disease  progresses  there  is  loss  of  muscular  power,  lowered  tone,  and 
inability  to  withstand  disease,  while  various  organic  changes  devel- 
op, especially  myocarditis  and  valvular  changes;  small,  weak,  di- 
crotic, and  irregular  pulse;  and  arteriosclerosis.  A  tendency  to 
nephritis,  lithaemia,  and  diabetes  is  often  noted.  The  thick  covering 
of  fat  favours  retention  of  internal  heat,  so  that  the  patients  readily 


1016  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

fall  victims  to  the  ravages  of  pneumonia  and  kindred  affections. 
The  course  of  the  disease  is  slow,  covering  years,  and  the  prognosis, 
unless  suitable  treatment  be  faithfully  followed  out,  is  far  from  good. 


SECTIOISr   X 

THE   IXTOXICATIOXS :   SUNSTEOKE 

Pkepaked  by  Frank  Whitfield  Shaw,  M.  D. 

I.  Alcoholism. — Varieties  axd  Symptoms. — A  periodical  ex- 
cessive consumption  of  alcoholic  liquor  is  known  as  dipsomania,  he- 
reditary or  acquired.  During  the  intervals  there  is  an  absence  of 
desire.  It  is  a  form  of  acute  alcoholism,  but  when  long  continued 
the  resulting  structural  changes  are  those  of  chronic  alcoholism. 

(I)  Acute  Alcoholism. — Symptoms. — These  are  disturbances  of  the 
mental  functions,  muscular  inco-ordination,  and  finally  unconscious- 
ness, with  deep  though  rarely  stertorous  breathing.  The  face  may 
be  flushed  or  pale,  and  the  pulse  is  usually  slow  and  full.  The 
pupils  are  equally  dilated.  The  temperature  is  rarely  elevated,  not 
infrequently  subnormal.  In  uncomplicated  cases  convulsions  are 
rare,  although  slight  muscular  twitchings  may  be  present.  The 
odour  of  the  breath  is  characteristic.  When  the  condition  is  well- 
marked  there  is  a  nearly  complete  loss  of  voluntary  muscular  power. 
By  persistent  effort  the  patient  may  be  aroused  to  incoherent  speech, 
followed  almost  immediately  by  a  return  to  the  narcotized  condition. 

(II)  Chronic  Alcoholism. — Symptoms. — There  is  unsteadiness  of 
the  muscles,  particularly  those  of  the  legs,  hands,  and  tongue,  mani- 
fested by  tremor,  which  for  a  time  can  be  temporarily  overcome 
by  taking  alcohol.  There  gradually  develop  mental  sluggishness. 
impaired  judgment  and  memory,  with  irritability  of  temper  and  a 
progressive  change  in  moral  character.  Indigestion  and  catarrhal 
gastritis  are  early  and  constant  findings.  The  breath  has  a  peculiar 
odour,  the  bowels  are  constipated,  the  tongue  is  furred,  and  there  is 
anorexia.  Gastrectasia  is  not  uncommon  in  habitual  beer  drinkers. 
The  most  constant  change  occurring  in  the  liver  is  cirrhosis,  pre- 
ceded, sometimes  for  years,  by  enlargement  and  tenderness.  The 
eyes  are  watery  and  red,  and  ante  rosacea  is  common. 

(III)  Delirium  Tremens  (Mania  a  potu). — A  result  of  long-con- 
tinued alcoholic  poisoning  of  the  brain  centres ;  is  a  common  attend- 
ant of  pneumonia  in  alcoholics,  and  may  be  induced  by  sudden 
fright,  shock,  or  accidents. 


THE  INTOXICATIONS  1017 

Symptoms. — Insomnia,  restlessness,  and  depression  are  early  pre- 
monitions. The  delirium  manifests  itself  by  constant  incoherent 
talking,  unnatural  activity  of  mind  and  body,  and  hallucinations  of 
sight  and  hearing.  There  is  a  disordered  imagination,  the  patient 
fancying  that  he  sees  and  hears  animals  (mice  or  snakes),  and  that 
he  is  being  pursued  by  enemies.  The  terror  induced  by  this  condi- 
tion may  be  so  marked  that  the  patient  in  his  efforts  to  escape  may 
do  himself  bodily  harm.  Insomnia  continues  during  the  active  pe- 
riod of  the  delirium,  which  may  last  for  several  days,  a  return  to 
natural  sleep  heralding  improvement.  The  temperature  usually 
ranges  from  101°  to  103°,  although  it  may  be  much  higher  in  fatal 
cases.  The  pulse  is  rapid  and  of  fairly  good  quality  at  first,  be- 
coming very  weak  if  the  delirium  is  prolonged.  Muscular  tremor 
and  a  tremulous  tongue  (usually  heavily  coated)  are  constant.  Fatal 
cases  end  by  heart  failure. 

Later  Symptoms  attending  Alcoholism. — Insanities,  dementia 
paralytica,  and  epilepsy  have  been  attributed  to  alcoholism.  Heredi- 
tary epilepsy  is  claimed  as  a  result  of  long-continued  dipsomania  in 
one  or  both  parents,  particularly  in  the  father.  Chronic  encephalo- 
meningitis  may  occur,  and  acute  alcoholic  neuritis  is  a  painful  con- 
dition attending  advanced  alcoholic  poisoning.  There  is  a  chronic 
form  of  alcoholic  neuritis  known  as  polyneuritis  potatorum  {pseudo- 
tabes, ataxia  of  drunkards).  It  presents  two  varieties,  the  paralytic 
and  the  ataxic.  There  are  pains  in  the  lower  extremities,  ataxia, 
areas  of  anaesthesia,  occasional  loss  of  the  superficial  reflexes,  and 
paralysis  and  atrophy,  chiefly  of  the  extensors  of  the  fingers  and  toes. 
Arteriosclerosis,  with  sequent  cardiac  dilatation  and  granular  kid- 
ney, is  not  infrequent. 

Diagnosis.— (1)  Acute  Alcoholism.— Usually  easy,  provided  the 
unconsciousness  is  not  complete.  It  is  based  mainly  upon  a  history 
of  alcoholic  excess,  the  odour  of  the  breath,  and  acute  gastric  dis- 
turbances (frequent  and  prolonged  vomiting),  with  muscular  inco- 
ordination and  confused  mentality.  There  is  a  pronounced  inclina- 
tion to  sleep,  an  indifference  as  to  location,  and  a  decided,  although 
good-natured,  resentment  of  interference.  A  sound  sleep  assures 
the  disappearance  of  most  of  these  symptoms  and  a  gradual  return 
to  the  normal.  Only  in  cases  associated  with  unconsciousness  and 
other  evidences  of  cerebral  or  constitutional  disturbances  is  there 
any  difficulty  in  the  differential  diagnosis.  It  must  be  borne  in 
mind  that  even  moderate  indulgence  in  alcohol  may  be  coincident 
with  apoplexy,  fracture  of  the  skull,  acute  uraemia,  or  sunstroke. 
In  cases  of  reasonable  doubt  the  patient  should  receive  the  benefit 
and  be  treated  as  if  suffering  from  the  graver  condition. 


1018  DIAGNOSIS,   DIRECT   AND  DIFFERENTIAL 

For  the  separation  of  acute  alcoholism  from  other  forms  of  coma^ 
especially  apoplexy^  urcsmia,  and  sunstroke,  see  pages  68  to  71. 

Fracture  of  the  Skull. — In  this  the  coma  may  be  profound,  pre- 
senting many  of  the  symptoms  of  cerebral  hemorrhage,  with  few  if 
any  evidences  of  external  injury.  If  there  is  no  improvement,  but 
rather  a  gradual  increase  in  the  symptoms  after  a  reasonable  length 
of  time,  a  suspicion  of  fracture  is  justifiable.  A  careful  examination 
of  the  entire  scalp  will  usually  reveal  a  point  of  circumscribed  oedema 
indicative  of  injury  to  the  bone.  Otherwise  the  differential  diagnosis 
is  similar  to  that  from  hemorrhage  (page  69). 

(2)  Diagnosis  of  Delirium  Tremens. — Occurs  only  in  more  or  less 
chronic  alcoholism,  not  in  persons  of  ordinarily  temperate  habits. 
In  addition  to  the  history  there  are  hallucinations  of  sight  and  hear- 
ing, incoherency  of  speech,  great  irritability  and  restlessness,  some 
fever,  insomnia,  prostration,  and  a  frequent,  feeble  pulse.  The  lungs 
should  be  examined  for  pneumonia  and  the  body  for  traumatisms. 

II.  Morphine  Habit  {Morjjhinomania,  Morphinism). — If  the 
use  of  morphine  is  discontinued  after  the  indications  for  its  employ- 
ment have  passed  no  injurious  effects  will  follow ;  otherwise  its  con- 
tinued taking  develops  a  craving  for  the  drug,  with  the  ultimate 
formation  of  the  morphine  habit. 

Early  Symptoms. — At  first  slight,  and  the  general  health  is  little,  if 
at  all,  impaired.  The  drug  produces  feelings  of  satisfaction  and  jier- 
sonal  comfort,  a  condition  which  lasts  as  long  as  it  is  given  in  suffi- 
cient quantities.  AVhen  discontinued,  feelings  of  lassitude  and  mental 
depression,  nausea,  and  sometimes  vomiting,  accompanied  by  epigas- 
tric distress,  ensue.  More  or  less  general  itching  of  the  skin,  par- 
ticularly about  the  nose,  is  a  quite  constant  symptom. 

Later  Symptoms. — As  the  necessity  for  larger  doses  becomes  more 
urgent  disturbances  of  the  general  health  are  manifest.  The  victim 
is  restless  and  irritable,  sleep  is  disturbed,  appetite  and  digestion 
deranged,  and  there  is  constant  mental  depression.  Chills  followed 
by  profuse  sweating  are  not  uncommon.  The  pupils  are  dilated, 
sometimes  unequally,  except  while  under  the  direct  influence  of  the 
drug,  when  they  are  minutely  contracted.  There  is  a  gradual  weak- 
ening of  the  moral  sense,  and  the  patient  becomes  an  inveterate  liar. 
In  women,  hysteria  and  neurasthenia  are  not  uncommon.  Ulti- 
mately a  condition  of  asthenia,  with  anorexia,  is  induced.  The  vic- 
tim gradually  becomes  emaciated,  sallow,  gray,  and  prematurely  aged, 
finally  dying  from  extreme  weakness. 

III.  Acute  Opium  Poisoning  {Opium  Xarcosis). — Due  to  an 
overdose,  and  may  occur  in  habitues  as  well  as  in  non-users. 

Symptoms. — The  period  between  the  taking  of  a  poisonous  dose 


THE  INTOXICATIONS  1019 

by  the  stomach  and  the  first  indication  of  symptoms  varies  from  a 
very  few  to  20  or  30  minutes.  When  taken  with  suicidal  intent  by 
subjects  of  alcoholic  mania,  there  is  often  a  marked  resistance  to  its 
narcotic  effects,  followed  by  sudden  and  complete  coma.  The  onset 
is  usually  abrupt.  The  patient  may  be  talking  naturally  one  mo- 
ment and  the  next  be  profoundly  unconscious.  The  jaws  may  at 
first  be  fixed  and  resist  efforts  to  open  them.  Later  relaxation  occurs. 
The  pupils  become  minutely  contracted,  do  not  react  to  light,  and 
sensation  is  lost  in  the  cornea.  Coincidently  the  respirations  drop  to 
10  or  12,  sometimes  4,  to  the  minute.  Tlie  heart  action  is  weak,  and 
the  pulse  feeble,  well-nigh  imperceptible. 

The  face  is  pale,  sometimes  cyanotic,  and  the  skin  dry  or  bathed 
in  perspiration.  The  coma  may  resist  everything  but  severe  bodily 
punishment.  When  partially  aroused  the  speech  is  incoherent,  and 
the  patient  relapses  quickly  into  narcosis.  There  is  retention  of 
urine,  later  associated  with  vesical  tenesmus,  lasting  for  several  hours. 
The  tongue  may  drop  back  into  the  pharynx,  seriously  diminishing 
the  already  impaired  oxygenation.  The  respiration  may  be  sterto- 
rous and  the  cheeks  flap.  Under  successful  treatment  the  coma 
gradually  lessens,  the  respirations  become  more  frequent,  the  colour 
of  the  skin  and  the  heart  action  improve.  Eelapses  are  frequent, 
and  hours  or  days  may  elapse  before  the  patient  is  out  of  danger. 
Opium  narcosis  following  alcoholic  excess  may  be  complicated  by 
acute  mania  or  peripheral  neuritis  of  one  or  more  of  the  extremities. 

Diagnosis. — It  may  be  necessary  to  differentiate  between  the  coma 
of  acute  opium  poisoning  and  that  of  uraemia,  alcohol,  sunstroke,  and 
cerebral  hemorrhage,  for  which  see  pages  68  to  71. 

IV.  Lead-poisoning  {Plumhism ;  Saturnism). — This  metal 
may  enter  through  the  lungs,  skin,  or  digestive  system.  It  is  found 
in  the  air  in  regions  where  lead  ore  is  being  smelted,  in  white-lead 
factories,  and  is  contained  in  water,  wines,  and  cider  which  have 
been  confined  for  some  time  in  lead  pipes  or  lead-lined  containers.  It 
may  enter  in  milk,  cosmetics,  hair  dyes,  thread,  false  teeth,  and  adul- 
terated food  or  food  products— e.  g.,  baking  powder  containing  chro- 
mate  of  lead.  Plumbism  is  not  common  in  children,  occurring  usu- 
ally between  30  and  40  years  of  age,  in  women  rather  than  men. 

Varieties  axd  Symptoms.— (I)  Acute  Lead-poisoning.— Symptoms 
may  appear  in  a  few  weeks  after  exposure,  or  be  absent  for  months  or 
years.  Anaemia,  sometimes  rapid,  may  follow  a  short  exposure.  Con- 
stipation, followed  by  severe  diarrlioea,  vomiting,  and  occasionally  ab- 
dominal tenderness  and  distention,  are  present.  Usually  the  abdomen 
is  contracted,  hard,  and  perhaps  scaphoid.  There  is  colic  {colica  Pic- 
tonum)  of  a  most  severe  type  felt  over  the  entire  abdomen.     It  inter- 


1020  DIAGNOSIS,    DIRECT  AND   DIFFERENTIAL 

mits,  with  dull  abdominal  pain  during  the  intervals.  It  is  a  true,  non- 
inflammatory colic  due  to  the  action  of  the  metal  upon  the  terminal 
nerves.  The  paroxysms  are  of  gradual  onset,  but  steadily  increase  in 
severity  and  frequency.  The  pain  is  twisting  or  grinding,  and  may 
be  accompanied  by  pain  or  cramps  in  the  extremities.  The  point  of 
maximum  intensity  of  the  pain  is  usually  in  the  region  of  the  umbili- 
cus, whence  it  radiates  in  all  directions,  but  may  be  in  other  parts  of 
the  abdomen.  It  is  relieved  by  deep  pressure,  and  sometimes  excited 
by  food.     The  temperature  is  not  elevated,  and  may  be  subnormal. 

Arteriosclerosis,  contracted  kidneys,  hypertrophy  of  the  heart, 
and  distinct  gouty  deposits  are  not  infrequent  results  of  continuous 
exposure.  Gouty  subjects  are  especially  liable  to  lead-poisoning. 
Albumin  is  frequently  found  in  the  urine,  due  either  to  the  irritation 
produced  by  the  elimination  of  the  lead  or  to  a  coexisting  nephritis. 
Other  symptoms  described  are  convulsions,  epilepsy,  and  delirium. 
Abdominal  distention  and  severe  entero-colitis  are  somewhat  rare,  and 
usually  occur  in  persons  recently  exposed. 

Acute  Lead-poisoning  in  Children. — If  slight,  this  may  easily  be 
overlooked.  A  not  uncommon  source  of  infection  in  the  very  young 
is  found  in  toys  composed  wholly  or  in  part  of  lead.  The  symptoms 
often  resemble  those  of  a  slight  indigestion.  There  may  be  indefi- 
nite malaise,  and  either  constipation  or  strong-smelling  diarrhoeal 
movements.  If  the  child  is  old  enough  he  may  complain  of  a  con- 
stant pain  in  the  region  of  the  umbilicus,  not  sufiiciently  severe  to 
cause  crying,  but  which  does  not  yield  to  simple  remedies.  The  child 
will  go  to  the  nurse  many  times  during  the  day  seeking  comfort  for 
a  distress  which  is  persistently  referred  to  the  abdomen.  There  is 
constant  slight  fever  (99°  to  101°),  which  at  the  beginning  of  the 
attack  may  reach  104°,  but  this  high  temperature  soon  responds  to 
simple  laxative  treatment.  It  may  be  confused  with  slight  malarial 
infection,  but  does  not  respond  to  quinine.  With  such  symptoms, 
if  careful  inquiry  is  made  as  to  the  toys  used  by  the  child,  a  source 
of  lead  infection  may  be  found. 

(II)  Chronic  Lead-poisoning. — The  symptoms  are  due  to  the  pro- 
longed absorption  of  small  quantities  of  lead,  and  usually  one  or 
more  of  these  predominate.  The  specific  effects  are  disturbances  of 
nutrition,  colic,  arthralgia,  paralyses,  and  lead  encephalopathy. 

(1)  Disturbances  of  Xutrition. — Anaemia  may  be  profound,  the 
red  cells  sinking  to  50  per  cent,  with  wasting,  especially  of  the  mus- 
cles, and  a  peculiar  yellowish  complexion.  The  latter  {icterits  satur- 
ninus)  is  not  due  to  the  deposit  of  bile  pigments.  Along  the  border 
of  the  gums  may  be  found  a  dark  or  bluish-black  line,  often  lacking 
in  persons  having  clean  teeth.     In  the  absence  of  teeth  it  is  not 


THE  INTOXICATIONS 


1021 


present.  It  may  be  confounded  with  a  line  on,  not  in,  the  gums, 
which  is  readily  removed  by  cleaning  the  teeth  (Osler)  ;  and  a  black 
line  found  in  miners,  due  to  deposition  of  carbon.  For  others 
see  page  222.  Certain  general  symptoms  are ;  Habitual  dryness  of 
the  mouth,  with  an  astringent,  sweetish,  or  faintly  metallic  taste, 
coated  tongue,  fetid  breath,  obstinate  constipation,  and  distressing 
dyspepsia.  As  the  disease  progresses  there  is  loss  of  muscular  power 
and  occasional  tremors.  The  patient  becomes  apathetic,  irritable, 
and  morose.  Coinciding  with  these  symptoms  there  may  have  been 
several  attacks  of  lead  colic,  followed  by  pains  in  the  muscles  or  joints, 
perhaps  by  evidences  of  beginning  paralysis. 

(2)  Lead  Colic  (Colica  satumina).— This  affection  {painter's  coUcy 
Devonshire  colic,  colica  Pictonmn)  follows,  as  a  rule,  a  period  of  mal- 
nutrition, dyspepsia,  and  constipation,  but  may  develop  suddenly, 
and  be  ushered  in  by  nausea  and  vomiting.  The  paroxysms  of  pain 
are  more  severe  in  the  afternoon  and  at  night.  Relapses  are  frequent, 
and  continued  exposure  may  lead  to  the  colic  becoming  chronio 
The  termination  of  an  attack  may  be  as  sudden  as  its  onset. 

(3)  Arthralgia  {Arthralgia  saturnina).—FaToxjsmal  pains,  with 
exacerbations  and  remissions,  are  not  infrequently  present  in  the 
joints  and  contiguous  muscles,  without  swelling,  redness,  or  fever. 
The  pain  may  be  increased  by  exercise  and  cold.  The  knees  are  most 
commonly  affected,  next  the  elbow  and  shoulder  joints ;  the  flexor 
muscles  more  frequently  than  the  extensors.  The  large  lumbar  mus- 
cles, the  intercostal,  and  those  of  the  neck  are  often  involved.  The 
pain  is  severe,  tearing,  and  burning. 

(4)  Paralysis  {Paralysis  saturnina  ;  Lead  Palsy). — Usually  a  later 
manifestation,  and,  with  few  exceptions,  limited  to  adults.  One 
attack  predisposes  to  others.  As  a  rule  there  is  no  fever.  The 
paralysis  may  be  local  or  general.  De  R.  is  marked,  muscular  atrophy 
begins  early,  and  the  wasting  may  be  so  decided  that  there  is  stretch- 
ing of  the  ligaments,  with  ultimate  partial  or  complete  dislocation  of 
the  bones.  Early  symptoms  are  coldness,  numbness,  and  hyperaes- 
thesia,  seldom  anaesthesia;  feebleness,  stiffness,  impairment  of  motor 
power,  and  tremor  of  the  affected  muscles.  The  symptoms  are  more 
marked  at  night.  If  persisting,  they  soon  lead  to  the  development 
of  the  characteristic  paralysis.  In  the  great  majority  of  cases  the 
extensor  muscles  are  affected,  one  or  more  of  the  muscles  of  a  group 
being  the  seat  of  the  paralysis.  The  following  localized  forms  have 
been  recognised  (Dejerine-Klumpke,  summarized  by  Osier) : 

Anti-hrachial. — In  this  the  musculo-spiral  nerve  is  involved,  with 
paralysis  of  the  extensors  of  the  fingers  and  wrist  (wrist-drop).  The 
supinator  longus  usually  escapes.    Distention  of  the  synovial  sheaths^ 


1022  DIAGNOSIS,   DIRECT   AND   DIFFERENTIAL 

causing  a  prominent  swelling  over  the  wrist  (Gruebler's  tumour), 
occasionally  follows  the  long-continued  flexion  of  the  carpus. 

Brachial. — The  muscles  involved  are  the  deltoid,  biceps,  brachi- 
alis  anticus,  and  supinator  longus.  The  atrophy  is  of  the  scapulo- 
humeral form  and  is  bilateral. 

Aran-Duchenne. — There  is  marked  atrophy  of  the  small  muscles 
of  the  hand  and  of  the  thenar  and  hypothenar  eminences,  resembling 
the  early  stage  of  poliomyelitis  anterior  chronica. 

Peroneal. — In  this  the  lateral  peroneal  muscles,  the  extensor 
communis  of  the  toes,  and  the  extensor  proprius  of  the  big  toe  are 
involved,  with  the  production  of  the  steppage  gait  ( (3),  page  34). 

Respiratory. — Paralysis  of  the  intercostal  and  laryngeal  muscles 
and  adductor  paralysis  of  the  larynx  nave  been  noted. 

Generalized  Palsies. — There  is  a  rare  type  of  palsy  pursuing  a 
course  like  that  of  ascending  paralysis,  with  rapid  wasting  of  all  four 
limbs.     A  febrile  form  of  general  paralysis  has  been  recognised. 

(5)  Encephalopathy  {Enceplialopatliia  Saturnina). — Extremely 
rare,  and  is  due  to  the  action  of  lead  upon  the  nerve  centres.  It 
embraces  lead  insanity,  delirium,  convulsions,  epilepsy,  and  coma. 
A  large  number  of  symptoms  may  precede  the  more  active  cerebral 
manifestations,  such  as  headache,  vertigo,  troublesome  insomnia,  dis- 
tressing dreams,  dimness  of  vision,  alterations  of  the  pupils,  tinnitus 
aurium,  dysphagia,  constriction  of  the  pharynx,  and  stupor  or  excite- 
ment.    Colic,  arthralgia,  and  palsy  are  also  prodromal. 

Lead  encephalopathy  may  be  divided  into  three  forms,  the  delir- 
ious, comatose,  and  convulsive.  The  delirium  is  at  first  tranquil, 
later  becoming  furious  and  paroxysmal,  with  intervals  of  somnolence. 
Finally,  true  sleep  supervenes,  followed  by  complete  restoration.  The 
coma  may  be  gradual  or  instantaneous ;  may  be  the  only  active 
indication  of  the  disease  ;  or  be  preceded  or  attended  by  convulsions 
or  delirium.  Convulsions  are  the  most  common  ;  are  occasionally  fol- 
lowed by  true  epilepsy ;  and  may  be  partial  or  general.  If  partial, 
the  face,  a  single  limb,  or  one  side  of  the  body  alone  may  be  in- 
volved. They  may  be  associated  with  dulness,  and  followed  by  more 
or  less  complete  coma.  Amblyopia,  usually  followed  by  recovery, 
has  been  noted,  but  occasionally  optic-nerve  atrophy  results. 

Diagnosis. — Excepting  colic,  which  may  occur  with  few  if  any 
prodromata,  little  difficulty  is  experienced  in  the  diagnosis  of  lead- 
poisoning.  The  history  and  the  subsequent  course  and  symptoms 
are  usually  sufficiently  distinctive.  The  abdominal  pain,  being 
purely  a  neurosis,  may  at  first  be  mistaken  for  flatulent  (page  798), 
hepatic  (page  805),  renal  (page  938),  or  appendicular  (page  788)  colic 
or  ectopic  gestation  (page  787). 


THE  INTOXICATIONS  1023 

^  .  Arsenic-poisoning. — Arsenic  in  poisonous  quantities  may 
enter  the  body  by  way  of  the  intestinal  or  respiratory  tracts.  It  is 
the  active  principle  of  Paris  green  and  Rough  on  Rats,  is  employed 
in  the  manufacture  of  coloured  papers  and  artificial  flowers,  and  is 
found  in  many  fabrics.  The  action  of  certain  moulds  upon  the 
arsenical  organic  matter  in  wall  paper  produces  a  volatile  oil  which 
renders  poisoning  through  the  lungs  possible. 

Varieties  and  Symptoms.— (I)  Therapeutic  Overaction.— Medici- 
nal doses  may  cause  symptoms  of  considerable  severity,  i.  e.,  a  metal- 
lic taste,  salivation,  nausea,  vomiting  of  glairy  mucus,  epigastric  pain 
and  soreness,  diarrhoea,  tenesmus,  and  at  times  dysenteric  stools. 
The  heart  is  irritable  and  feeble,  with  palpitation,  cough,  oppressed 
breathing,  oedema  of  the  eyelids,  and  occasionally  general  oedema. 
There  may  be  itching  of  the  eyelids,  urticaria,  eczema,  pityriasis, 
psoriasis,  falling  out  of  hair  and  nails,  trembling,  stiffness,  contrac- 
tion of  joints,  disorders  of  sensibility,  and  herpes  zoster  (Bartholow). 

(II)  Acute  Arsenic-poisoning. — The  gastro-intestinal  symptoms 
are  intense  epigastric  and  abdominal  pain,  uncontrollable  vomiting, 
colic,  diarrhoea,  tenesmus,  dryness  of  the  mouth  and  fauces,  intense 
thirst,  intestinal  irritation,  bloody  and  offensive  stools,  retracted  ab- 
domen, strangury,  priapism,  suppression  of  urine  or  bloody  urine, 
monorrhagia  in  women,  and  involuntary  evacuations.  Without  gas- 
tro-intestinal symptoms  the  condition  may  become  suddenly  one  of 
profound  coma  very  similar  to  that  of  extreme  opium  narcosis. 
Later  symptoms  may  be  paralysis,  neuralgic  pains,  and  numbness. 

(III)  Chronic  Arsenic-poisoning. — Pronounced  and  common  symp- 
toms are  debility  and  anaemia,  with  some  gastro-intestinal  irritation 
and  pain,  disturbed  mucous  secretion,  redness  or  bleeding  of  the 
gums,  sensory  disorders,  such  as  tingling  or  numbness,  and  oedema 
or  puffiness  of  the  eyelids.  Later  symptoms  are  multiple  neuritis,  pig- 
mentation, stiff  joints,  neuralgic  pains,  and  arsenical  paralysis.  The 
latter  resembles  that  of  chronic  lead-poisoning,  except  that  the  legs, 
rather  than  the  arms  or  wrists,  are  usually  affected.  It  attacks  the 
extensors  and  the  peroneal  muscles,  causing  the  "steppage  gait" 
(page  34).  De  R.  is  usually  present.  A  tolerance  is  at  times  ac- 
quired, which  will  render  harmless  an  ordinarily  poisonous  dose. 

Diagnosis. — Based  mainly  upon  the  history  and  the  form  in 
which  the  poison  is  taken.  Attention  should  be  given  to  wall  paper, 
artificial  flowers,  and  wearing  apparel.  Paris  green,  in  common  use 
by  suicides,  gives  an  intensely  green  colour  to  the  vomitus. 

YI.  Food-poisoning  {Bromatotoxismns,  Vaughan). — Food,  in- 
cluding milk,  may  contain  the  active  organisms  of  tuberculosis, 
trichinosis,  typhoid  fever,  scarlet  fever,  and  diphtheria ;  may  be  in- 


1024  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

fected  with  the  bacteria  of  putrefaction  or  by  certain  fungi,  and, 
finally,  actively  poisonous  ptomaines  may  exist  in  shellfish  and  fish. 

(1)  Meat-poisoning  {Kreotoxismus). — Arises  commonly  from  de- 
composed sausages  {botulism^  allantiasis),  ham,  pork  pie,  and  head- 
cheese ;  occasionally  beef,  veal,  and  mutton. 

Symptoms. — The  primary  symptoms  (Ballard,  Vaughax,  Osler)  in 
a  mild  type  are  vomiting,  diarrhoea,  abdominal  pains,  muscular  weak- 
ness, thirst,  and  headache,  preceded  by  a  period  of  incubation  varying 
from  13  to  -iS  hours,  during  which  there  are  no  prodromes.  In  other 
cases  there  are  languor,  anorexia,  nausea,  chilliness,  dyspnoea,  vertigo, 
faintness,  cold  sweat,  headache,  pain  in  the  trunk  or  abdomen,  dys- 
phagia, and  intense  thirst.  A  single  case  seldom,  if  ever,  presents  all 
of  these  symptoms.  At  the  close  of  the  incubation  period  more 
active  symptoms  develop,  beginning  with  abdominal  pain,  constant 
diarrhoea,  and  vomiting.  The  pain  (crampy,  tearing,  burning)  in  the 
chest  or  between  the  shoulders  causes  extreme  prostration  and  faint- 
ness. The  diarrhoea  is  frequently  uncontrollable,  with  dark  and  very 
offensive  stools.  Headache,  intense  thirst,  and  restlessness  are  fre- 
quent.    There  is  fever,  and  the  pulse  reaches  100  to  128. 

Less  frequent  symptoms  are  "  excessive  sweating,  cramps  in  the 
legs,  or  in  both  legs  and  arms,  convulsive  fiexion  of  the  hands  or 
fingers,  muscular  twitching  of  the  face,  shoulders,  or  hands,  aching 
pains  in  the  shoulders,  joints,  or  extremities,  a  sense  of  stiffness  of 
the  joints,  pricking  or  tingling  or  numbness  of  the  hands  lasting  far 
into  convalescence,  a  sense  of  general  compression  of  the  skin,  drowsi- 
ness, hallucinations,  imperfection  of  vision,  and  intolerance  of  light. 
In  other  cases  yellowness  of  the  skin,  either  general  or  confined  to 
the  face  and  eyes,  appeared.  In  the  fatal  cases  death  was  preceded 
by  collapse  like  that  of  cholera,  pinched  features,  and  blueness  of  the 
fingers  and  toes  and  around  the  sunken  eyes  "  (Osler). 

Symptoms  similar  to  those  just  described  have  been  observed  in 
cases  of  poisoning  by  canned  meats.  In  other  cases  poisonous  symp- 
toms may  arise  from  eating  certain  game  birds. 

(II)  Poisoning  by  Milk  Products  — The  symptoms  of  poisoning  by 
milk  {galactotoxismiis),  cheese  (tyrotoxistmis),  custard,  and  ice  cream 
do  not  differ  from  those  occurring  in  meat-poisoning. 

(III)  Poisoning  by  Shellfish  and  Fish.— (l)  Oysters.— These,  if 
they  have  undergone  decomposition,  may  become  poisonous.  The 
symptoms  are  usually  gastro-intestinal,  and  differ  only  in  degree  from 
those  of  meat-poisoning. 

(2)  Mussels  {Mytilus  edulis). — The  edible  mussel  becomes  poison- 
ous in  filthy  water.  The  symptoms,  unlike  those  of  meat-poisoning, 
are  seldom   gastro-intestinal.     The  onset  is  acute,  and  death  may 


THE  INTOXICATIONS— SUNSTROKE  1025 

occur  within  a  few  hours  with  symptoms  of  collapse  (see  page  151). 
Even  in  cases  that  recover  these  symptoms  are  usually  present, 

(3)  Fish  {Ichthyotoxismiis). — Putrefaction  occurring  in  fish,  espe- 
cially haddock,  maciierel,  and  cod,  results  in  the  production  of  toxic 
ptomaines.  The  symptoms  observed  are  usually  referable  to  the 
nervous  system,  the  gastro-intestinal  tract  being  seldom  involved. 

(IV)  Grain-poisoning  {Sitotoxismus). — (I)  Ergotism. — The  ergot 
fungus  {claviceps  purpurea)^  found  in  certain  grains,  may  cause  severe 
symptoms  if  food  containing  it  has  been  used  for  a  long  time.  Two 
varieties  are  recognised,  gangrenous  and  convulsive. 

Gangrenous. — Symptoms  are  spasmodic  muscular  contractions, 
pain,  tingling,  occasionally  anaesthesia ;  finally  blood  stasis  and  gan- 
grene, usually  in  fingers  and  toes,  sometimes  in  nose  and  ears. 

Convulsive. — During  the  early  stages  the  symptoms  may  be  those 
of  the  gangrenous  form,  followed  by  pronounced  nervous  disturb- 
ances. The  prodromal  period  (1  to  2  weeks)  usually  presents  head- 
ache, slight  fever,  and  occasional  tingling  or  pain,  soon  succeeded 
by  muscular  cramps  and  spasm,  the  latter  continuing  either  for  a 
few  hours  or  for  several  days.  In  severe  cases  there  may  be  early 
delirium  or  epilepsy  (sometimes  fatal) ;  but  dementia  or  melancholia 
are  somewhat  more  frequent  occurrences.  Death  is  not  uncommon 
in  chronic  ergotism.  Degeneration  of  the  posterior  columns  may 
ensue,  resulting  in  a  condition  not  unlike  that  of  tabes  dorsalis. 

(II)  Lathyeism  (Lupinosis). — A  condition  due  to  the  presence 
in  the  food  of  the  seeds  of  the  Lathy rus,  and  occurs  in  India,  Italy, 
and  Algiers.  Its  most  constant  symptom  is  spastic  paraplegia,  result- 
ing from  what  is  probably  a  slow,  toxic,  spinal  sclerosis. 

(III)  Pellagea  (Maidismus ;  Italian  leprosy;  Alpine  scurvy). 
— Due  to  the  use,  as  food,  of  diseased  maize.  It  is  unknown  in 
America,  but  common  in  France,  Spain,  and  Italy.  The  body 
becomes  almost  coal-black,  and  the  victims  suffer  from  prostration 
and  melancholia.  The  skin  is  thickened  and  rough,  and  finally 
exfoliates.  Suppuration,  with  the  formation  of  black  crusts,  is  not 
uncommon.  There  are  also  diarrhoea,  indigestion,  and  salivation. 
Mild  cases  may  persist  for  months,  and  the  more  severe  are  attended 
by  spasms,  pain  in  the  back  and  head,  paralysis  (chiefly  a  paraplegia), 
and  melancholia  or  suicidal  mania. 

VII.  Sunstroke  (Heat  Exhaustion;  Tliermic  Fever;  Insolation; 
Coup  de  .S'o?f?7).— Contributing  causes  are  excessive  bodily  fatigue, 
insufficient  diet,  and  overuse  of  beer  and  whisky.  Two  forms  are 
recognised  :  (1)  Heat  exhaustion  and  (2)  Sunstroke. 

Symptoms  —(I)  Heat  Exhaustion.— The  attack  may  occur  in  bed, 
or  at  work,  or  while  walking.     Nausea  and  vomiting,  usually  pre- 


1026  DIAGNOSIS,   DIRECT  AND   DIFFERENTIAL 

ceded  by  dizziness  and  fulness  or  pain  in  the  head,  are  early  symp- 
toms. There  is  a  feeling  of  oppression  and  great  weakness,  the 
patient  falling  or  sitting  down.  The  skin  is  either  flushed  or  pale, 
and  may  be  hot  and  dry  or  bathed  in  cold  perspiration.  The  pulse 
is  usually  rapid  and  feeble,  the  respirations  shallow  and  sighing. 
The  temperature  ranges  from  subnormal  to  102°.  In  many  cases 
the  condition  is  one  of  collapse  (page  151).  The  unconsciousness 
is  usually  not  profound  and  yields  readily  to  treatment.  In  mild 
cases  the  pupils  react  to  light  and  are  moderately  dilated. 

(II)  Sunstroke. — Symptoms. — The  patient  is  usually  found  uncon- 
scious. The  symptoms  of  heat  exhaustion  may  have  preceded  the 
attack,  but,  as  a  rule,  the  insensibility  develops  very  rapidly.  The 
face  is  hot  and  flushed,  the  pulse  rapid  and  bounding,  and  the  res- 
pirations either  loud,  slow,  and  stertorous,  or  feeble,  gasping,  and 
laboured.  In  extreme  cases  the  symptoms  of  collapse  (page  151)  may 
be  present.  Even  in  the  cases  which  recover  there  frequently  occur, 
during  the  period  of  coma  and  high  temperature,  tonic  or  clonic 
contractions  of  the  muscles,  either  localized  or  general.  With  a 
drop  in  the  temperature  the  muscular  spasm  becomes  less  frequent 
and  the  insensibility  less  profound.  Eelapses  of  high  temperature,^ 
often  with  a  return  of  coma  and  collapse,  are  not  uncommon  even 
after  restoration  to  complete  consciousness. 

Complications. — These  are  :  repeated  relapses,  persistent  vomiting, 
retention  of  urine,  general  convulsions,  cyanosis,  active  delirium, 
failure  to  respond  to  stimulation,  pneumonia,  pulmonary  oedema, 
and  fatal  intestinal  hemorrhage. 

Sequelce. — Sequelae  do  not  always  occur,  as  the  recovery  is  often 
complete.  The  most  constant  sequel  is  an  intolerance  of  high,  or 
moderately  high,  temperatures.  Less  frequent  are  peripheral  neu- 
ritis, meningitis,  muscular  atrophy  or  tremor,  wrist-  or  foot-drop, 
difficulty  of  speech,  long-continued  acceleration  of  pulse  and  respi- 
ration, headache,  vertigo,  epilepsy,  spinal  irritation,  cutaneous  anaes- 
thesia or  hyperaesthesia,  enfeebled  memory,  deafness,  cardiac  lesions, 
indigestion,  impaired  nutrition,  and  anaemia. 

DiAG>fosis. — This  is  based  upon  the  existing  temperature  and 
atmospheric  conditions  and  the  mode  of  onset.  Heat  exhaustion 
with  moderately  low  body  temperature  may  be  mistaken  at  first 
for  acute  alcoholism,  uraemia,  or  apoplexy.  The  history  and  the 
course  of  the  attack  are  sufficiently  distinctive  for  the  discrimination. 
Sunstroke,  with  its  sudden  onset,  extremely  high  temperature,  and 
accompanying  symptoms,  should  rarely  be  misdiagnosed. 


DISEASES  DUE  TO  ANIMAL   PARASITES  1027 

SECTION  XI 
DISEASES  DUE  TO   THE  AXIMAL  PAEASITES 
Pkepaked  by  Frank  Whitfield  Shaw,  M.  D. 

I.  Distomiasis. — (I)  Liver  Flukes. — Some  of  these  are  the 
Fasciola  hepatica  (in  ruminants),  Distomum  lanceolatum  (sheep  and 
cattle),  and  Distoma  fellneum  (in  cats).  Among  the  symptoms  as- 
signed are  emaciation,  diarrhoea,  ascites,  and  jaundice.  The  liver 
becomes  enormously  enlarged,  and  chronic  cholangitis  may  coexist. 

(2)  Blood  Flukes  {Schistosoma  hmmatohium). — Found  in  the  blood 
of  the  portal  vein  and  the  veins  of  the  spleen,  bladder,  kidneys,  and 
mesentery.  Hasmaturia,  with  dysuria,  resulting  from  irritation  due 
to  the  ova  of  this  parasite  in  the  blood,  is  a  serious  and  constant 
symptom,  second  only  to  the  progressive  ansemia  attending  it. 

(3)  Bronchial  Fluke  Distomum  Westermanni,  Parasitic  Hemop- 
tysis).— Found  in  the  bronchial  tubes,  and  produces  attacks  of 
haemoptysis,  which  are  endemic  in  many  Eastern  countries. 

II.  Nematodes. — (I)  Ascaris  Lumbricoides  {Roundworm). — This 
worm  (see  (i),  page  136)  is  most  frequently  found  between  the  3d 
and  10th  years  of  childhood,  but  is  rare  during  infancy.  The  symp- 
toms may  be  very  indefinite,  the  condition  not  being  suspected  until 
a  worm  is  vomited  or  is  found  in  the  stools.  There  may  be  a  wide 
range  of  symptoms :  chills,  hysterical  attacks,  epileptiform  convul- 
sions, strabismus,  and  perhaps  temporary  paralyses.  More  commonly 
the  usual  indications  are  grinding  of  the  teeth,  picking  of  the  nose, 
irritability,  and,  in  extremely  nervous  children,  mild  convulsive 
attacks.  The  diagnosis  is  simple  when  the  worm  or  its  ova  (B,  Fig. 
220,  page  619)  are  found.  If  not,  the  administration  of  full  doses  of 
santonin,  followed  by  a  purgative,  will  establish  the  diagnosis. 

(II)  Oxyuris  Vennicularis  {Pimvorm).  —  The  worms  (see  page 
138)  are  found  principally  in  the  rectum  and  colon.  The  more  pro- 
nounced symptoms  are  irritability  and  restlessness,  intense  irritation 
and  itching  about  the  anus  and  external  genitals,  incontinence  of 
urine,  and,  in  the  female,  vaginitis.  The  latter  is  probably  due  to 
the  Bacillus  coli  commune  with  which  the  oxyuris  is  freely  covered, 
rather  than  to  the  worm  itself.  The  diagnosis  presents  no  difficulties 
when  the  stools  are  properly  examined,  the  worms  with  their  ova  (A, 
Fig.  220,  page  610)  being  easily  detected. 

(III)  Trichlniasis.—^S'vw/j/om.?.— These  depend  entirely  upon  the 
number  of  trichinse  which  reach  maturity  in  the  intestinal  canal. 


X028  DIAGNOSIS,    DIRECT  AND  DIFFERENTIAL 

If  only  a  small  number  enter  the   stomach,  and  but  few  of  these 
reach  the  muscles,  there  may  be  no  symptoms. 

The  more  marked  early  symptoms  are  abdominal  pain,  cardialgia, 
nausea,  vomiting,  and  marked  muscular  exhaustion.  The  period  of 
incubation  varies  from  3  to  14  days.  An  exhausting  diarrhoea  may 
appear  early,  and,  if  not  fatal,  may  be  followed  by  obstinate  constipa- 
tion. The  muscles  become  swollen,  tense,  and  painful  to  the  touch. 
The  muscles  of  mastication  and  respiration  may  be  involved,  with 
serious  impairment  of  their  functions.  Fever  may  be  slight  or  reach 
104°.  Profuse  sweating  is  an  early  and  persistent  symptom.  The 
urine  is  usually  decreased.  Early  oedema  of  the  eyelids  and  face, 
appearing  later  in  the  lower  limbs,  is  said  to  be  almost  pathogno- 
monic. In  grave  cases  the  symptoms  may  resemble  those  of  typhoid 
fever.  The  group  of  symptoms  which  render  the  diagnosis  fairly 
clear  are  oedema  of  eyelids  and  face,  great  prostration,  violent  mus- 
cular pain  from  motion  or  pressure,  catarrhal  symptoms  of  the  bron- 
chi, marked  dyspnoea,  continued  sweating,  and  extreme  restlessness. 
The  most  marked  change  in  the  blood  is  a  leucocytosis  with  a  large 
increase  of  the  eosinophilic  cells.  The  differential  diagnosis  is  to 
be  made  from  cholera  by  the  profuse  perspiration  and  by  the  mus- 
cular symptoms;  from  simple  rheumatism  by  the  gastro-intestinal 
symptoms  and  extreme  exhaustion  ;  from  myositis  by  the  presence  of 
eosinophilia  and  the  finding  of  trichinae  in  the  muscles  and  stools ; 
and  from  typhoid  fever  (see  page  668).  The  complications  are  :  long- 
continued  diarrhoea,  extreme  dyspnoea,  difficult  deglutition,  marked 
typhoid  symptoms,  bronchitis,  pleurisy,  pneumonia,  sleeplessness,  and 
general  exhaustion. 

(IV)  Anchylostomiasis  ( Uncinaria  duodenalis). — Anaemia  is  the 
most  characteristic  and  alarming  symptom,  the  parasite  extracting 
the  blood  by  suction.  The  disease  is  known  variously  as  Egyptian 
chlorosis,  brickmaker's  anaemia,  tunnel  anaemia,  miner's  cachexia, 
and  mountain  anaemia.  (Edema  and  dyspnoea  may  be  jjresent,  asso- 
ciated with  gastro-intestinal  symptoms.  There  are  extreme  pallor, 
wasting,  and  debility.  The  diagnosis  depends  upon  the  persistent 
anaemia,  and  the  presence,  in  the  stools,  of  the  eggs  of  the  parasite. 

(V)  Filariasis  (Filaria  hancrofti,  Filaria  dinrna,  and  Filaria 
perstans). — There  are  three  conditions,  which  may  be  classed  as 
symptoms,  due  to  this  parasite :  liaimatocliyluria,  the  occasional  pas- 
sage in  the  urine  of  blood  clots,  the  urine  being  of  an  opaque  white 
or  milky  appearance,  and  showing  a  slightly  reddish  deposit  on  set- 
tling ;  lymph  scrotum,  showing  enormous  thickening  of  tissues  and 
distended  lymph  vessels ;  and  elephantiasis.     See  also  page  591. 

(VI)  Tricocephalus   Dispar   ( Whipivorm). — The   symptoms    are 


DISEASES  DUE  TO  ANIMAL  PARASITES  1029 

few  and  rare.  By  some  it  is  thought  to  be  the  cause  of  beri-beri. 
Profound  anaemia  with  diarrhoea  have  been  associated  with  this 
worm.  The  diagnosis  depends  upon  the  presence  in  the  stools  of 
the  eggs  (see  C,  Fig.  220,  page  619). 

(VII)  Dioctophyme  Gigas.— The  worm,  male,  about  1  foot  long, 
female  nearly  3  feet,  is  in  man  usually  found  in  the  region  of  the 
kidney,  and  has  been  known  to  entirely  destroy  that  organ. 

(VIII)  Strongyloides  Intestinalis.— This  worm  is  found  abun- 
dantly in  the  diarrhoea  of  hot  countries,  and  is  sometimes  associated 
with  miner's  anaemia.  When  found  in  large  numbers  it  is  usually 
responsible  for  severe  diarrhoea  and  anaemia. 

III.  Cestodes  {Tapeworms). — The  cestodes,  or  tapeworm  group 
of  intestinal  parasites,  possess  a  twofold  clinical  interest  based  upon 
their  regional  distribution  and  condition  of  maturity.  The  mature 
worm  occupies  the  small  intestine,  the  symptoms  to  which  it  gives 
rise  depending  largely  upon  the  size  and  number  present,  and  even 
when  abundant  they  seldom  prove  directly  fatal ;  but,  per  contra,  the 
visceral  distribution  of  the  larvcB  or  immature  parasite  frequently 
causes  grave  and  important  symptoms.  The  following  group  includes 
the  more  important  varieties  of  the  mature  tapeworm,  the  symp- 
toms arising  from  each  being  much  the  same. 

(I)  Intestinal  Cestodes  (Tapeworms). — Tcenia  saginata :  In  its 
larval  condition  it  is  known  as  Cysticercus  sagifiata  or  beef  measle 
worm.  It  is  the  most  common  form  of  tapeworm  in  man,  being 
derived  from  beef  used  as  food  (see  also  page  138).  Twnia  solium  : 
The  pork  or  armed  tapeworm  (see  also  page  139).  In  its  larval  con- 
dition it  is  known  as  Cysticercus  cellulosm.  Tcenia  cucumerina  (dog) 
and  Twnia  elliptica  (cat)  are  by  some  considered  as  the  same  species. 
They  are  found  in  both  adults  and  children.  TcBuia  flavojninctata : 
A  small  variety  of  taenia ;  when  found  it  is  usually  in  children,  giv- 
ing rise  to  few  symptoms.  Bothriocephalus  lafus :  Is  also  known  as 
the  T(B?iia  Ma  or  broad  tapeworm.  It  is  a  very  common  worm  in 
Sweden  and  Switzerland. 

Symptoms. — The  symptoms  arising  from  this  group  of  intestinal 
parasites  are  all  of  the  same  general  character,  are  both  local  and 
general,  and  persist  until  the  entire  parasite  has  been  removed. 

(1)  Local  Symptoms. — The  diagnostic  local  symptoms  are  the 
finding  of  segments  in  the  stools,  or  at  times  in  the  clothing,  the 
segments  extruding  themselves  from  the  anus,  particularly  in  the 
case  of  the  Tcenia  saginata;  and  the  occasional  vomiting  of  segments, 
especially  in  women.  In  the  latter  case,  if  it  is  the  Twnia  solium, 
portions  are  likely  to  remain  in  the  stomach,  rendering  the  patient 
liable  to  measles  or  cvsticerci.     There  may  be  distressing  itching 


1030  DIAGNOSIS,   DIRECT  AND  DIFFERENTIAL 

about  the  anus,  with  abdominal  uneasiness,  fulness,  or  pain,  nausea, 
vomiting,  and  diarrhoea.  At  times  there  may  be  a  sense  of  move- 
ment in  the  intestine  due  to  the  worm,  this  condition  being  in- 
creased by  fasting  and  often  relieved  by  a  full  meal. 

(2)  General  Symptoms. — The  appetite  is  variable,  the  breath 
fetid,  and  the  tongue  usually  furred.  The  patient  may  be  pale  and 
emaciated,  showing  discolorations  about  the  eyes.  Anaemia  is  not 
uncommon  in  long-continued  cases,  with  dizziness,  fulness  in  the 
head,  buzzing  in  the  ears,  twitching  of  the  face,  and  dull  headache. 
A  fatal  form  of  anaemia  may  be  due  to  the  bothriocephalus  (Schau- 
mann).  There  may  be  great  mental  depression,  even  hypochondria- 
sis, in  chlorotic  and  hysterical  persons,  and  not  infrequently  some 
uterine  disorder.     Fainting,  chorea,  and  epileptic  fits  are  rare. 

(II)  Visceral  Cestodes. — The  larvae  of  two  of  the  cestodes  may 
infest  the  solid  organs,  producing  affections  that  may  be  serious,  the 
Tmnia  solium  and  the  Tcenia  echinococcus.  The  larva  of  the  former 
is  known  as  the  Cysticercus  celhdosm  or  pork  measle  worm ;  that  of 
the  latter  as  the  echinococcus. 

Cysticercus  Cellulos.^. — Infection  occurs  by  swallowing  the 
eggs  or  mature  segments  of  the  tapeworm.  They  have  been  found 
in  the  brain,  muscles,  eyes,  liver,  kidneys,  lungs,  heart,  and  subcu- 
taneous tissues.  When  present  in  large  numbers  in  the  muscles 
there  are  stiffness,  pain,  general  weakness,  numbness  and  tingling, 
and  painful  nodules  containing  cysticerci  are  found  in  the  sub- 
cutaneous tissues.  When  in  the  brain  and  cord  they  may  give  rise 
to  obscure  symptoms — e,  g.,  evidences  of  diabetes  and  anomalous 
nervous  manifestations.  The  cysticercus  has  been  found  pressing 
upon  the  floor  of  the  4th  ventricle.  It  may  be  present  in  the  vitre- 
ous humour  of  the  eye.  The  diagnosis  of  the  condition  when  affect- 
ing the  internal  viscera  is  practically  impossible ;  but  they  can  be 
detected  in  the  eye,  so  also  in  a  subcutaneous  nodule  after  excision. 

EcHiJsroGOCCUS. — Derived  from  the  Tcenia  echinococcus  or  hydatid 
tapeworm,  and  is  the  cause  of  hydatid  tumours.  The  mature  worm 
is  found  in  the  dog,  infection  occurring  by  swallowing  the  eggs. 
Hydatid  tumours  are  most  common  in  the  liver,  but  may  occur  in 
the  lungs,  kidneys,  spleen,  omentum,  subperitoneal  tissue,  heart, 
brain,  spinal  canal,  pelvic  viscera,  and  bones. 

Symptoms  and  Diagnosis. — Small  and  few  cysts  in  the  liver  cause 
little  or  no  disturbance.  If  very  large,  there  may  be  a  feeling  of 
weight  or  pressure  in  the  region  of  the  liver.  If  near  the  surface, 
there  is  a  distinct  tumour  which  may  have  a  firm,  tense,  sometimes 
fiuctuating,  feeling.  If  situated  to  the  left  of  the  suspensory  liga- 
ment, they  may  press  upward  on  the  heart  and  increase  the  area  of 


DISEASES  DUE  TO  ANIMAL   PARASITES  1031 

cardiac  dulness.  If  suppuration  of  the  cyst  occurs,  pyaemic  symp- 
toms rapidly  follow,  i.  e.,  jaundice,  rigours,  sweating,  rapid,  feeble 
pulse,  and  loss  of  weight.  The  cysts  may  perforate  any  of  the  sur- 
rounding hollow  organs — stomach,  bile  passages,  colon,  pleura, 
bronchi,  pericardium,  or  peritoneum.  Perforation  into  the  inferior 
vena  cava  or  pericardium  is  rapidly  fatal.  They  may  open  exter- 
nally. External  rupture  and  aspiration  of  the  cysts  are  frequently 
followed  by  urticaria.  The  general  health  may  be  good.  In  simple 
echinococcus  the  liver  is  irregularly  enlarged ;  in  the  multilocular 
variety  the  enlargement  is  regular  and  smooth  ;  jaundice  is  a  com- 
mon symptom,  there  are  progressive  emaciation  and,  later  in  the  dis- 
ease, frequent  hemorrhages.  It  is  confined  almost  entirely  to  the 
liver,  the  symptoms  being  not  unlike  those  of  tumour  or  cirrhosis. 
The  hydatid  thrill  or  fremitus  (page  442)  is  a  diagnostic  sign  when 
it  can  be  elicited.  The  sudden  development  of  septic  symptoms 
where  there  has  been  an  enlargement  of  the  liver  associated  with 
previously  good  health  is  suggestive  of  suppurating  hydatids.  In 
the  same  connection  a  sudden  intense  jaundice  may  indicate  perfo- 
ration into  the  bile  passages. 

When  the  larvae  develop  primarily  in  the  pleura  the  early  symp- 
toms may  be  those  of  compression  of  the  lungs  and  displacement  of 
the  heart.  The  physical  signs  are  those  of  effusion,  and  the  condi- 
tion readily  may  be  mistaken  for  simple  hydrothorax.  Hydatid  dis- 
ease of  the  right  lobe  of  the  liver  may  encroach  upon  the  right  pleural 
cavity  and  pass  for  primary  involvement  of  the  pleura.  Examina- 
tion of  aspirated  fluid,  which  reveals  a  non-albuminous  liquid  (see 
also  (8),  page  653),  is  sufficient  for  differentiation.  The  hydatid 
may  rupture  through  the  chest  wall,  in  which  case  echinococcus 
cysts  are  frequently  found  in  the  discharge. 

Development  of  the  cysts  in  the  lungs  is  attended  by  symptoms 
of  compression,  later  by  the  formation  of  cavities,  and  occasionally 
gangrene.  Pulmonary  hemorrhage  may  follow  extensive  destruction 
of  lung  tissue.  Most  of  the  cases  of  primary  hydatid  formation  in 
the  lung  are  during  life  mistaken  for  gangrene  or  tuberculosis. 
Occasional  rupture  occurs,  either  into  the  pleura  with  resulting 
empyema,  or  into  a  bronchus.  In  the  latter  case  there  is  a  discharge 
of  fluid  containing  fragments  of  cyst  membrane,  and  sometimes  par- 
tial or  complete  booklets.  The  majority  of  these  cases  are  fatal, 
rupture  into  the  pericardium  inevitably  so. 

In  the  order  of  frequency,  hydatid  development  in  the  Jcidneys  is 
second  only  to  that  occurring  in  the  liver.  The  kidney  may  reach 
an  enormous  size  and  resemble  a  hydronephrosis.  An  exploratory 
puncture  is  necessary  to  a  positive  diagnosis.     When  rupture  occurs 


1032  DIAGNOSIS,   DIRECT  AND  DIPFEREXTIAL 

into  the  pelvis  of  the  kidney,  cysts  or  membrane  may  be  passed  in 
the  urine,  attended  by  colicky  pains  resembling  renal  colic.  The 
general  health  is  not  usually  much  impaired. 

In  the  hrain  the  symptoms  are,  as  a  rule,  those  of  tumour,  i.  e., 
convulsions,  distressing  headache,  and  gradually  developing  blind- 
ness. There  is  nothing  to  distinguish  this  condition  from  other 
forms  of  brain  tumours. 

IV.  Parasitic  Arachnida. — (I)  Sarcoptes  (Acarus)  Scablei 
{Itch  Insect). — This  is  the  common  parasite  of  itch,  and  is  found 
ordinarily  in  the  folds  of  the  skin,  or  where  the  skin  is  delicate. 
The  insect,  usually  the  female,  is  about  0.45  mm.  in  length,  pearly 
white  in  colour,  easily  detected  by  the  naked  eye,  and  occupies  a 
small  burrow  in  the  epidermis.  The  principal  symptoms  are  dis- 
tressing itching  and  an  eruption  which  may  be  papular,  vesicular,  or 
pustular,  and  general  irritation  of  the  skin  resulting  from  the  scratch- 
ing. There  is  seldom  any  doubt  as  to  the  diagnosis,  the  appearance  of 
the  parasite  under  the  skin,  accompanied  with  the  evidences  of  irri- 
tation and  scratching,  being  usually  sufficient. 

(II)  Demodex  Folliculorum  {Steatozodti). — Principal  habitat  is  in 
the  sebaceous  glands  of  the  face,  neck,  and  chest,  which  present 
minute  elevations,  containing  in  their  centres  exposed  blackish 
points  {comedones  or  Machheads). 

V.  Parasitic  Insects. — (I)  PedicuH  {Body  Lice). — These  are : 
Pediculus  Capitis. — Found  in  regions  containing  long  hair,  prin- 
cipally in  the  head.  They  multiply  rapidly  by  the  deposit  of  eggs 
which  cling  to  the  body  of  the  long  hairs,  appearing  as  white  specks, 
sometimes  called  nits.  The  symptotns  are  itching  and  irritation  of 
the  scalp.  If  abundant,  an  eczema  or  pustular  dermatitis,  with 
crusts  and  scabs,  may  appear  on  the  head,  resulting  in  a  dense  mat- 
ting and  tangling  of  the  crusts  and  hair,  known  as  the  plica  polonica. 
There  is  no  difficulty  in  diagnosis,  the  eggs  or  nits  clinging  to  the 
shafts  of  the  hair  being  distinctly  visible  to  the  naked  eye. 

Pediculus  Corporis. — Lives  in  the  clothing  and  sucks  blood  from 
the  body.  The  resulting  hemorrhagic  specks  are  very  common  on 
the  back,  abdomen,  and  neck,  and  create  a  distressing  desire  for  con- 
stant scratching.  Urticaria  may  follow  as  a  result  of  the  irritation. 
The  so-called  vagabond's  disease — morbus  errorum — occurs  in  cases  of 
long  standing,  and  is  characterized  by  a  rough,  thickened,  often  pig- 
mented skin.  The  diagnosis  depends  upon  the  finding  of  the  para- 
site in  the  clothing,  and  the  irritation  and  peculiar  hemorrhagic 
spots  on  the  skin.  The  only  condition  with  which  it  may  be  con- 
founded is  the  bronzing  of  Addison's  disease  (page  922). 

Pediculus  Pubis. — The  symptoms  produced  by  this  louse  resemble 


DISEASES  DUE  TO  ANIMAL  PARASITES  1033 

those  just  mentioned.     They  occupy  the  sites  of  the  shorter  hairs, 
especially  the  pubes,  occasionally  the  axilla  and  eyebrows. 

(II)  Cimex  Lectularius  {Common  Bedbug). — The  symptoms  due  to 
the  sting  of  this  bug  vary  according  to  personal  susceptibility.  In 
some  individuals  there  is  little  or  no  reaction,  in  others  there  may  be 
intense  urticaria  and  hyperaemia  of  the  skin.  The  bite  resembles 
somewhat  a  papular  urticaria,  but  has  in  its  centre  a  dark  pin-point 
discoloration  made  by  the  proboscis  of  the  animal.  The  diagnosis 
depends  upon  the  finding  of  the  bug  and  inspection  of  the  bite. 

(III)  Pulex  Irritans  ( Common  Flea). — Easily  transferred  from  one 
person  to  another  during  temporary  crowding  in  public  places.  The 
irritation  following  a  bite  is  similar  to  that  of  (II),  preceding. 

(IV)  Pulex  Penetrans  {Sand  Flea-jigger). — Much  smaller  than  (III) 
and  usually  attacks  the  feet.  It  penetrates  the  skin  and  burrows, 
producing  inflammation,  sometimes  vesicular  or  pustular  swelling. 


INDEX 


Abdomen,  absent  respiratory  motion  of,  429 ; 
auscultation  of,  444;  auscultatory  percus- 
sion of,  432 ;  bony  landmarks  and  surface 
markings  of,  423  ;  causes  of  distention  of, 
433 ;  causes  of  pain  in,  45 ;  condition  of 
walls'of,  432 ;  distention  of,  from  tumours, 
437 ;  enlarged  arteries  of  wall  of,  429 ;  en- 
larged veins  of,  428;  examination  of  tu- 
mours of,  439. 

Abdomen,  "  flicking "  percussion  of,  432 ; 
friction  sounds  over,  444;  general  disten- 
tion of,  433  ;  indications  from  the  situation 
of  tumours  of,  443,  444;  inspection  of,  tech- 
nic,  427  ;  mensuration  of,  431 ;  methods  of 
indicating  location  of  lesions  in,  426 ;  mo- 
bility of  tumours  of,  441 ;  pain  in,  45 ;  pal- 
pation of,  technic,  430. 

Abdomen,  percussion  of,  technic,  431 ;  results 
of  general  palpation  and  percussion  of,  432: 
results  of  inspection  of,  in  disea.se,  428 ;  re- 
traction of,  433 ;  rigid  recti  muscles,  433 ; 
skin  of,  428  ;  tenderness  of,  53 ;  the  normal, 
427  ;  topographical  anatomy  of,  425 ;  topo- 
graphical areas  of,  424  ;  tumours  of,  which 
move  with  respiration,  439;  visible  peri- 
stalsis over,  429. 

Abscess,  atheromatous,  900  ;  mediastinal,  869  ; 
of  brain,  998;  of  liver,  809  ;  of  lung,  853; 
of  aural  meatus,  176;  of  ovary,  787  ;  perine- 
phritic,  941 ;  retropharyngeal,  754 ;  sub- 
phrenic, 823 ;  puncture  of,  649. 

Acarus  scabei,  1032. 

Accommodation,  loss  of  power  of,  198. 

Acetone  and  acetouuria,  638. 

Achylia  gastrica,  614. 

Acid,  acetic,  significance  of,  in  gastric  con- 
tents, 616;  test  for,  612. 

Acid,  butyric,  significance  of,  in  stomach 
contents,  616  ;  test  for,  612. 

Acid,  diacetic,  in  urine,  638. 

Acid,  glycosuric,  in  urine,  mistaken  for  glu- 
cose, 637. 


Acid,  hydrochloric ;  determining  amount  of 
free,  608 ;  determining  amount  of  com- 
bined, 610 ;  tests  for  free,  607  ;  variations 
in  amount  of,  in  gastric  juice,  615. 

Acid,  lactic,  significance  of,  in  stomach  con- 
tents, 616 ;  tests  for,  608. 

Acid,  o.\ybutyric,  in  urine,  638. 

Acid,  uric,  amount  of,  in  urine,  631. 

Acid  salts,  determining  amount  of,  in  stomach 
contents,  610. 

Acidity,  determining  total,  of  stomach  con- 
tents, 609. 

Acids,  determining  amount  of  organic,  ia 
stomach  contents,  610. 

Acne  rosacea,  1016. 

Acoria,  113. 

Acromegaly,  958 ;  shape  of  head  and  face  in 
156. 

Acting  nares,  214. 

Actinomyces,  examination  for,  in  sputum, 
601. 

Actinomycosis,  symptoms  and  diagnosis,  745. 

Acute  and  subacute  articular  rheumatism, 
710. 

Addison's  disease,  922. 

Adenitis,  tuberculous  cervical,  symptoms  and 
diagnosis,  734. 

Adenoids  of  pharynx,  756. 

Adipose  tissue,  amount  and  character  of,  26. 

Adrenals,  tuberculosis  of,  736. 

iEstivo-autumnal  malarial  fevers,  706. 

After-sensation,  535. 

Age,  its  influence  on  disease,  15. 

Ageusia,  232. 

Albuminuria,  631 ;  febrile,  toxic,  and  circula. 
tory,  632 ;  neurotic,  functional  (cyclic,  di- 
etetic,  transitory),  organic,  and  extra-renal, 
633. 

Albumosuria,  634. 

Alcohol,  coma  of,  68. 

Alcoholism,  1016. 

Alimentary  canal,  tuberculosis  of,  735. 
1035 


1036 


INDEX 


Alkaptonuria,  637. 

Allantiasis,  1024. 

Allochiria,  535. 

Alpine  scurvy,  1025. 

Amaurosis,  207. 

Amblyopia,  207. 

Amenorrhoea,  as  a  symptom,  147. 

Amoeba  coli,  in  sputum,  601. 

Amyloid  kidney,  935 ;  urine  in,  646. 

Amyosthenia,  946 ;  definition  of,  520. 

Amyotrophic  lateral  sclerosis,  9'76. 

Amyotrophy,  progressive  spinal,  973. 

Anachlorhydria,  615. 

Anaemia,  908 ;  brickmaker's,  miner's,  tunnel, 
or  mountain,  1028, 1029  ;  progressive  per- 
nicious, 910;  splenic,  924. 

Anaemic  headache,  43. 

Anaesthesia,  531 ;  bilateral,  533 ;  dolorosa, 
534 :  irregular,  533. 

Analgesia,  534,  535. 

Anamnesis,  the,  5. 

Anarthria,  246. 

Anasarca,  87. 

Anatomy,  topographical,  of  heart,  318;  of 
intestines,  456 ;  of  kidneys,  475 ;  of  liver, 
461 ;  of  lungs,  382 ;  of  pleura,  384. 

Anchylostomiasis,  1028. 

Aneurism,  arterio-venous,  908;  of  abdominal 
aorta,  907 ;  of  heart,  893 ;  of  splenic  artery, 
908 ;  of  thoracic  aorta,  902 ;  of  thoracic 
aorta,  dulness  of,  339 ;  pulse  of,  378  ;  tho- 
racic, vertigo  in,  59  ;  varieties  of,  901. 

Aneurismal  varix,  902. 

Angina  Ludovici,  755. 

Angina  pectoris,  894. 

Angio-ataxia,  550. 

Angio-cholitis,  simple,  801. 

Angio-neurotic  (circumscribed)  oedema,  957. 

Angio-paralysis,  549. 

Angio-sclerosis,  900. 

Angio-spasm,  550. 

Anidrosis,  82. 

Anisocoria,  188. 

Ankle  clonus,  541. 

Anomalies,  congenital,  of  heart,  896. 

Anorexia  nervosa,  112 ;  symptoms,  773. 

Anosmia,  217. 

Anthracosis,  848. 

Anthrax,  743. 

Anuria,  143. 

Anxiety  neurosis,  949. 

Aorta,  abdominal,  aneurism  of,  907 ;  dulness 
of  aneurism  of  thoracic,  339  ;  neurotic  (dy- 
namic) pulsation  of  abdominal,  907  ;  neu- 
rotic (dynamic)  pulsation  of  thoracic,  906 ; 
thoracic,  aneurism  of,  902. 


Aortic  incompetency  (regurgitation),  879; 
pulse  of,  378 ;  vertigo  in,  59. 

Aortic  stenosis,  880  ;  pulse  of,  378. 

Aortic  stenosis  and  incompetency,  direct 
effect  of,  upon  the  heart,  313. 

Apex-beat,  character  and  extent  of,  324;  dis- 
placement of,  323  ;  position  of,  322. 

Aphasia,  246 ;  auditory,  255 ;  causes  of,  255 ; 
conduction,  255 ;  examination  for,  252 ;  mo- 
tor, 254 ;  varieties  of,  251  ;  visual,  254. 

Aphonia,  243  ;  hy.sterical,  946. 

Aphthous  stomatitis,  750. 

Apoplexy,  cerebral ;  coma  of,  69  ;  from  em- 
bolism, 997  ;  from  hemorrhage,  994 ;  from 
thrombosis,  997  ;  pulmonary  apoplexy,  842, 

Appendicitis,  acute,  782;  chronic,  788;  re- 
current, 788,  789. 

Appendicular  hypochondriasis,  789. 

Appendix,  ensiform,  as  a  landmark,  304. 

Appendix  vermiformis,  situation  of,  456. 

Appetite,  abnormalities  in,  112. 

Apraxia,  250  ;  examination  for,  252. 

Aprosexia,  757. 

Arachnida,  parasitic,  1032. 

Arcus  senilis,  184. 

Argyll-Kobertson  pupil,  188,  987. 

Arm,  miscellaneous  signs  and  symptoms  con- 
nected with,  278. 

Arrhythmia,  372. 

Arsenic-poisoning,  1023. 

Arsenic,  therapeutic  overaction,  1023. 

Arterial  tension,  310  ;  estimation  of,  368. 

Arteries,  "  beading  "  of,  363  ;  diseases  of,  900 ; 
enlarged,  of  abdominal  wall,  429 ;  in.spec- 
tion.  palpation,  and  auscultation  of,  363 ; 
normal  palpable  pulsation  of,  363;  pain  in 
disease  of,  48;  pulsation  of  retinal,  210; 
syphilis  of,  741 ;  thickened,  373. 

Arterio-capillary  fibrosis,  900. 

Arterio-sclerosis,  900 ;  pulse  of,  378 ;  vertigo 
in,  59. 

Arterio-venous  aneurism,  902,  908. 

Arteritis,  of  coronary  arteries,  892.^ 

Artery,  carotid,  pulsation  of,  267 ;  embolism 
and  thrombosis  of  the  central,  of  retina, 
210;  femoral,  tliickened  and  pulsating, 
280 ;  full  and  empty,  376 ;  of  cerebral  hem- 
orrhage, 507;  splenic,  aneurism  of,  908; 
superior  mesenteric,  embolism  or  throm- 
bosis of,  797. 

Arthralgia  saturnina,  1021. 

Arthritis  deformans,  1012. 

Arthritis,  localized,  of  shoulder  joint,  1014. 

Artliropatliies,  987. 

Articular  sense,  disturbance  of,  535;  test- 
ing, 529. 


INDEX 


1037 


Ascaris  lumbricoides,  description  of,  138; 
symptoms,  1027. 

Ascites,  causes  of,  436,  827;  character  of 
fluid  in,  827  ;  chylous,  or  chyloid,  651 ;  di- 
agnosis of,  433. 

Aspirated  fluids,  examination  and  characters 
of,  650. 

Aspiration,  diagnostic,  of  cavities,  648. 

Associated  movements,  518. 

Astasia-abasia,  535. 

Asthenic  bulbar  paralysis,  976. 

Asthenopia,  201. 

Asthma,  bronchial,  839 ;  "  cardiac,"  840 ; 
"  hay,"  830  ;  "  renal,"  840  ;  "  thymic,"  833, 
928,  929. 

Ataxia,  cerebellar,  530 ;  hereditary  (Fried- 
reich's), 989 ;  of  drunkards,  1017  ;  varieties 
of,  and  testing,  530. 

Ataxic  gait,  33. 

Atelectasis,  pulmonary,  849. 

Atheromatous  abscess,  900  ;  ulcer,  900. 

Athetosis,  516. 

Athyrea,  926. 

Atonic  dyspepsia,  776. 

Atrophies,  occupation  muscular,  971. 

Atrophy,  arthritic  muscular,  971 ;  atonic, 
974 ;  facial  hemi-,  957 ;  infantile  progress- 
ive muscular  (Duchenue),  971 ;  of  muscles, 
509 ;  progressive  hereditary  muscular,  of 
leg  type  (Charcot-Marie-Tooth),  975;  pro- 
gressive muscular,  973;  progressive  mus- 
cular, spastic  form  (Charcot),  976 ;  tonic, 
974. 

Auricles,  hypertrophy  of,  887. 

Auscultation,  of  arteries,  364 ;  of  heart,  839 ; 
of  intestines,  460  ;  methods  and  technic  of, 
294 ;  of  stomach,  452 ;  of  liver  and  gall- 
bladder, 463  ;  of  lungs,  technic  of,  409. 

Auscultatory  percussion,  291 ;  of  heart,  334. 

Bacelli's  sign,  418. 

Bacillus,    Boas-Oppler,     614,     leprae,    745; 

mallei,  744;  tuberculosis,  examination  for, 

in  sputum,  601. 
Back,  acute  or  chronic  atiflFness  of,  285 ;  signs 

and  symptoms  connected  with,  283,  284; 

swellings  in,  286 ;  tenderness  in,  53. 
"  Bad  tastes,"  233. 
Basedow's  disease,  925. 
Bearing-down  sensation,  55. 
Bedbug,  1033. 

Bednar's  ulcer  of  hard  palate,  752. 
Beefy  tongue,  231. 
Behaviour,  general,  diagnostic    hints  from, 

24. 
Belching,  120. 


Bell-tympany,  409. 

Bell's  palsy,  968. 

Ben- ben,  748. 

Biermer's  phenomenon,  408. 

Bile-duct,  common,  impacted  gallstones  in, 
807;  symptoms  of  complete  and  incom- 
plete obstruction  of,  802. 

Bile-duct,  cystic,  impacted  gallstones  in,  807. 

Bile-ducts,  acute  catarrh  of,  801 ;  chronic 
catarrh  of,  802;  di.seases  of,  800;  stenosis! 
and  obstruction  of,  803 ;  suppurative  in- 
flammation of,  803. 

Bilious  attack,  1011. 

"  Bilious  headaches,"  944. 

Birth  palsies,  1000. 

Blackheads,  1032. 

Bladder,  urinary,  cancer  and  tuberculosis  of, 
urine  in,  648  ;  pain  in  disease  of,  52 ;  indi- 
cations from  inflammation  or  irritation  of, 
480 ;  tuberculosis  of,  733. 

Bleeders,  918. 

Blepharitis,  180. 

Blood,  ascertaining  specific  gravity  of,  570  v 
diseases  of,  908;  in  the  stools,  134,  185;. 
obtaining,  for  bacteriological  examination, 
594;  table  of  cellular  elements  of,  576. 

Blood  cells,  red,  giant,  578 ;  nucleated,  578 ;. 
variations  in  number  of,  577 ;  variations  in 
shape  of,  577  ;  variations  in  size  of,  578. 

Blood  cells,  white,  classification  of  the,  580  v 
difl"erential  count  of,  583;  in  disease,  584; 
in  health,  583 ;  transition  forms,  581 ;  va- 
rieties of,  579. 

Blood  dust,  Muller's,  587. 

Blood  examination,  counting  red  cells,  659  ; 
counting  white  cells,  564;  diagnostic  sig- 
nificance of  results  of,  575 ;  estimating  the 
haemoglobin,  567;  estimating  the  volume 
of  the  cells,  567  ;  in  special  disea.ses  (table), 
695 ;  microscopical,  571 ;  order  of  proce- 
dure in,  574 ;  teciinic  of,  559. 

Blood  films,  preparing,  fixing,  and  staining, 
571-574. 

Blood  plates,  587. 

Blood  tests,  for  diabetes,  593. 

Blood-vessels,  innervation  of,  311. 

"  Blue  disease,"  897. 

Blue  cedema,  946. 

Blue  or  waxy  fingers,  274. 

Boas-Oppler  bacillus,  614. 

Boas's  test  breakfast,  605. 

Body,  congenital  and  acquired  abnormalities- 
in  the  conformation  of,  27. 

Boils,  86. 

Bones,  of  leg,  curvatures  of,  280 ;  pain  in  dis- 
ease of,  52. 


1038 


INDEX 


Botulism,  1024. 

Brachycardia,  371 ;  essential,  372. 
Brain,  abscess  of,  998  ;  acute  softening,  997  ; 
blood-supply  of,  506  ;  diseases  of  substance 
of,  994;  etfect  of  valvular  lesions  upon, 
318 ;  hydatids  (echmococcus)  of,  1032 ;  in- 
flammation of  membranes  of,  992 ;  syph- 
ilis of,  740 ;  tuberculosis  of,  736 ;  tumour 
of,  1001. 
"Bread-crumbling"  movement,  954. 

Breast, "  hysterical,"  534. 
"  Breast-pang,"  894. 

Breath,  odour  of,  219. 

Breath  sounds,  amphoric,  414 ;  bronchial,  in 
disease,  413 ;  bronchial,  in  health,  410 ; 
broncho- vesicular,  in  disease,  415 ;  broncho- 
vesicular,  in  health,  411 ;  characteristics  of 
the  normal,  410  ;  "  cog-wheel,"  416 ;  harsh, 
416;  indeterminate,  415;  puerile,  416; 
vesicular,  in  disease,  415;  vesicular,  in 
health,  410. 

Breathing,  abdominal,  388;  Cheyne-Stokes, 
391 ;  jerky,  stertorous,  stridulous,  wavy, 
392;  rhythm  of,  390;  simple  irregularity 
of,  391 ;  thoracic,  387. 

Bremer's  test  for  diabetes,  593. 

Brick-dust  deposit  in  urine,  625. 

Bright's  disease,  acute,  932 ;  urine  in,  648. 

Bright's  disease,  chronic  difl'use  (parenchym- 
atous), 934 ;  urine  in,  646. 

Bright's  disease,  chronic  interstitial,  934; 
urine  in,  646. 

Bromatoto.xismus,  1023. 

Bronchi,  diseases  of,  833. 

Bronchia,  obstruction  of,  838. 

Bronchiectasis,  836. 

Bronchitis,  acute,  833 ;  "  capillary,"  833,  847 ; 
chronic,  834;  fibrinous  (plastic),  837;  pu- 
trid, 835. 

Bronchophony,  417. 

Broncho-pneumonia,  844. 

Bronchorrhoea,  835. 

Bronzing  of  skin,  81. 

Brown-Sequard  paralysis,  983. 

■Jiruit  d'airain.  409. 

Bruit  de  diable,  366. 

Bruit  de  galop,  345. 

Bubonic  plague,  symptoms,  705. 

Buccal  cavity,  eruptions,  ulcers,  and  sloughs 
in,  221 ;  petechial  and  pigmented  spots  in, 
220. 

Bulb  (medulla),  diseases  of,  972. 

Bulbar  paralysis,  asthenic,  976  ;  progressive, 
975;  progressive  upper,  977. 

Bulimia,  112;  paroxysmal,  773. 

Burning,  Ungling,  numbness,  56. 


Cachexia,  malarial,  707  ;  miners',  1028 ;  stru- 
mipriva,  928  ;  syphilitic,  737. 

Cachexias,  29. 

Csecum,  position  of,  456. 

Calculi,  of  pancreas,  820 ;  renal,  938. 

Calculus,  renal,  urine  in,  647;  vesical,  urine 
in,  647. 

Calf,  increase  in  size  of,  281. 

Cancer,  Lobstein's,  827. 

Cancer  of  stomach,  765. 

Cancrum  oris,  751. 

"  Canker  "  sore  mouth,  750. 

Capsulitis  (perihepatitis),  815. 

Caput  MedusjB,  428. 

Caput  quadratum,  1014. 

Carbuncles,  86. 

Carcinoma,  of  gall-bladder,  805 ;  of  intestine, 
794;  of  pancreas,  818  ;  of  peritoneum,  826; 
of  rectum,  796 ;  of  stomach,  765. 

Card  outfit,  6. 

Cardia,  spasm  of,  775. 

Cardiac  crisis,  987. 

Cardiac  cycle,  308. 

Cardio-pulmonary  murmur,  362. 

Carotids,  abnormal  pulsation  of,  267. 

Carphologia,  153,  517. 

Carpo-pedal  spasm,  833. 

Case  histories,  keeping,  6. 

Casts  in  urine,  642. 

Catalepsy,  519. 

Catarrh,  acute  nasal,  828 ;  apical,  731 ;  chronic 
nasal,  829  ;  suifocative,  845. 

Catarrhal  gastritis,  chronic,  761. 

Catarrhal  stomatitis,  750. 

Cavities  in  lung,  signs  of,  730. 

Cayenne  pepper  deposit  in  urine,  625. 

Cerea  ilexibilitas,  519. 

Cerebellar  ataxic  gait,  33. 

Cerebral  abscess,  998 ;  apoplexy,  994 ;  embo- 
lism and  thrombosis,  997  ;  localization,  553 ; 
syphilis,  740  ;  tumours,  1001. 

Cerebral  and  spinal  lesions,  summary  of 
diagnostic  points  bearing  upon  nature  and 
location  of,  555. 

Cerebro-spinal  fluid,  652. 

Cerebro-spinal  meningitis,  672. 

Cervical  glands,  enlargement  of,  265. 

Cestodes,  intestinal,  1029 ;  visceral,  1030. 

Chalicosis,  848. 

Chalk  stones,  1011. 

Charcot's  disease,  976. 

Charcot-Marie-Tooth  type  of  muscular  atro- 
phy, 975. 

Cheeks,  puffing,  220. 

Chest,  anatomical  landmarks  of,  304 ;  causes 
of  pain  in,  45 ;  distended  or  enlarged  veins 


INDEX 


1039 


-of,  303;  emphysematous,  850;  flat,  ptery- 
goid or  alar,  299 ;  mensuration  of,  297 ;  ob- 
taining outline  of  transverse  section  of,  298 ; 
oedema  of,  303  ;  pain  in,  45  ;  paralytic,  299 ; 
phtliisical,  299  ;  rachitic,  300 ;  semi-circum- 
ference and  diameters  of,  298 ;  unilateral  or 
localized  swellings  or  prominences  of,  301. 

•Cheyne-Stokes  respiration,  391. 

Chicken  pox,  683. 

■"  Child  crowing,"  833. 

Chills,  significance  of,  13 

Chloasma,  163. 

Chloro-ausemia,  909. 

Chlorosis,  909 ;  Egyptian,  1028 ;  rubra,  164 

"  Choked  disc,"  209. 

Cholangitis,  chronic  catarrhal,  802;  suppu- 
rative, 803. 

Cholecystitis,  acute,  804 

Cholelithiasis,  805. 

Cholera  Asiatica,  703. 

Cholera  infantum,  779. 

Cholerine,  704 

Chorea,  habit,  951 ;  Huntington's  (heredi- 
tary), 951;  maniacal,  950;  paralytic,  951; 
senile,  951 ;  Sydenham's,  950. 

Choreic  movements,  517. 

Choroidal  tubercles,  211. 

Chromidrosis,  82. 

Chronic  hydrocephalus,  999. 

Chylous  and  chyloid  exudates,  652. 

Chyluria,  639. 

Cimex  lectularius,  1033. 

Circulation,  symptom  group  of  obstructed 
portal,  153. 

Circulatory  system,  examination  of,  308;  dis- 
eases of,  870. 

Claviceps  purpurea,  1025. 

Clavicle,  swellings  on  or  above,  264 

Claw  hand,  272,  512. 

Clay-coloured  stools,  133. 

"  Clear  "  percussion  note,  287. 

Clergyman's  sore  throat,  754 

Clonu-s  ankle,  541. 

Clubfoot,  282. 

Coccygodynia,  958. 

Coeliac  affection,  the,  780. 

"Coiled"  posture,  31. 

Coin  percussion,  408. 

Coldness  of  hands  and  feet,  272. 

Coldness,  or  cold  sensations,  55. 

Colic,  appendicular,  788 ;  flatulent,  798 ;  gall- 
stone, 805;  hepatic,  805;  intestinal,  798; 
lead-.  1019:  mucous,  799;  renal,  988. 

Colica  Pictonum,  1019. 

Colitis,  778 ;  simple  ulcerative,  782. 

Collapse,  symptom  group  and  causes  of,  151. 


Colon,  cordlike,  777  ;  dilatation  of,  796 ;  per- 
cussion of,  459 ;  position  of,  457 ;  V-shaped, 
459,  777. 

Coloptosis,  777. 

Colour  analysis  of  leucocytes,  583. 

Colour  inde.x,  576. 

Coma,  66;  alcoholic,  68;  diabetic,  71;  diag- 
nosis of  varieties  of,  67 ;  epileptic,  70 ;  from 
apoplexy,  69 ;  from  gas  poisoning,  71 ;  from 
opium,  68;  from  sunstroke,  71 ;  hysterical, 
70 ;  significance  of,  66 ;  symptom  group  of, 
149 ;  ursemic,  49. 

Coma  vigil,  66. 

Combined  scleroses  (Putnam's),  989. 

Comedones,  1032. 

Compensation,  broken,  o(  valvular  defects, 
315,  316. 

Conjugate  deviation,  195. 

Consciousness,  disturbances  of,  $6. 

Constipation,  causes  of,  126 ;  headache  of,  44 ; 
nervous,  797. 

Constitutional  diseases,  1007. 

Contractures,  519. 

Convulsion  of  epilepsy,  72;  of  hysteria,  73; 
of  infancy,  73  ;  of  strychnine  poisoning,  74; 
of  tetanus,  74 ;  of  uraemia,  73  ;  puerperal,  73. 

Convulsions,  the  causes  and  varieties  of  gen- 
eral, 71. 

Convulsive  tic,  163. 

Coprolalia,  168. 

Coprophagy,  113. 

Cornea,  affections  of,  184;  ulcers  of,  185. 

Corrigan's  pulse,  880. 

Coryza,  acute,  828. 

Cough,  character  and  varieties  of,  256 ;  direct 
and  indirect  causes  of,  258. 

Coup  de  soleil,  1025. 

Cracked-pot  sound,  diagnostic  significance 
of,  406. 

Cramp,  37,  518 ;  writer's,  954. 

Cranial  nerves,  motor  functions  of,  501. 

Craniotabes,  160,  1014. 

Cranium,  notles  on,  160. 

Crepitant  rale,  420. 

Crepitation,  prsecordial,  362. 

Cretinism,  927 ;  shape  of  head  and  face  in 
sporadic,  155. 

Crises,  104;  vesical,  140. 

Crisis,  in  locomotor  ataxia,  987 ;  gastric,  dis- 
tinguished from  gastric  ulcer,  764. 

"  Cross-legged  "  (spastic)  gait,  34,  988. 

Crossed  paralysis,  171. 

Croup,  membranous,  690 ;  spasmodic,  830. 

Crystals,  Charcot-Leyden,  cholesterin,  hsem- 
atoidin,  and  fatty  acid,  in  sputum,  600. 

Curschmann's  spirals,  599. 


1040 


INDEX 


Cyanosis,  causes  of,  77. 

Cycloplegia,  198. 

Cylindroids,  644. 

Cyrtometry,  298. 

Cyst,  hydatid,  fluid  in,  653 ;  ovarian,  fluid  in, 

653 ;  of  pancreas,  fluid  in,  652. 
Cysticercus  cellulosee,  symptoms,  1030. 
Cystinuria,  688. 
Cystitis,  urine  in,  647. 
Cysts,  mesenteric,  796;  of  kidney,  940;   of 

pancreas,  819 ;  puncture  of,  649. 

Dactylitis  syphilitica,  739. 

Dead  fingers,  956. 

Deafness,  nervous,  177 ;  non-nervous,  179. 

Death,  facies  of  impending,  162. 

Debiles,  508. 

Debility,  symptoms  of,  152. 

Decreased  mobility,  520. 

Defecation,  125;  painful,  131. 

Degeneracy,  stigmata  of,  507. 

Degenerates,  508.  ' 

Delayed  conduction,  535. 

Delirium,  64. 

Delirium  tremens,  1016, 

Delusions,  64. 

Demodex  folliculorum,  1032, 

Dengue,  672. 

Dentition,  early,  delayed,  or  difficult,  223, 

Depression,  mental,  63. 

De  K.  (reaction  of  degeneration),  548. 

Devonshire  colic,  1021. 

Dextrocardia,  339. 

Diabetes  insipidus,  1008  ;  urinalysis  in,  647. 

Diabetes  mellitus,  1009  ;  blood  tests  for,  593 ; 
coma  of,  71 ;  dietetic  test  for,  637 ;  uri- 
nalysis in,  647. 

Diaceturia,  638. 

Diagnosis,  definition  of,  1 ;  descriptive  terms 
applied  to,  2 ;  difficulties  in,  3 ;  methods 
and  order  of  obtaining  evidence  for  a,  5 ; 
methods  of  reasoning  in,  4. 

Diaphragm,  enlarged  capillaries  along  line 
of  attachment  of,  303 ;  signs  of  paralysis  of, 
387,  388. 

Diaphragmatic  hernia,  866, 

Diarrhoea,  acute  dyspeptic,  779 ;  causes  of, 
129 ;  chronic,  778  ;  "  hill,"  781 ;  lienteric, 
134;  "morning,"  797  ;  nervous,  797, 

Diastolic  shock  of  aneurism,  343. 

Diatheses,  28. 

Diazo-reaction  in  urine,  value  of,  639. 

Dietl's  crisis,  629. 

Digestion,  physiology  of,  604. 

Digestive  system,  diseases  of,  750 ;  examina- 
tion of,  444. 


Digiti  mortui,  956, 

Dilatation  of  heart,  889. 

Diniethyl-amido-azobenzol  test  for  free  HCl, 
607. 

Dioctophyme  gigas,  1029. 

Diphtheria,  690. 

Diphtheroid  sore  throat,  754. 

Diplegia,  definition  of,  520 ;  facial,  174. 

Diplegias,  infantile  cerebral,  1000. 

Diplococcus  pneumoniae,  examination  for,  in. 
sputum,  603. 

Diplopia,  194, 

"  Dipping,"  431. 

Dipsomania,  1016. 

Discharges  from  the  nose,  215. 

Disease,  Charcot's,  976  ;  diurnal  exacerbation 
of,  22 ;  Ducheune- Aran's,  973 ;  Friedreich's, 
1007 ;  Gilles  de  la  Tourette's,  953 ;  Little's, 
988  ;  manner  of  obtaining  the  evidences  of, 
5 ;  Marie's,  958  ;  Morvan's,  984 ;  Parkin- 
son's, 953 ;  policeman's,  959  ;  Raynaud's, 
956 ;  seasonal  prevalence  of,  22 ;  Thom- 
sen's,  1007;  vagabond's,  1032 ;  varieties  of 
gait  in,  33. 

Diseases,  attacks  of,  which  render  subsequent 
attacks  probable,  20 ;  attacks  of,  which 
render  subsequent  attacks  unlikely,  20; 
constitutional,  1007 ;  due  to  animal  para- 
sites, 1027 ;  hereditary,  14 ;  incident  to 
active  occupations,  18 ;  incident  to  infancy 
and  childhood,  15  ;  incident  to  middle  age, 
16  ;  incident  to  old  age,  16. 

Diseases,  incident  to  puberty  and  adoles- 
cence, 16 ;  incident  to  sedentary  occupa- 
tions, 18 ;  incident  to  special  occupations, 
18  ;  influence  of  occupation  in  causing,  18  ; 
most  common  in  females,  17 ;  most  common 
in  males,  17  ;  of  arteries,  900 ;  of  blood  and 
ductless  glands,  908  ;  of  circulatory  system, 
870  ;  of  digestive  system,  750  ;  of  esophagus, 
767 ;  of  heart,  875 ;  of  heart  valves,  879  ; 
of  kidney,  929, 

Diseases  of  liver,  gall  bladder,  and  bile  ducts, 
800 ;  of  mediastinum,  867 ;  of  muscles, 
1005 ;  of  nervous  system,  942 ;  of  peri- 
cardium, 870 ;  of  peripheral  motor  neurones, 
963 ;  of  peripheral  sensory  neurones,  958 ; 
of  pharynx,  753;  of  salivary  glands,  753; 
of  spinal  cord  and  bulb  (medulla),  972  ;  of 
spleen,  923  ;  of  thymus  gland,  928  ;  of  thy- 
roid gland,  925 ;  of  tongue,  752  ;  of  tonsils, 
755. 

Diseases,  ophthalmoscopic  signs  of  extra- 
ocular, 208 ;  purpuric,  of  newborn,  916  ;  sea- 
sonal prevalence  of,  22 ;  special,  the  urine 
in,  645 ;    systemic,    of  spinal    cord,   985 ; 


INDEX 


1041 


■which  may  have  sequeliB,  21 ;  which  should 
be  diagnosed  with  special  caution,  21 ;  with 
diurnal  exacerbations,  22  ;  with  which  pain 
is  associated,  47. 
Distoma  pulmonale  in  sputum,  600. 
Distomiasis,  1027. 
Dittrich's  plugs,  836. 
Double  sensibility,  535. 
Dress,  diagnostic  hints  from,  24. 
Dropsy,  87. 
Drug  eruptions,  85. 
Drunkard's  ataxia,  1017. 
"Dry-mouth,"  113,753. 
"Dry  retching,"  762. 
Duchenne,    infantile    progressive    muscular 

atrophy  of,  971. 
Duchenne- Aran's  disease,  973. 
Dulness,  areas  of  cardiac,  330 ;  of  spleen,  473 ; 

over  lung,  401 ;  mental,  63. 
Dumbness,  246. 

Duodenal  ulcer,  symptoms  of,  765. 
^Duodenitis,  777. 
Dupuytren's  contraction,  276. 
J)ura  mater,  cerebral,  inflammation  of,  993. 
Dysacusis,  180. 
Dysentery,  700. 

Dysmenorrhoea  as  a  symptom,  147. 
-Dyspepsia,  760 ;  atonic,  776  ;  nervous,  770. 
Dysphagia,  its  causes,  237. 
Dyspnoea,  faeies  of,  161 ;  symptom  group  of, 

149  ;  varieties  and  causes  of,  392 ;  ursemic, 

932. 
Dystrophies,  509  ;  progressive  muscular,  969. 
Dystrophy,    facio  -  scapulo  -  liumeral    (Lan- 

douzy-Dejerine),     971 ;     scapulo-humeral 

(juvenile  of  Erb),  971. 
Dysuria,  139. 

Ear,  abscess  of  meatus,  176 ;  causes  of  pain 
in,  175 ;  colour  of,  175 ;  discharges  from, 
176;  haematoma  of,  175;  hemorrhage  from, 
176;  shape  of  the,  176. 

Earache,  175. 

Ecchymoses,  83;  subconjunctival,  184. 

Ecliinococcus  (hydatids),  in  sputum,  600;  of 
brain,  1032;  of  kidneys,  1031;  of  liver, 
1030 ;  of  lungs,  1031 ;  of  pleura,  1031 ; 
symptoms,  1030, 1031. 

Echokinesis,  168. 

Echolalia,  168. 

Eclampsia,  infantile,  puerperal,  73. 

Ectopic  gestation,  787. 

Effusion,  pericardial,  signs  of,  872. 

Egopliony,  418. 

Ihrlich's  diazo-reaction,  639;  triple  stain, 
573,  580. 


Electro-diagnosis,  indications  from,  547 ;  re- 
action of  degeneration,  548 ;    technic  of, 
642. 
Elephantiasis,  1028. 
Emboli,  pulmonary,  non-septic,  and  septic, 

843. 
Embolism,  cerebral,    997;    in    endocarditis, 
evidences  of,  877 ;  of  superior  mesenteric 
artery,  797 ;  pulmonary,  843 ;  septic,  signs 
of,  698. 
Embryocardia,  345. 
Emotional  state,  significance  of  the,  63. 

Emphysema,  atrophic,  852;  compensatory, 
852;  hypertrophic,  850;  interstitial,  850; 
of  skin,  92 ;  pulmonary,  849. 

Emphysematous  chest,  850. 

Emprosthotonus,  31. 

Empyema,  necessitatis,  862 ;  of  gall  bladder, 
804;  of  pleura,  862;  pulsating,  862. 

Encephalitis,  acute  exudative,  of  gray  mat- 
ter, 997;  acute  exudative,  with  hem- 
orrhage, 997  ;  acute  suppurative,  998. 

Encephalocele,  160. 

Encephalopathia  saturnina,  1022. 

Endocarditis,  chronic,  878;  malignant  (ul- 
cerative), 876 ;  simple  (benign),  875. 

Enophthalmos,  191. 

Ensiform  appendix,  as  a  landmark,  304. 

Enteralgia,  798. 

Enteritis,  acute  catarrhal,  777 ;  chronic  ca- 
tarrhal, 778  ;  croupous,  781 ;  diphtheritic, 
781 ;  membranous,  799 ;  phlegmonous,  781 ; 
varieties  of,  in  infancy  and  childhood,  779 ; 
with  "  peritoneal "  symptoms,  778. 

Entero-colitis,  acute,  780. 

Enteroplosis,  776. 

Enterospasm,  797. 

Eosinophiles,  582. 

Eosinophilia,  586. 

Ephemeral  fever,  749. 

Epigastric  pulsation,  328. 

Epilepsy,  942  ;  coma  from,  70 ;  convulsion  of, 
72;  Jacksonian,  516;  psychical,  942. 

Epiphora,  184. 

Epistaxis,  215. 

Episternal  notch,  pulsation  in,  267. 

Epithelioma  of  eyelid,  182. 

Erb,  juvenile  dystrophy  of,  971. 

Erb's  palsy,  966. 

Ergotism,  1025. 

Erroneous  projection,  195. 

Eructations,  120;  nervous,  775. 

Eruptions,  83 ;  from  drugs,  85. 

Erysipelas,  of  face  and  head,  175,  698. 

Erythema,  85. 

Erythema  nodosum,  278. 


1042 


INDEX 


Erythromelalgia,  282,  956. 

Esophagitis,  acute,  757. 

Esophagus,  acute  inflammation  of,  757 ;  anat- 
omy of,  445 ;  cancer  of,  758 ;  dilatation 
of,  759 ;  diseases  of,  757 ;  diverticula  of, 
759 ;  instrumental  examination  of,  446 ; 
palpation  and  auscultation  of,  445;  rup- 
ture of,  760 ;  spasm  of,  757 ;  stricture  of, 
758 ;  ulceration  of,  757. 

Esophoria,  201. 

Ether  pneumonia,  718. 

Euchlorhydria,  615. 

Evidences  of  disease,  the,  manner  of  ascer- 
taining, 5. 

Ewald's  test  breakfast,  605. 

Examinations,  synopsis  or  schedule  of,  xix. 

Exanthemata,  the,  85. 

Excitement,  mental,  63. 

Exophoria,  202. 

Exophthalmic  goitre,  925;  facies  of,  161. 

Exophthalmos,  191. 

Expansion,  deflcient  respiratory,  389 ;  in- 
creased respiratory,  390. 

Expiration,  prolonged,  416. 

E.xtremities,  causes  of  pain  in,  45 ;  signs  and 
symptoms  found  in  the,  271 ;  tenderness 
in,  54. 

Exudative  encephalitis,  997. 

Eye,  conjugate  deviation  of,  195;  dryness 
and  moisture  of,  184;  pain  in  and  around, 
190;  signs  and  symptoms  referable  to, 
180. 

Eyeball,  mechanism  of  normal  conjugate, 
lateral  movements  of,  192;  position  of,  192; 
protrusion  of,  191 ;  recession  of,  191. 

Eyelid,  epithelioma  of,  182  ;  initial  lesion  of 
syphilis  on,  183;  swelling  and  pufflness  of, 
180;  verruca  upon,  181. 

Eye  muscles,  to  test,  198. 

Eye  strain,  vertigo  in,  59. 

Eyes,  duskiness  under,  183 ;  irregular  or 
spasmodic  movements  of,  198. 

Face,  colour  of,  163;  ecchymoses  of,  164; 
flushing  of  the,  164;  in  acromegaly,  156 ; 
in  facial  hemiatrophy,  156  ;  in  hydroceph- 
alus, shape  of,  154;  in  leprosy,  shape  of, 
158;  in'rayxoedema,  156;  in  osteitis  de- 
formans, 156;  in  rachitis,  155;  in  sporadic 
cretinism,  155;  miscellaneous  affections  of 
the  head  and,  175 :  myopathic,  971 ;  oedema 
or  swellings  of,  166  ;  skin  of,  164. 

Facial  diplegia,  174. 

Facial  expression,  significance  of,  62. 

Facial  hemiatrophy,  progressive,  957 ;  shape 
of  face  in,  156. 


Facial  paralysis,  varieties  and  causes  of,  169. 

Facial  spasm,  951 ;  varieties  and  causes  of,. 
167. 

Facies,  of  special  diseases,  160;  of  acute  peri- 
tonitis, 161 ;  of  dyspnoea,  161 ;  of  exophthal- 
mic goitre,  161 ;  of  hereditary  syphilis,  163 ; 
of  hysteria,  161 ;  of  impending  death,  162;. 
of  phthisis,  162;  of  pneumonia,  162;  of 
renal  disease,  162. 

Fsecal  obstruction,  793. 

Faeces,  incontinence  of,  130 ;  microscopical 
examination  of,  618;  Plasmodium  malariae- 
and  amoeba  coli  in,  620 ;  other  micro-organ- 
isms in,  620,  621. 

Faintness,  56. 

Fallopian  tubes,  tuberculosis  of,  734. 

False  angina,  896. 

Family  history,  13. 

Farcy,  744. 

Fat,  in  stools,  137 ;  febricula,  749. 

Fatty  diarrhoea,  137. 

Fatty  heart,  891. 

Females,  diseases  most  common  in,  17. 

Femur,  periostitis  of,  281. 

Festination,  34. 

Fetid  stomatitis,  750. 

Fever,  "  break- bone,"  671;  causes  of,  105;. 
cerebro-spinal,  672;  diagnostic  classifica- 
tion of,  106;  ephemeral,  749;  facies  of 
typhoid,  162 ;  general  symptoms  of,  100 ;. 
hectic,  symptom  group  of,  153;  malarial, 
705 ;  malarial  intermittent,  types  of,  706. 

Fever,  manner  of  invasion,  course  and  ter- 
mination of,  104 ;  mountain,  749  ;  one-night,, 
of  infants,  749 ;  pernicious  malarial,  707 ; 
relapsing,  670 ;  remittent  malarial,  706 ; 
rheumatic,  acute  and  subacute,  710  ;  simple 
continued,  749;  suppurative,  symptom 
group  of,  153. 

Fever,  symptom  group  of,  149;  terminology 
of,  102 ;  thermic,  1025  ;  types  of  (continued, 
remittent,  intermittent,  recurring,  irregu- 
lar), 102,  103;  typhoid,  655;  typhoid,  facies. 
of,  162;  typhus,  668;  yellow,  699. 

Fevers,  sestivo-autunmal,  706. 

Fibrinuria,  634. 

Filaria  hominis  sanguinis,  591. 

Filariasis,  1028. 

Finger,  flexed,  276;  initial  lesion  of  syphilis- 
on,  272. 

Finger  nails,  condition  of,  271. 

Fingers,  blue  or  waxy,  274  :  clubbing  of,  274 ;:. 
distortion  of,  275. 

Fish,  poisoning  by,  1025. 

"  Fit  of  passion,"  833. 

Flat-foot,  282. 


INDEX 


1043 


Flatulence,  460. 
Flea,  1033. 

"  Flicking  "  percussion  of  abdomen,  432. 
"Flint"  murmur,  353,  880. 
Fluid  vein,  347. 

Fluids,  aspirated,  character  of  cerebro-spinal 
and  pancreatic,  652 ;  of  dropsical  and  in- 
flammatory, 650;  of  serous,  hemorrhagic, 
purulent,  putrid,  and  chylous,  651 ;  from 
hydatid  cyst,  distended  gall  bladder,  hy- 
dronephrosis, and  ovarian  cyst,  653. 
Flukes,  1027. 
Follicular  stomatitis,  750. 
Follicular  tonsilitis,  755. 
Fontanels,  significance  of  prominent  or  bulg- 
ing, 158 ;  sunken,  large,  or  delaved  closure 
of,  160. 
Food-poisoning,  1023. 

Foot  and  leg,  miscellaneous  signs  and  symp- 
toms connected  with,  279. 
Foot,  changes  in  shape  or  deformities  of,  282 ; 

gangrene  of,  281. 
Foot-drop,  513,  968. 
Forced  positions  or  movements,  518. 
Formication  and  itching,  causes  of,  56. 
Fracture  of  skull,  symptoms)  1018. 
Fractures,  spontaneous,  987. 
Fremissement  cataire,  329. 
Fremitus,  bronchial  (rhonchal),  396 ;  friction, 
395 ;  hydatid,  442 ;  vocal,  394 ;  vocal,  in- 
crease or  absence  of,  395. 
Friction  fremitus,  329,  330. 
Friction  sound,  subphrenic,  362. 
Friction  sounds,  character  and  seat  of,  422  ; 
over  abdomen,  444;  mediastinal,  874;  peri- 
cardial, 361  ;  pleuro-pericardial  and  pleural, 
362. 
Friction,  subpleural,  422. 
Friedreich's  ataxia,  989 ;  disease,  1007 ;  phe- 
nomenon, 408 :  sign,  874. 
Fulne-ss,  sensation  of,  causes,  56. 
Funnel  chest,  301. 
Furuncles. 

Gabbett's  method  of  staining  for  tubercle 
bacillus,  602. 

Gait,  cross-legged,  988 ;  in  hysterical  para- 
plegia, 946 ;  varieties  of,  in  disease,  33. 

Galactotoxismus,  1024. 

Galacturia.  639. 

Gallopinir  rhythm,  345. 

Gall  bladder,  acute  infective  inflammation 
of,  804:  carcinoma  of,  805;  discrimination 
of  distended,  from  movable  kidney,  479; 
diseases  of,  800 ;  dropsy  of,  807  ;  dropsy  of, 
fluid  in,  653;  empyema  of,  804;  examina-  | 


tion  of,  463 ;  pain  in  diseases  of,  50 ;  palpa- 
tion of,  467;  percussion  of,  465;  position 
of,  463. 
Gallstone,  ball-valve,    action    of,  802;    im- 
pacted, in  cystic  duct,  807;  impacted,  in 
common  duct,^807;  intestinal  obstruction 
from,  793 ;  occasional  sequelae  and  compli- 
cations of,  808;  search  for,  in  stools,  187; 
symptonjs  and  diagnosis,  805. 
Gangrene  of  lung,  853. 
Gangrenous  stomatitis,  751. 
Gas  poisoning,  coma  from,  71. 
Gastralgia,  distinguished  from  gastric  ulcer, 

764 ;  symptoms  and  diagnosis  of,  774. 
Gastrectasia,  examination  for,  456 ;  symptoms 

and  diagnosis,  768,  769. 
Gastric  crisis,  987. 

Gastric  juice,  acidity  of,  614 ;  normal  flndings 
617;    quantity  of,  614;    testing  digestive 
power  of,  609. 
Gastric  neuroses,  770. 

Gastritis,  acute  catarrhal,  760;  atrophic  or 
sclerotic,  762;  chronic  catarrhal,  761; 
chronic,  distinguished  from  gastric  ulcer, 
765 ;  diphtheritic,  761 ;  mucous,  7(>2 ; 
phlegmonous  or  suppurative,  761 ;  simple, 
762 ;  toxic,  761. 
Gastro-duodenitis,  777. 
Gastroptosis,  776 ;  results  of  examination  for, 

456. 
Gastrosuccorrhoea,  614,  772. 
Gastroxynsis,  772. 
General  aching,  40. 
General  appearance,    diagnostic  indications 

from,  24. 
Genitalia,  pain  in  disease  of,  52. 
Genitalia,  symptoms  referable  to,  in  males, 

144;  in  females,  146. 
Geographical  tongue,  753. 
Gerhardt's  phenomenon,  408. 
Gestation,  ectopic,  symptoms  of,  787. 
Gigantoblast,  578. 
Gilles  de  la  Tourette's  disease,  953. 
Girdle  sensation,  causes  of,  56. 
Gland,  mammary,  position  of,  305 ;  mammary, 
tuberculosis  of,  736;  parotid,  gaseous  tu- 
mours of,  753;    prostate,  tuberculosis  of, 
733 ;  thymus,  diseases  of,  928 ;  thyroid,  dis- 
eases of,    925 ;  thyroid,   enlargement   or 
atrophy  of,  264. 
Glanders,    symptoms    and    diagnosis,    744; 

prognosis,  745. 
Glands,  cervical  lymphatic,  enlargement  of, 
265,  266;    ductless,  diseases  of,  908;  in- 
guinal, enlargement  of,  279 ;  tuberculosis  of 
cervical,  tracheo-bronchial,  and  mesenteric, 


1044 


INDEX 


734,  735 ;  mediastinal,  inflamed,  869 ;  sali- 
vary, diseases  of,  753. 

Glaucoma,  185. 

*'  Glenard's  disease,"  776. 

Glossitis,  varieties  and  symptoms,  752. 

Glosso-labio-laryngeal  paralysis,  975. 

Glossy  skin,  274. 

Glycosuria,  637. 

Goitre,  exophthalmic,  925;  facies  of  exoph- 
thalmic, 161 ;  simple,  925. 

*'  Goose  "  gait,  34. 

Gout,  1010 ;  acute,  1010 ;  chronic,  1011 ;  ir- 
regular, 1011;  rheumatic  (arthritis  deform- 
ans), 1012  ;  suppressed  (retrocedent),  1011. 

Gouty  diathesis,  1011. 

Gowers'  solution,  561 ;  table  of  laryngeal  pa- 
ralyses, 243. 

Grain-poisoning,  1025. 

Grande  mal,  942. 

Granulations  of  leucocytes,  579. 

"  Gravel  "  from  kidney,  938. 

Graves's  disease,  925. 

Gray  skin,  81. 

*'  Green  sickness,"  911. 

Green  stools,  134. 

Groin,  enlarged  glands  in,  279. 

Gums,  colour,  sponginess,  ulceration  of,  222. 

Gunzberg's  test  for  free  IICI,  607. 

Gurgling  in  right  iliac  fossa,  458. 

Habit  chorea,  951. 

Habit  spasm,  168,  951. 

Habits,  influence  of,  upon  disease,  20. 

Hsemanalysis  chart  and  card,  559. 

Hsemateinesis,  causes  of,  122. 

Hfem'atidrosis,  83. 

Hsematochyluria,  1028. 

Hsematocrit,  the,  567. 

Hsematoglobinurla,  636. 

Hasmatoma  auris,  175. 

Hsematomyelia,  982. 

IliBmatoporphyrinuria,  636. 

Haematorrhachis,  981. 

Hiematuria,  635. 

Hsemin,  test  for,  123. 

"  Haemoconien,"  587. 

Hajmocytometer,  Thoma-Zeiss,  559. 

Ha-moglobin,  variations  in  amount  of,  576. 

Haemoglobinuria  neonatorum,  916. 

Hsemometer      (or      hsemoglobinometer),    v. 

Fleischl's,  567 ;  Gower.s',  569. 
Haemopericardium,  874. 
Hsemophilia,  918. 
Haemoptysis,  causes  of,   262 ;   diagnosis  of, 

261 ;  parasitic,  1027. 
Haemothorax,  863. 


Hair,  colour  and  loss  of  the,  165;  tumour- 
like mass  of  swallowed,  768. 

Hallucinations,  64. 

Hand,  accoucheur's,  518 ;  atrophy  of,  272 ; 
claw  (main-en-ffrife),  272  ;  of  arthritis  de- 
formans, 276 ;  of  pulmonary  osteo-arthrop- 
athy,  274 ;  spade,  272. 

Hands,  coldness  of,  273 ;  excessive  sweating 
of,  274. 

Handwriting,  defects  in,  278. 

Harrison's  sulcus,  300. 

Hay  asthma,  830. 

Hay  fever,  829. 

Hayem's  fluid,  587. 

Head,  abnormal  fixity  or  retraction  of,  167; 
abnormal  movements  of,  166;  in  acromeg- 
aly, shape  of,  156 ;  in  hydrocephalus,  shape 
of,  154;  in  idiocy,  shape  of,  155  ;  in  leon- 
tiasis  ossea,  shape  of,  158;  miscellaneous 
afiections  of  the  face  and,  175. 

Head,  nodding  spasm  of,  166  ;  in  rachitis, 
shape  of,  155;  in  osteitis  deformans,  car- 
riage of,  156  ;  in  sporadic  cretinism,  shape 
of,  155  ;  pain  in,  causes  of,  40 ;  sweating  of, 
excessive,  175 ;  tenderness  in,  53. 

Headache,  causes,  40  ;  character  of,  40  ;  defi- 
nition of,  40  ;  from  constipation,  44 ;  loca- 
tion of,  42  ;  varieties  of,  43. 

Hearing,  disorders  of,  176. 

Heart,  aneurism  of,  893;  auscultation  of,  339 ; 
auscultatory  percussion  of,  334 ;  dilatation 
of,  889;  direct  eftects  of  valvular  lesions 
upon,  312 ;  diseases  of,  875 ;  displaced, 
causes  of,  323 ;  dulness,  areas  of,  330  ;  fatty, 
891 ;  fibroid,  892  ;  hypertrophy  of,  886. 

Heart,  increase  of  dulness  of,  335,  338 :  in- 
nervation of,  310  ;  irritable,  890  ;  lessened 
percussion  dulness  of,  338 ;  limitations  of 
percussion  of,  335  ;  mobility  of,  320  ;  neu- 
roses of,  893 ;  pain  in  disease  of,  48 ;  per- 
cussion of,  Sansom's  method,  334;  phys- 
ical examination  of,  321. 

Heart,  pulsations  in  the  neighbourhood  of, 
325;  percussion  of,  technic  and  choice  of 
methods,  331,  382;  rupture  of,  893;  shape 
and  relations  of,  318,  319;  sounds  of  nor- 
mal, 308 ;  syphilis  of,  741  ;  topographical 
anatomy  of,  318;  valves,  areas  of  audibil- 
ity of,  340 ;  valves,  position  of,  339. 
Heartburn,  121. 

Heart  sounds,  reduplication  of,  344;   varia- 
tions in  intensity  and  character  of,  341. 
Heat  exhaustion,  1025. 
Heat,  subjective  sensations  of,  56. 
Heberden's  nodes,  276, 1012. 
Hebetude,  63. 


INDEX 


1045 


Height,  25. 

Hemiageusia,  233. 

Hemiausestbesia,  531. 

Hemianopia,  203. 

"  Hemianopic  pupillary  inaction,"  205. 

Hemianopsia,  203. 

Hemicrania,  943. 

llemiopia,  203. 

Hemiplegia,  cerebral,  994 ;  crossed,  definition 
of,  520 ;  definition  of,  520  ;  gait  in,  34 ;  in- 
fantile, 1000 ;  significance  of,  524. 

Hemorrhage,  artery  of  cerebral,  507  ;  broncho- 
pulmonary, 261;  from  ear,  176;  from  in- 
testines, 134;  from  nose,  215 ;  from  stom- 
ach, 122;  intracranial,  994;  retinal,  208; 
spinal,  981;  subconjunctival,  184;  symp- 
tom group  and  causes  of  internal,  150. 

Hemorrhages,  cutaneous,  83. 

Haemorrhagic  encephalitis,  997 ;  pericarditis, 
873 ;  pleurisy,  863 ;  purpura,  917. 

Henoch's  purpura,  917. 

Hepatoptosis,  776. 

Hereditary,  ataxic  paraplegia,  990;  diseases, 
14;  spinal  ataxia,  989. 

Hernia,  diaphragmatic,  866. 

Herpes,  facialis,  84  ;  of  pharynx,  235. 

Herpes  zoster,  175,  960. 

Heteropiioria,  201. 

Hiccough,  causes  of,  121. 

Hippus,  188. 

History,  clinical,  manner  of  recording,  6 ;  of 
present  illness,  22 ;  the  family,  13. 

Hoarseness,  243. 

Hodgkin's  disease,  913. 

«  Holding  the  breath,"  833, 

Hordeolum,  180. 

Humerus,  enlargement,  swelling,  and  pain 
of,  278. 

Hutchinson's  ("screw-driver")  teeth,  224. 

Huxley,  definition  of  scientific  reasoning,  4. 

Hydatid  thrill,  or  fremitus,  442. 

Hydatid  (echinococcus)  disease,  1030. 

Hydatids  (echinococcus),  of  brain,  1032;  of 
kidneys,  1031 ;  of  liver,  1030 ;  of  lungs, 
1031;  of  pleura,  1031. 

Hydreneephalocele,  160. 

Hydrencephaloid  state,  780. 

Hydrocephalus,  chronic,  999 ;  shape  of  head 
and  face  in,  154;  spurious,  780. 

Hydronephrosis,  937 ;  fluid  in,  653 ;  urine  in, 
647. 

Hydropericardium,  874. 

Hydrophobia,  747. 

Hydrothorax,  864. 

Hyperacusis,  180. 

Hyperemia,  of  kidney,  930. 
68 


Hyperesthesia,  534;  gastric,  774;  ocular  or 
retinal,  191. 

Hyperalgesia,  534. 

Hyperchlorhydria,  015;  symptoms  and  diag- 
nosis of,  771, 772. 

Hyperidrosis,  82. 

Hyperleucocytosis,  584. 

Hyperosmia,  217. 

Hyperphoria,  202. 

Hyperpyrexia,  110;  symptom  group  of,  150. 

Hypersecretion  of  gastric  juice,  614;  varieties 
and  symptoms,  772. 

Hyperthyrea,  925. 

Hypertrophy,  of  auricles,  887 ;  of  heart,  886 ; 
of  left  ventricle,  886 ;  of  muscles,  509  ;  of 
right  ventricle,  887. 

Hypochlorhydria,  615,  773. 

Hypochondriasis,  appendicular,  789. 

Hypochondrium,  bulging  of  right,  301. 

Hypoleucocytosis,  586. 

Hysteria,  944 ;  coma  of,  70 ;  convulsion  of, 
73;  facies  of,  161 ;  headache  of,  43;  major, 
945 ;  major,  crises  of,  947 ;  minor,  945 ; 
traumatic,  949. 

Hystero-epilepsy,  947. 

Hysterogenic  zones,  534,  945. 

Ichthyotoxismu.s,  1025. 

Icterus,  78;  ne<matorum,  803;  saturninos, 
1020 ;  simplex  and  gravis,  80, 

Idiocy,  shape  of  head  in,  155, 

Ileo-colitis,  777. 

Hlusions,  64. 

Immobility  of  body,  32. 

Impending  death,  facies  of,  162. 

Impotence,  146. 

Incompetency,  aortic,  879 ;  mitral.  881 ;  pul- 
monary, 886 ;  of  pylorus,  776 :  tricuspid, 
885. 

Incontinence  of  urine,  141. 

Indican  and  indicanuria,  629. 

Ineffectual  systole,  882. 

Infancy  and  childhood,  diseases  incident  to, 
15. 

Infantile  cerebral  palsies,  1000. 

Infantile  hemiplegia,  1000. 

Infarction,  intestinal,  797 ;  pulmonary,  843. 

Influenza,  epidemic,  675 ;  bacillus,  examina- 
tion for,  in  sputum,  603. 

Insects,  parasitic,  1032. 

Insolation,  1025. 

Insomnia,  65. 

Inspection  and  palpation  of  veins,  865. 

Inspection,  of  abdomen,  technic  of,  427 ;  of 
intestines,  457 ;  of  kidney,  477 ;  of  liver, 
463 ;  of  stomach,  448 ;  of  thorax,  296. 


1046 


INDEX 


Intellection,  disorders  of,  64. 

Intercostal  spaces,  bulging  and  retraction  of, 
390. 

Intermenstrual  pain,  148. 

Intermittent  malarial  fever,  Y05  ;  differential 
diagnosis,  709. 

Internal  hemorrhage,  symptom  group  and 
causes  of,  150. 

Interspaces,  identitication  of,  305. 

Intestine,  acute  obstruction  of,  its  causes,  792 ; 
carcinoma  of,  794 ;  causes  of  obstruction  in 
large,  791 ;  causes  of  obstruction  in  small, 
791 ;  chronic  obstruction  of,  its  causes,  792 ; 
diminished  sensibility  of,  798 ;  neuroses  of, 
797 ;  strangulation  of,  792 ;  ulceration  of, 
781 ;  ulcers  of,  781. 

Intestines,  auscultation  of,  460 ;  determining 
cause  of  obstruction  of,  791 ;  determining 
site  of  obstruction  of,  791 ;  diseases  of,  776  ; 
effect  of  valvular  lesions  on,  316 ;  examina- 
tion of,  457 ;  inspection  of,  457 ;  obstruction 
of,  causes,  789,  790 ;  obstruction  of,  from 
gallstones,  793. 

Intestines,  obstruction  of,  from  stricture  or 
tumour,  793 ;  obstruction  of,  rare  causes, 
793 ;  pain  in  disease  of,  49 ;  palpation  of, 
458 ;  percussion  of,  458  ;  practical  obstruc- 
tion of,  from  paresis  of  muscular  coat,  793 ; 
topography  of,  456 ;  tuberculosis  of,  736. 

Intoxications,  1016. 

Intussusception,  792. 

Iridoplegia,  accommodative,  with  preserved 
light  reflex,  188 ;  reflex  and  accommodative, 
186. 

Iris,  inflammation  of,  186 ;  physiology  of,  186. 

Iritis,  186. 

Italian  leprosy,  1025. 

Itch  insect,  1032. 

Itching  and  formication,  causes  of,  56. 

Janeway,succussion  sound  in  subphrenic  ab- 
scess, 824. 

Jaundice,  78 ;  symptom  group  of,  153;  with 
reference  to  its  origin,  78 ;  with  reference 
to  its  severity,  80. 

Jaw,  paralysis  of,  225. 

Joint,  shoulder,  stiffness  and  pain  in,  278. 

Joints,  examination  of,  and  the  signiflcance  of 
joint  symptoms,  93  ;  pain  in  diseases  of,  52. 

Jugular  veins,  collapse  of,  268 ;  distention, 
respiratory  movement  or  pulsation  of,  269  ; 
diastolic  collapse  of,  271. 

Jugulars,  pulsating,  269. 

June  cold,  829. 

Kakosmia,  218. 


Keel  breast,  300. 

Kelling's  test  for  lactic  acid,  608. 

Keratitis,  intei"stitial,  185. 

Kernig's  sign,  283. 

Kidney,  amyloid,  935 ;  urine  in,  646. 

Kidney,  cancerous,  tuberculous,  cystic,  urine 
in,  647. 

Kidney,  congestion  (hyperemia)  of,  930; 
cysts  of,  940 ;  discrimination  of  movable 
right,  from  distended  gall  bladder,  479 ; 
diseases  of,  929 ;  effect  of  valvular  lesions 
on,  317;  embolism  of,  urine  in,  647;  en- 
larged, causes  of,  480 ;  enlarged,  to  dis- 
tinguish from  spleen,  480. 

Kidney,  hyperaemia,  acute  and  passive,  urine 
in,  646;  large  white,  934;  movable,  929; 
movable,  urine  in,  645 ;  movable  and  float- 
ing, to  examine,  478 ;  pain  in  disease  of,  50 ; 
palpable,  to  examine,  477 ;  perinephritic 
abscess,  941 ;  tuberculosis  of,  733  ;  tumours 
of,  639. 

Kidneys,  hydatids  (echinococcus)  of,  1031; 
inspection  of,  477  ;  palpation  of,  477 ;  phys- 
ical examination  of,  476  ;  syphilis  of,  741 ; 
topography  of,  475. 

Koplik's  spots,  221. 

Kreotoxismus,  1024. 

Kyphosis,  283,  284. 

Lachrymation,  causes  of,  184. 

Lactosuria,  637. 

Lacunar  tonsilitis,  755. 

Ladder  pattern  in  abdomen,  429. 

Lagophtlialmos,  183. 

Landouzy-Dejerine  type  of  dystrophy,  971. 

Landry's  paralysis,  965. 

Larvffi  of  tapeworms,  1029. 

Laryngeal  crisis,  987. 

Laryngeal  paralysis,  causes  of,  242. 

Laryngeal  vertigo  (syncope,  epilepsy),  60. 

Laryngismus  stridulus,  833. 

Laryngitis,  acute  catarrhal,  830;  acute,  with 
spasm  of  glottis  (spasmodic  croup),  830; 
chronic,  831;  syphilitic,  832;  tuberculous, 
832. 

Larynx,  autoscopy  (Kirstein)  of,  239 ;  dis- 
eases of,  830 ;  examination  of,  238 ;  inspir- 
atory descent  of,  265 ;  oedema  of,  831 ;  pa- 
ralyses of,  varieties  and  causes,  240,  242 ; 
tumours  of,  832. 

Lateral  spinal  sclerosis,  988. 

Lathyrism,  1025. 

Lead  colic,  1019,  1021. 

Lead  palsy,  1021. 

Lead-poisoning,  1019;  acute,  in  children, 
1020;  chronic,  1020. 


INDEX 


1047 


Leg  and  foot,  miscellaneous  signs  and  symp- 
toms connected  with,  279. 

Leg,  peripheral  palsies  of,  968;  varicose 
veins  of,  281. 

Leontiasis  ossea  shapeof  head  and  face  in,158. 

Leprosy,  745 ;  Italian,  1025  ;  shape  of  face  in, 
158. 

Leptomeningitis,  acute  spinal,  991 ;  cerebral, 
993 :  chronic  spinal,  992. 

Lethargy,  66. 

LeucflEmia,  spleno-medullary  (myelogenous), 
911;  lymphatic  (lymphsemia),  913. 

Leucocytes,  basophilic,  582 ;  classification  of, 
580 ;  count  of,  in  acute  appendicitis,  786 ; 
differential  count  of,  583 ;  in  disease,  584 ; 
in  health,  583 ;  pigment-bearing,  590,  591 ; 
transition  forms,  581 ;  varieties  of,  579. 

Leucocytosis,  584 ;  absence  of,  in  typhoid 
fever,  658. 

Leucopenia,  586. 

Leucoplakia  buccalis,  753. 

Lice,  1032. 

Lientery,  134. 

Lipaciduria,  633. 

Lips,  colour,  218 ;  foam  on,  219 ;  herpes,  fis- 
sures, chancre,  mucous  patches,  epithelioma 
of,  219 ;  open,  218  ;  swelling  of,  219  ;  twitch- 
ing, 218;  unilateral  deviation  of,  218. 

Lipuria,  639. 

Lithaemia,  1011. 

Little's  disease,  988. 

Liver,  abnormal  consistence  or  roughnees  of, 
469  ;  abscess  of,  809 ;  acute  yellow  atrophy 
of,  816;  amyloid,  813;  auscultatory  per- 
cussion of,  465;  carcinoma  of,  814;  cirrho- 
sis of,  811 ;  cirrhosis  of,  distinguished  from 
gastric  ulcer,  765 ;  diminished  size  of,  469 ; 
efiect  of  valvular  lesions  on,  316;  enlarge- 
ment of,  467 ;  examination  of,  463. 

Liver,  fatty,  813;  hydatids  (echinococcus) 
of,  1030;  hypersemia,  active  and  passive, 
of,  808;  hypertrophic  cirrhosis,  812;  irreg- 
ular shape  of,  469 ;  "  lacing  "  or  "  corset," 
800 ;  movable  or  floating,  801 ;  "  nutmeg," 
608:  ordinary  percussion  of,  464;  pain  in 
disease  of,  50 ;  palpation  of,  466  ;  pulsation 
of,  328;  puncture  of,  649  ;  syphilis  of,  740 ; 
topographical  anatomy  of,  461 ;  tubercu- 
losis of,  736. 

Liver  and  spleen,  combined  enlargement  of, 
475. 

"  Liver  cough,"  259. 

"  Liver  spots,"  163. 

Lobar  pneumonia,  712. 

Lobstein's  cancer,  827. 

Local  asphyxia,  956;  syncope,  956. 


Lockjaw,  225. 

Locomotor  ataxia,  985. 

Loeffler's  solution,  603. 

Lordosis,  284. 

Lumbago,  1008. 

Lumbar  bulging,  285. 

Lung,  abscess  of,  853;  hydatids  (echino- 
coccus)  of,  1031 ;  gangrene  of,  853 ;  new 
growths  in,  854. 

Lungs,  acute  miliary  tuberculosis  of,  725,726 ; 
auscultation  of,  tech nic,  409  ;  changes  in  po- 
sition of  borders  of,  399 ;  congestion  of,  ac- 
tive and  passive,  841 ;  disease  of,  results  of 
percussion  in,  399  ;  diseases  of,  841 ;  effect  of 
valvular  lesions  on,  316 ;  hemorrhage  or  in- 
farction of,  842 ;  inspection  and  palpation  of, 
386 ;  oedema  of,  842 ;  pain  in  disease  of,  49. 

Lungs,  percussion  of,  increased  resonance, 
403;  percussion  of,  decreased  resonance, 
401 ;  phthisis,  acute  and  chronic,  726,  727 ; 
physiology  of,  384 ;  results  of  percussion  in 
normal,  398 ;  signs  of  cavities  in,  730 ; 
syphilis  of,  740 ;  technic  of  auscultation  of, 
409;  technic  of  percussion  of,  396;  topo- 
graphical anatomy  of,  382. 

Lupinosis,  1025. 

Lymph  glands,  cervical,  enlargement  of,  265 ; 
in  groin,  279 ;  tuberculosis  of,  734. 

Lymph  scrotum,  1028. 

Lymphflemia,  913. 

Lymphocytes,  580. 

Lymphocytosis,  585. 

Lymphoedema,  89. 

Lysis,  104. 

Lyssophobia,  748. 

Macrocytes,  578. 

Maidismus,  1025. 

Main-en-gnfe,  272,  968. 

Malar  bone,  tenderness  of,  53. 

Malarial  cachexia.  707. 

Malarial  fever,  705. 

Males,  diseases  most  common  in,  17. 

Malignant  pustule,  743. 

Mania  a  potu,  1016. 

Marie's  disease,  958. 

Mast  cells,  582. 

Mastodynia,  960. 

Mastoid  process,  tenderness  of,  63. 

Masturbation,  146. 

McBurney's  point,  456. 

Measles,  688. 

Meckel's  diverticulum,  792. 

Mediastinal  abscess,  869 ;  glands,  inflamma- 
tion of,  869 ;  lympliadenitis,  869 ;  tumonrs, 
867. 


1048 


INDEX 


Mediastino-pericarditis,  indurative,  873. 
Mediastinum,  diseases  of,  867. 
Medulla  (bulb),  diseases  of,  972. 
Megaloblast,  578. 
Megalocytes,  578. 
Megalogastria,  456. 
Megalonychosis,  272. 
Megastria,  456. 
Melaeua,  134. 

Membrane,  character  of,  in  mucous  colic,  799. 
Membranous  enteritis,  799. 
Memory,  loss  of,  64. 
Menidrosis,  83. 
Meniere's  disease,  59. 

Meningitis,  acute  tuberculous,  724,  725;  cere- 
bral, 992 ;  cerebral,  sei'ous  (alcoholic),  992 ; 

external  spinal,  990  ;  internal  spinal,  991. 
Meningocele,  cerebral,  160  ;  spinal,  981. 
Meningo-myelitis,  chronic,  992. 
Meningo-myelocele,  spinal,  981. 
Menorrhagia  as  a  symptom,  148. 
Mensuration  of  chest,  297. 
Mental  depression  and  excitement,  63. 
Meralgia,  960. 
Mercurial  stomatitis,  752. 
Merycism,  120,  775. 
Mesentery,  diseases  of,  796. 
Metallic  tinkling,  421. 
Meteorism,  causes  of,  436. 
Methsemoglobinuria,  636. 
Metrorrhagia  as  a  symptom,  148. 
Microcytes,  578. 

Middle  age,  diseases  incident  to,  16. 
Migraine,  943. 
Migrainoid  states,  944.  . 
Milk-poisoning,  1024. 
Mimic  spasm,  167. 
Mimic  tic,  951. 
Mind  blindness,  deafness,  anosmia,  ageusia, 

and  atactilia,  250. 
Miosis,  189. 
Mirror  writing,  278. 
Mitral  incompetency,  881 ;  direct  effect  of, 

upon  the  heart,  314. 
Mitral  regurgitation,  881. 
Mitral  stenosis,  883 ;    direct  effect  of,  upon 

the  heart,  315  ;  pulse  of,  378. 
Moisture  of  skin,  82. 
Monoplegia,  definition  of,  520;   significance 

of,  526. 
Morbus  cseruleus,  897. 
Morbus  cox£E  senilis,  1013. 
Morbus  errorum,  1032. 
Morbus  maculosus  neonatorum,  916  ;  Werl- 

hofl,  917. 
Morphine  habit,  1018. 


Morton's  neuralgia,  959. 

Morvan's  disease,  984. 

Mo.squito  as  carrier  of  malaria,  589. 

Motility,  increased,  514. 

Motor  functions  of  cranial  nerves,  501. 

Motor  localization  in  spinal  cord,  486. 

Motor  neuroses,  950. 

Motor  path,  the,  483. 

Motor  points  of  muscles,  547. 

Motor  power  of  stomach,  test  for,  612. 

Mountain  fever,  749 ;  sickness,  749. 

Mouth,  diseases  of,  750. 

Moutli,  dryness  of,  221 ;  "  tapir,"  971. 

Mouth- breathing,  162;  causes  and  symp- 
toms of,  756 ;  fades  of,  162. 

Movable  kidney,  629. 

Movements,  forced,  or  associated,  518. 

Moving,  mode  of,  32. 

Mucous  colic,  799. 

Mucous  patches,  738. 

Mucus,  in  gastric  contents,  616. 

Muguet,  751. 

Multiple  (disseminated)  sclerosis,  1003. 

Mumps,  678. 

Murmur,  of  high  pressure,  359  ;  the  "  Flint," 
353. 

Murmurs,  aortic  diastolic,  356 ;  aortic  systolic, 
355 ;  cardio-pulmonary,  362 ;  combined, 
359,  360;  discrimination  between  organic 
and  functional,  350  ;  do  they  accompany  or 
replace  the  valve  sounds,  349 ;  mitral  pre- 
systolic, 352  ;  mitral  systolic,  853 ;  phy.sical 
causes  of,  347  ;  point  of  maximum  intensity 
and  line  of  propagation,  350 ;  pulmonary 
diastolic,  359;  pulmonary  systolic,  358; 
time,  quality,  and  intensity  of,  348 ;  tri- 
cuspid, 357. 

Muscffi  volitantes,  202. 

Muscles,  atrophy  and  hypertrophy  of,  509 ; 
atrophy  of  leg,  281 ;  diseases  of,  1005 ;  ex- 
amination of,  509 ;  ocular,  insufficiencies  of, 
201 ;  ocular,  paralysis  of,  198 ;  of  calf, 
atrophy  of,  281;  ot  eye,  to  test,  198;  of 
hand,  atrophy  of,  272  ;  of  larynx,  paralysis 
of,  240,  242. 

Muscles,  the,  innervated  by  special  nerves, 
503 ;  motor  points  of,  547 ;  pain  in  disease 
of,  52 ;  rigid  recti,  433 ;  servatus  magnus, 
paralysis  of,  967  ;  tables  showing  evidences 
of  deficient  action,  their  innervation  and 
representation  in  spinal  cord,  492-500 ; 
testing  motor  power  of,  510 ;  tone  or  tension 
of,  510  ;  testing  power  of  individual,  511. 

Muscular  atrophies,  occupation,  971. 

Muscular  atrophy,  arthritic,  971 ;  infantile 
progressive  (Duchenne),  971 ;  progressive, 


INDEX 


1049 


973;  progressive  hereditary,  of  leg  type 

(Chareot-Marie- Tooth),  975;   progressive, 

spastic  form  (Charcot),  976. 
Muscular  sense,  disturbances  of,  535 ;  testing, 

529. 
Muscular  tissue,  amount  and  character  of,  26. 
Mussels,  poisoning  by,  1024. 
Mutism,  246. 
Mycotic  stomatitis,  751. 
Mydriasis,  188. 
Myelitis,  978 ;  acute  transverse,  978 ;  chronic, 

980 ;  compression,  980  ;  subacute,  980. 
Myelocytes,  582. 
Myelocytosis,  586. 
Myocarditis,  891 ;  pulse  of,  378. 
Myoclonia,  1007. 
Myoidema,  518. 

Myositis,  1005  ;  ossificans,  1006. 
Myotonia,  1007. 
Mytilus  edulis,  1024. 
Myxoedema,  926;    operative,  928;  shape  of 

face  in,  156. 

Nails,  diagnostic  appearances  of,  271. 

Narcosis,  opium,  1018. 

Nares,  acting,  214. 

Nasal  cavities,  examination  of,  211. 

Nasal  discharges,  215. 

Nasal  stenosis,  215. 

Nationality,  influence  of,  upon  disease,  18. 

Naunyn,  distinctive  signs  of  impacted  gall- 
stones in  common  duct,  807. 

Neck,  pulsating  arteries  of,  267 ;  rigidity  of, 
264 ;  shape  of,  263 ;  tenderness  in,  53 ;  veins 
of,  condition  of,  267. 

Nematodes,  1027. 

Nephritic  headache,  43. 

Nephritis,  acute,  932 ;  urine  in,  648. 

Nephritis,  clironic  diffuse  (parenchymatous), 
934;  urine  in,  646. 

Nephritis,  chronic  interstitial,  934 ;  urine  in, 
646. 

Nephritis,  facies  of,  162. 

Nephrolithiasis,  938. 

Nephroptosis,  776. 

Nerve,  anterior  crural,  paralysis  of,  968; 
eighth  (or  auditory),  to  test,  552;  fifth  (or 
trigeminus),  to  test,  551 ;  fourth,  paralysis 
of,  200,  201 ;  median,  paralysis  of,  967 ; 
musculo-spiral,  paralysis  of,  967 ;  ninth  (or 
glossopharyngeal),  to  test,  552;  obturator, 
paralysis  of,  968. 

Nerve,  phrenic,  paralysis  of,  966;  posterior 
thoracic,  paralysis  of,  967  ;  si.xth,  paralysis 
of,  201  ;  spinal  part  of  accessory,  paralysis 
of,  965;  suprascapular,  paralysis  of,  967; 


tenth  (or  pneumogastric),  to  test,  562 ;  third, 
paralysis  of,  198,  201 ;  ulnar,  paralysis  of, 
967. 

Nerves,  brachial,  combined  paralysis  of,  966 ; 
brachial  plexus,  paralysis  of  single,  967; 
cranial,  functions  of,  550 ;  cranial,  motor 
functions  of,  501  ;  lumbar,  paralyses  of, 
968 ;  motor  functions  of  mixed  spinal,  502 ; 
muscles  innervated  by  special,  503;  pe- 
ripheral, 500 ;  sensory  distribution  of  mixed 
spinal,  506;  vaso-coustrictor  and  dilator, 
311. 

Nervous  dyspepsia,  770. 

Nervous  eructations,  775. 

Nervous  prostration  (neurasthenia),  948. 

Nervous  syphilis,  1004. 

Nervous  system,  diseases  of,  942;  examina- 
tion of,  487,  507;  pain  in  "disease  of,  47; 
sympathetic,  500 ;  syphilis  of,  1004. 

Nervous  vomiting,  775. 

Neuralgia,  cervico-brachial,  961 ;  cervico- 
occipital,  961 ;  congestive,  956 ;  crural  (fem- 
oral), 960 ;  definition  of,  40 ;  digital,  961 ; 
intercostal,  960 ;  lumbo-abdominal,  960 ; 
mammary,  960 ;  Morton's,  959 ;  plantar, 
960 ;  rectal  or  pubic,  79? ;  red,  of  feet,  956. 

Neuralgias,  958 ;  of  the  trigeminus,  962. 

Neurasthenia,  948 ;  headache  of,  43 ;  vertigo 
from,  58. 

Neuritis,  dermatitic,  960 ;  epidemic  multiple 
(beri-beri),  748;  migrating,  965 ;  multiple, 
963 ;  optic,  209 ;  spontaneous  ulnar,  964. 

Neurone,  the,  481. 

Neurones,  central  and  peripheral,  481. 

Neuroses,  cardiac,  893 ;  intestinal,  797 ;  motor, 
950 ;  of  occupations,  955 ;  of  stomach,  770  ; 
seusori-motor,  942  ;  traumatic,  949. 

Neurotic  angina,  896. 

Neusser's  basophilic  granules,  582. 

Neutrophiles,  polymorphonuclear,  581. 

Newborn,  purpuric  diseases  of  the,  916. 

New  growths  of  pleura,  866. 

Nipple,  position  of.  305. 

Nodding  spasm,  166,  952. 

Nodes,  Heberden'.s,  1012;  on  skull,  161;  on 
tibia,  280. 

Noma,  751. 

Normoblasts,  578. 

Nose,  discharges  from  the,  215  ;  diseases  of, 
828;  examination  of,  211;  pain  in  or 
around,  213 ;  regurgitation  of  fluids 
through,  214;  shape,  colour,  ulceration  of, 
213 ;  stenosis  of,  215. 

Nucleo-albuminuria,  634. 

Numbness,  tingling,  burning  sensations,  56. 

Nystagmus,  definition  and  causes  of,  197. 


1050 


INDEX 


Obesity,  1015. 

Obstruction,  bronchial,  838. 

Obstruction,  causes  of,  in  large  intestine,  791 ; 
causes  of,  in  small  intestine,  791. 

Obstruction,  intestinal,  acute,  789 ;  chronic, 
790;  causes  of  acute,  792;  determining 
cause  of,  791 ;  determining  site  of,  791 ; 
from  gallstones,  793 ;  from  stricture  or  tu- 
mour, 793 ;  rare  causes  of,  793  ;  faecal.  793  ; 
practical,  from  paresis  of  muscular  coat, 
793. 

Occupation  neuroses,  955. 

Occupations,  diseases  incident  to  active,  18 ; 
diseases  incident  to  sedentary,  18  ;  diseases 
incident  to  special,  18. 

Ocular  headache,  44. 

Ocular  muscles,  insufficiencies  of  the,  201. 

Ocular  vertigo,  59, 195. 

Oculo-motor  paralysis,  199. 

Odour,  of  breath,  219 ;  of  stools,  133 ;  of  vom- 
itus,  125. 

CEdema,  angio-neurotic  (circumscribed),  957 ; 
"  blue,"  946 ;  causes  and  varieties,  87 ;  of 
one  arm  and  hand,  278 ;  pulmonary,  842 ; 
topographical  occurrence  of,  89. 

Old  age,  diseases  incident  to,  16. 

Oligoeythaemia,  577. 

Oliguria,  622. 

Omentum,  cordlike,  829, 

Onanism,  146. 

Onychia,  272. 

Ophthalmoplegia,  progressive,  977  ;  varieties 
of,  198. 

Ophthalmoscopic  signs  of  extra-ocular  dis- 
eases, 209. 

Opisthotonus,  31, 

Opium,  coma  of,  68. 

Opium-poisoning,  acute,  1018, 

Oppression,  sense  of,  57. 

Optic  atrophy,  210. 

Orthophoria,  201. 

Orthopnoea,  32, 

Osteitis  deformans,  shape  of  head  and  face 
in,  156. 

Osteophytes,  1013. 

Otorrhoea,  176. 

Ovaries,  tuberculosis  of,  734. 

Ovary,  abscess  of,  787. 

Oxaluria,  628. 

O.xyuris  vermicularis,  description  of,  138; 
symptoms,  1027. 

Oysters,  poisoning  by,  1024. 

Ozaena,  215. 

Pachymeningitis,  externa,  cerebral,  993  ;  spi- 
nal, 990 ;  interna,  spinal,  991. 


Pain,  34;  diagnostic  import  of  character  of, 
36 ;  diagnostic  import  of  the  seat  of,  38 ; 
differences  in  susceptibility  to,  35 :  diseases 
associated  with,  47  ;  in  abdomen,  causes  of, 
45  ;  in  chest,  causes  of,  45 ;  in  extremities, 
causes  of,  45;  in  sole  of  foot,  28?,  inter- 
menstrual, 148 ;  manner  oi  btatement,  35 ; 
miscellaneous  causes  of  52 ;  transferred, 
38 ;  varieties  of,  36. 

Pain  areas.  Head's,  38. 

Pain  sense,  529  ;  disturbances  of,  534. 

Painter's  colic,  1019,  1021. 

Palate,  anaesthesia  of,  235;  perforation  or 
paralysis  of,  234;  ulcers  of  (Parrott,  Bed- 
nar),  752 ;  vesicles  on,  235. 

Pallor  of  skin,  75. 

Palpation  of  abdomen,  technic,  430 ;  of  gall 
bladder,  467  ;  of  intestines,  458 ;  of  kidney, 
477 ;  of  liver,  466 ;  points  to  be  determined 
by,  287 ;  of  spleen,  471 ;  of  stomach,  449  ; 
theory  and  practice  of,  286. 

Palpatory  percussion,  293. 

Palpitation  of  heart,  893. 

Palsies,  facial,  968;  peripheral,  of  leg,  968. 

Palsy,  Erb's,  966 ;  facial  (Bell's),  968 ;  lead, 
1021 ;  pressure,  1015  ;  shaking,  953. 

Pancreas,  carcinoma  of,  818;  cysts  of,  819; 
diseases  of,  816;  hemorrhage  into,  818; 
pain  in  disease  of,  50;  physical  examina- 
tion of,  471 ;  relations  of,  470. 

Pancreatic  calculi,  820. 

Pancreatitis,  chronic,  818 ;  gangrenous,  818 ; 
hemorrhagic,  817  ;  suppurative,  817. 

Papilla  duodenalis,  794. 

Papillitis,  209.  : 

Paraesthesia,  trigeminal,  963. 

Paraj.sthesias,  diagnostic  significance  of,  55. 

Parageusia,  233. 

Paragraphia,  252,  253. 

Paralyses,  functional,  523 ;  infantile  cerebral, 
1000;  laryngeal,  Gowers'  table  of  243;  of 
lumbar  nerves,  968. 

Paralysis,  511 ;  acute  ascending  (Landry's), 
965 ;  a-sthenic  bulbar,  976 ;  Brown-Sequard, 
983;  combined,  of  brachial  nerves,  966; 
crossed,  171 ;  diagnostic  significance  of  the 
type  of,  522 ;  diphtheritic,  692 ;  double,  of 
face,  174;  Erb's,  966;  facial,  varieties  and 
causes,  169;  glosso-labio-laryngeal,  975; 
lower  neurone,  peripheral,  spinal,  fiaccid, 
or  atrophic,  521 ;  ocular,  198. 

Paralysis,  oculo-motor,  199;  of  anterior  cru- 
ral, 968  ;  of  circumflex,  967  ;  of  diaphragm, 
signs  of,  387,  388 ;  of  fourth  nerve,  200 ;  of 
jaw  muscles,  225 ;  of  median,  967  ;  of  mus- 
culo-spiral,967 ;  of  obturator,  968 ;  of  phrenic 


INDEX 


1051 


nerve,  966 ;  of  posterior  thoracic,  967 ;  of 
single  brachial  plexus  nerves,  967 ;  of  sixth 
nerve,  201 ;  of  soft  palate,  234. 

Paralysis,  of  spinal  part  of  accessor}-,  965 ;  of 
suprascapular,  967;  of  third  nerve,  198;  of 
ulnar,  967 ;  of  vocal  cords,  240 ;  progressive 
bulbar,  975;  pseudo-hypertrophic,  969; 
spastic,  514 ;  spastic  spinal,  988  ;  upper 
neurone,  central,  cerebral,  or  spastic,  520; 
varieties  of,  520 ;  vasomotor,  549. 

Paralysis  agitans,  953 ;  faciesof,  161 ;  manner 
of  talking  in,  246. 

Paralysis  saturnina,  1021. 

Paralytic  chest,  229. 

Paramyoclonus  multiplex,  1007. 

Paraphasia,  252,  253. 

Paraplegia,  definition  of,  520 :  liereditary 
ataxic,  990 ;  significance  of,  526. 

Parasites,  animal,  diseases  due  to,  1027 ;  in 
the  stools,  138;  in  vomitus,  125. 

Parasitic  arachnida,  1032. 

Parasitic  haemoptysis,  1027. 

Parasitic  stomatitis,  751. 

Paresis,  511 ;  definition  of,  520;  of  intestines, 
793. 

Parkinson's  disease,  953. 

Parkinson's  mask,  161. 

Parosmia,  218. 

Parotid  gland,  gaseous  tumours  of,  753. 

Parotitis,  chronic,  753;  epidemic,  678;  sup- 
purative, 753 ;  symptomatic,  753. 

Parrott's  ulcer  of  hard  palate,  752. 

Parry's  disease,  925. 

Patient,  interrogation  of  the,  5. 

Patterns  of  tumidity  in  abdomen,  429, 

Pectoriloquy,  417. 

Pediculi,  1032. 

Peliomata,  659. 

Pellagra,  1025. 

Pemphigu.s,  739. 

Pepsin,  absence  of,  616 ;  determining  pres- 
ence of,  in  gastric  juice,  609. 

Peptonuria,  634. 

Percussion,  auscultatory,  291 ;  auscultatory, 
of  abdomen,  432 ;  auscultatory,  of  heart, 
334 ;  auscultatory,  of  stomach,  451 ;  coin, 
408 ;  "  flicking,"  of  abdomen,  432 :  of  ab- 
domen, technic  of,  431 ;  of  colon,  459 ;  of 
intestines,  458 ;  of  liver  and  gall  bladder, 
463. 

Percussion,  of  lungs,  decreased  resonance, 
401 ;  of  lungs,  increased  resonance,  403  ;  of 
lungs,  technic  of,  396;  of  heart,  330;  of 
heart,  its  limitations,  335  ;  of  spleen,  473  ; 
ordinary,  of  stomach,  450:  palpatory  and 
direct,  293 ;  practice  of,  288 ;  results  of,  in 


disease  of  lungs  and  pleura,  399 ;  results  of; 
in  normal  lungs,  898 ;  sense  of  resistance  in, 
293. 

Percussion  sound  or  note,  amphoric,  405; 
elements  and  varieties  of,  289  ;  "  wooden," 
402. 

Percussion  sounds,  muffling  of,  290. 

Percussion  stroke,  proper  strength  of,  290. 

Percussion,  theory  of,  287. 

Perforating  ulcer  of  foot,  281. 

Pericardial  cavity,  puncture  of,  648. 

Pericardial  effusion,  signs  of,  338. 

Pericardial  friction  sounds,  361. 

Pericarditis,  acute  plastic,  870 ;  chronic  ad- 
hesive, 873 ;  hemorrhagic,  873 ;  in  general, 
870 ;  purulent,  873 ;  sero-fibrinous  (with 
effusion),  871. 

Pericardium,  diseases  of,  870 ;  tuberculosis  of, 
731. 

Perihepatitis,  815. 

Periuephritic  abscess,  941. 

Periodic  vomiting,  775. 

Periostitis,  acute,  of  femur  or  tibia,  281 ; 
syphilitic,  280. 

Peristalsis,  visible,  over  abdomen,  429. 

Peristaltic  unrest,  775. 

Peritoneal  cavity,  free  gas  in,  487. 

Peritoneum,  carcinoma  of,  826 ;  diseases  of, 
820 ;  examination  of,  457  ;  tuberculosis  of, 
symptoms  and  diagnosis,  732. 

Peritonitis,  acute  diffuse,  820 ;  acute  diffuse, 
facies  of,  161 ;  acute  localized,  823 ;  chronic 
diffuse,  826 ;  chronic  local,  825 ;  "  hysteri- 
cal," 823 ;  subphrenic,  823. 

Perityphlitis,  788. 

Pernicious  ansemia,  910. 

Pernicious  malarial  fever,  707. 

Pertussis,  677. 

Pes  equinus  (talipes),  varus,  valgus,  and  cal- 
caneus, 282. 

Petechioe,  83. 

Petit  mal,  942. 

Phantom  tumour,  438. 

Pharyngitis,  acute,  754;  chronic,  754;  mem- 
branous, 754. 

Pharynx,  acute  infectious  phlegmon  of,  754 ; 
adenoids  of,  756 ;  antesthesia  of,  236 ;  diag- 
nostic appearances  of,  235 ;  diseases  of,  758 ; 
distended  veins  of,  753;  examination  of, 
233;  hypera!mia  of,  753;  motor  and  sen- 
sory disorders  of,  236 ;  paralysis  of,  237  ; 
retropharyngeal  abscess,  754;  ulcers  in, 
236 ;  visible  pulsation  in,  754. 
Phenomenon,  Biermer's,  408;  Friedreich's, 
408 :  Gerhardt's,  408  ;  Wintrich's,  406,  408. 
Phlebitis,  of  deep  veins  of  leg,  281. 


1052 


INDEX 


Phlebosclerosis,  900. 

Phlegmonous  gastritis,  Vtil. 

Phloroglucin-vanilliu  test  for  free  HCl,  607. 

Phonendoscopc,  in  auscultation,  295 ;  in  aus- 
cultatory percussion,  293. 

Phosphaturia,  627. 

Photophobia,  190. 

Plithisical  chest,  299. 

Phthisis,  acute  pulmonary  (pneumonic  and 
broncho-pneumonic),  726 ;  chronic  pul- 
monary, 727 ;  flbroid,  731. 

Phthisis,  facies  of,  162. 

Physical  signs,  definition  of,  1 ;  descriptive 
terms  applied  to,  3. 

Pia  mater,  cerebral,  inflammation  of,  993 ; 
spinal,  acute  inflammation  of,  991 ;  chronic, 
992. 

Pica,  113. 

Pigeon  breast,  300. 

Pinworm,  1027. 

Pituitary  body,  disease  of,  958. 

Plague,  bubonic,  705. 

Plantar  neuralgia,  960. 

Plasmodium  malariae,  clinical  relations  of, 
590 ;  how  detected  in  the  blood,  589 ;  vari- 
eties and  life  history  of,  587. 

Plehn's  double  stain,  574,  580. 

Plessor,  288. 

Pleura,  diseases  of,  856 ;  hydatids  (echino- 
coccus)  of,  1031 ;  new  growths  of,  866 ;  pain 
in  disease  of,  49 ;  topographical  anatomy 
of,  384  ;  tuberculosis  of,  731. 

Pleural  and  pleuro-pericardial  friction 
sounds,  362. 

Pleural  cavity,  puncture  of,  649. 

Pleural  efl'usions,  estimating  amount  of,  859 ; 
physical  signs  of,  858. 

Pleurisy,  acute  fibrinous,  857 ;  adhesive,  864 ; 
chronic,  863 ;  diaphragmatic,  859 ;  en- 
cysted, 860 ;  hemorrhagic,  863 ;  in  general, 
856;  interlobar,  860;  latent,  859;  pulsat- 
ing,  862 ;  purulent,  862 ;  sero-fibrinous 
(with  efi"usion),  857 ;  tuberculous,  731. 

Pleurodynia,  1008. 

Pleuropneumonia,  719. 

Pleximeter,  288 ;  Sansom's,  method  of  use, 
334. 

Pleximeter  finger,  288. 

Plica  polonica,  1032. 

Plugs,  Dittrich's,  836. 

Plumbism,  1019. 

Pneumatosis,  437,  775. 

Pneumaturia,  626. 

Pneumococcus,  examination  for,  in  sputum, 
603. 

Pneumonia,  "aspiration,"  844;    chronic  in- 


terstitial, 847 ;  broncho-,  844 ;  "  ether,"  844 ; 
facies  of,  162;  hypostatic,  841;  lobar,  712. 

Pneumonokoniosis,  848. 

Pneumopericardium,  875. 

Pneumothorax,  865. 

Poikilocytosis,  577. 

Poisoning,  arsenic-,  1023;  by  oysters  and 
mussels,  1024;  by  phosphorus,  816;  fish-, 
1025;  food-,  1023;  grain-,  1025;  lead-, 
1019;  meat-,  1024;  milk-,  1024;  opium-, 
acute,  1018;  strychnine-,  convulsion  of, 
74  ;  irritant,  symptom  group  of,  153. 

Policeman's  disease,  959. 

Polio- encephalitis,  997;  inferior,  972;  supe- 
rior, 972. 

Poliomyelitis  anterior,  acute,  972 ;  chronic, 
973. 

Polytesthesia,  535. 

Polycythaemia,  577. 

Polyneuritis  potatorum,  1017. 

Polyphagia,  112. 

Polyuria,  622. 

Portal  circulation,  symptoms  of  obstructed, 
153. 

Positions,  forced,  518. 

Posterior  spinal  sclerosis,  985. 

Posture,  in  bed,  30  ;  "  coiled,"  31. 

Prsecordial  bulging,  301. 

Prfecordial  constriction,  sense  of,  57. 

Pnecordial  crepitation,  362. 

Prsecordial  splashing  sounds,  363. 

Prsecordium,  shape  of,  301. 

Pregnancy,  extra-uterine,  symptoms  of,  787. 

Present  illness,  history  of,  22. 

Pressure  palsy,  1015. 

Priapism,  145. 

Proctitis,  778. 

Proctospasm,  797. 

Progressive  ophthalmoplegia,  977 ;  upper 
bulbar  palsy,  977. 

Propulsion,  34. 

Pseudo-angina,  896. 

Pseudo-leucaemia  (Hodgkin's  disease),  913. 

Pseudo-hydrophobia,  748. 

Pseudo-hypertrophy,  510. 

Pseudo-muscular  hypertrophy,  969. 

Pseudo-tabe.s,  1017. 

Psychical  condition,  62. 

Psychical  epilepsy,  942. 

Psychro-sesthesias  and  psychro-algia,  55. 

Ptosis,  192;  alternating,  200. 

Ptyalism,  221. 

Puberty  and  adolescence,  diseases  incident 
to,  16. 

Putting  cheeks,  220. 

Pulex  irritans,  1033. 


INDEX 


1053 


Pulex  penetrans,  1033. 

Pulmonary  atelectasis,  849. 

Pulmonary  congestion,  acute,  719. 

Pulmonary  incompetence  (regurgitation), 
886. 

Pulmonary  stenosis,  886. 

Pulmonary  stenosis  and  insufficiency,  direct 
effect  of,  upon  the  heart,  315. 

Pulsation,  carotid,  267 ;  epigastric,  328 ;  in 
episternal  notch,  267;  of  liver,  328. 

Pulsations,  determining  the  rhythm  of,  325; 
in  the  neighbourhood  of  the  heart,  325. 

Pulse,  bigeminal,  372 ;  capillary,  271 ;  centrip- 
etal venous,  365 ;  Corrigan's  or  "  water- 
hammer,"  880;  dicrotic,  368;  decreased 
frequency  of,  371 ;  elements  and  technic  of 
examination  of  the,  367;  "gaseous,"  376; 
high-tension,  significance  of,  373 ;  increased 
frequency  of,  370;  intermittent  or  irregu- 
lar, 372. 

Pulse,  large,  small,  376 ;  low-tension,  signifi- 
cance of,  376  ;  paradoxical,  372,  373 ;  sig- 
nificance of  variations  in,  369 ;  slow,  quick, 
377  :  subungual,  271 ;  the  normal,  369 ;  uni- 
lateral abnormalities  of,  377. 

Pulses  of  special  diagnostic  value  (mitral 
stenosis,  aortic  stenosis,  and  incompetency, 
arteriosclerosis,  aneurism,  myocarditis), 
378. 

Pulsus,  altemans,  372 ;  bigeminus,  372 ;  bis- 
feriens,  376 ;  celer,  377 ;  durus,  373 ;  fre- 
quens,  369 ;  magnu.s,  376 ;  mollis,  376 ;  par- 
adoxus, 372,  373 ;  parvus,  376 ;  pleuus,  376 ; 
varus,  371 ;  tardus,  377  ;  trigeminus,  372 ; 
vaeuas,  376. 

Puncture,  diagnostic,  results  of  examination 
of  fluid  obtained  by,  649;  diagnostic, 
technic  of,  648 ;  lumbar,  649. 

Pupil,  absent  skin  reflex  of,  190;  Argyll- 
Kobertson,  987;  contracted,  189;  dilated, 
188 ;  response  to  accommodation,  and  skin 
reflex,  186;  response  to  light,  185;  skin 
reflex  of,  186. 

Pupillary  skin  reflex,  186, 190. 

Purpura,  916;  arthritic  (rheumatic),  917; 
erythematosa,  917 ;  fulminans,  917  ;  hem- 
orrhagic, 917;  rheumatica,  917;  simplex, 
917 ;  symptomatic,  916. 

Purpuric  diseases  of  newborn,  916. 

Pustule,  malignant,  743. 

Putnam's  combined  scleroses,  989. 

Pyamia,  695,  696:  arterial,  877;  symptom 
group  of,  153. 

Pyelitis,  936 ;  urine  in,  649. 

Pyelonephritis,  936. 

Pylorus,  hypertrophic  stenosis  of,  768;  in- 
competency of,  776 ;  spasm  of,  775. 


Pyonephrosis,  936. 
Pyopneumothorax,  865. 
Pyrosis,  121. 
Pyuria,  640. 

Quadruplegia,  definition  of,  520. 
Quincke,  lumbar  puncture,  649. 
Quinsy  sore  throat,  756. 

Rabies  (hydrophobia),  747. 

Rachitis  (rickets),  1014;  shape  of  head  and 
face  in,  155. 

Radius,  enlargements  of,  278 ;  pain  over  head 
of,  278. 

Railway  spine,  949. 

Rale,  crepitant,  420. 

Rales,  dry,  418;  moist,  420;  varieties  and 
significance,  418. 

Rashes,  83. 

Raspberry  tongue,  231. 

Raynaud's  disease,  956. 

Reaction  of  degeneration,  548. 

Reaction  of  stools,  133. 

Rectum,  carcinoma  of,  796;  examination  of 
and  findings  in,  460 ;  neuralgia  of,  798 ; 
spasm  of,  797 ;  syphilis  of,  741. 

Red  neuralgia  of  feet,  956. 

Redness  of  skin,  76. 

Reduplication  of  heart  sounds,  344 

Reflex,  patellar,  539. 

Reflexes,  536;  deep,  diagnostic  significance 
of  alterations  in,  539;  deep  (or  tendon), 
537 ;  significance  of  the  superficial,  537 ; 
testing  superficial,  536;  testing  deep  (or 
tendon),  538. 

Regurgitation,  aortic,  879 ;  of  fluids  through 
the  nose,  214;  of  food,  120;  pulmonary^ 
886 ;  tricuspid,  885. 

Relapsing  fever,  670 ;  spirilla  or  spirochsettt 
of,  591. 

Remittent  malarial  fever,  706. 

Renal  colic,  938. 

Renal  disease,  facies  of,  162. 

Renal  insufficiency,  624. 

Rennin,  absence  of,  616  ;  test  for,  612. 

Residence,  diseases  incident  t»,  19. 

Resonance,  amphoric,  405 ;  osteal,  287  :  "  Sko- 
daic,"  405 :  tympanitic  and  pulmonary,  288. 

Resonance,  vocal,  varieties  and  significance 
of,  417. 

Resorcin  test  for  free  HCl,  607. 

Respiration,  abdominal,  388 ;  absent  abdom- 
inal, 429;  amphoric,  414;  bronchial,  in 
disease,  413 ;  broncho-vesicular,  in  disease, 
415;  Cheyne-Stokes,  391;  "cog-wheel," 
416 ;  harsh,  416 ;  jerking,  stertorous,  strid- 
ulus, and  wavy,  392 ;  movements  of,  387. 


1054 


INDEX 


Eespiration,  muscles  of,  386 ;  normal  fre- 
quency of,  386  ;  puerile,  416 ;  rapid,  387 ; 
rhythm  of,  890 ;  simple  irregularity  of,  391 ; 
slow,  887;  in  health,  410 ;  in  disease,  413; 
thoracic,  887 ;  vesicular,  in  disease,  415. 

Respiratory  centre,  385. 

Respiratory  expansion,  388. 

Respiratory  system,  diseases  of,  828. 

Restlessness,  32. 

Retinal  hemorrhage,  208. 

Retinitis,  varieties  and  significance  of,  209. 

Retraction,  causes  of  cervical,  167. 

Retroperitoneal  sarcoma,  827. 

Retropharyngeal  abscess,  754. 

Retropulsion,  34. 

Rhachischisis  posterior,  981. 

Rhagades,  739. 

Rheumatic  fever,  710. 

Rheumatic  gout  (arthritis  deformans),  1012. 

Rheumatic  purpura,  917. 

Rheumatism,  acute  and  subacute  articular, 
710;  chronic,  1007 ;  gonorrhceal,  742  ;  mus- 
cular, 1008. 

Rhinitis,  acute,  828 ;  atrophic,  829  ;  hyper- 
trophic, 829. 

Rhinoscopy,  anterior,  211 ;  posterior,  212. 

Ribbon-shaped  stools,  132. 

Ribs,  flexibility  of,  803  ;  identification  of,  304. 

Rickets  (rachitis),  1014;  fcetal,  927. 

Rigid  recti  muscles,  433. 

Ringworm,  165. 

Risus  sardonicus,  68. 

Rontgen  light,  uses  of,  654. 

Romberg  symptom  (static  ataxia),  530. 

Rose  cold,  829. 

Roseola,  85. 

Rotheln,  689. 

Roundworm,  1027. 

Rubella,  689. 

Rubeola,  688. 

Rumination,  120,  775. 

"  S  "  curve,  in  pleural  effusions,  858. 

Saccharomyces,  614. 

Salaam  convulsion,  166. 

Salivary  glands,  diseases  of,  753. 

Salivation,  221. 

Sallowness,  168. 

Salol  test,  for  motor  power  of  stomach,  612. 

Salpingitis,  symptoms  of,  787. 

Saltatory  spasm,  951. 

Sand  flea-jigger,  1088. 

Sansom's  pleximeter,  method  of  use,  334. 

Sarcina  ventriculi,  613. 

Sarcoma,  retroperitoneal,  827. 

Sarcoptes  scabei,  1032. 


Saturnism,  1019. 

Scalp,  distended  veins  of,  175 ;  tenderness 
of,  53. 

Scanning  speech,  246. 

"  Scaphoid  "  abdomen,  433. 

Scapula,  position  of,  306. 

Scapulae,  prominence  of,  284. 

Scarlatina,  684. 

Scarlet  fever,  684. 

Scars,  significance  of,  86. 

Schedule  of  examinations,  xix. 

Schistosoma  hsematobinum,  1027. 

Schonlein's  disease,  917. 

Sciatica,  959. 

Scleroderma,  278. 

Scleroses,  amyotrophic  lateral,  976 ;  lateral 
spinal,  988  ;  multiple  (disseminated),  1003  ; 
posterior  spinal,  985. 

Scleroses,  combined  (Putnam's),  989. 

Sclerotic,  colour  of,  183. 

Scoliosis,  284 ;  sciatic,  959. 

Scotoma,  flittering,  202. 

Screw-driver  teeth,  224. 

Scurvy,  Alpine,  1025 ;  in  adults,  920 ;  infan- 
tile, 918. 

Scybala,  182. 

Semi-lunar  (Traube's)  space,  402. 

Sensation,  disturbances  of,  527. 

Sense,  disturbances  of  pain-,  534;  disturb- 
ances of  temperature-,  534 ;  of  tempera- 
ture-, testing,  529 ;  testing  articular  and 
tendinous,  529 ;  testing  muscular,  529 ; 
testing  pain-,  529;  testing  tactile  (contact 
and  pressure),  528,  529. 

Senses,  disturbances  of  articular,  muscular, 
and  tendinous,  535;  tactile,  temperature, 
pain,  muscular,  articular,  and  tendinous, 
527. 

Sensibility,  diminished  intestinal,  798. 

Sensori-motor  neuroses,  942. 

Sensory  localization  in  spinal  cord,  500. 

Sensory  path,  the,  481. 

SepticEcmia,  694. 

Serous  meningitis,  cerebral,  992. 

Serous  stools,  133. 

Serum  test  for  typhoid  fever,  592. 

Sex,  influence  on  disease,  16. 

Shingles,  960. 

Shock,  symptom  group  and  causes  of,  151. 

Shoulder,  stiflrness  and  pain  in,  278. 

Sick  Jieadache,  943. 

Sickness,  mountain,  749. 

Siderosis,  848. 

Sighing,  391. 

Sign,  Bacelli's,  418 ;  Kemig's,  283. 

Simple  continued  fever,  749. 


INDEX 


1055 


Sitotoxismus,  1025. 

Skin,  colour  of,  75;  emphysema  of,  92; 
liemorrliages  into  or  beneath,  83 ;  heat  of, 
81 ;  moisture  of,  82 ;  of  abdomen,  inspec- 
tion of,  428. 

Skin  reflex,  of  pupil,  186. 

*'  Skodaic  "  percussion  note,  405. 

Skull,  fracture  of,  1018. 

Sleep,  starting  in,  65. 

Smallpo.x,  679. 

Smell,  disturbances  of  the  sense  of,  217. 

Smoker's  patch,  230. 

Sneezing,  214. 

"  Snuffles,"  215,  739. 

Somnambulism,  943. 

Somnolence,  66. 

Soor,  751. 

Sordes,  225. 

Sore  throat,clergyman'8,754;  diphtheroid,754. 

Spade  hand,  272. 

Spasm,  carpo-pedal,  518, 833 ;  habit,  168, 961 ; 
localized,  516  ;  mimic,  167;  nodding,  166; 
of  stomach,  775;  saltatory,  951 ;  tonic  and 
clonic,  514;  facial,  167. 

Spasmodic  tic,  with  coprolalia,  953. 

Spasmodic  torticollis,  166. 

Spasmus  nutans,  952. 

Spastic  gait,  34. 

Spastic  spinal  paralysis,  988. 

Speech,  alterations  in  manner  of,  246 ;  normal 
mechanism  of,  247. 

Spermatorrhoea,  145. 

Spermatozoa  in  urine,  644. 

Sphygmograms,  374,  375. 

Sphygmograph,  378;  diagnostic  indications 
from,  381 ;  normal  trace  and  its  elements, 
380  ;  teehnic  of,  379. 

"  Spilling"  the  intestines,  431. 

Spina  bifida,  286,  981. 

Spinal  and  cerebral  lesions,  summary  of  diag- 
nostic points  bearing  upon  nature  and  loca- 
tion of,  555. 

Spinal  ataxia,  hereditary,  989. 

''  Spinal  concussion,"  946. 

Spinal  cord,  automatic  centres  of,  500. 

Spinal  cord,  diseases  of,  972;  inflammation 
of,  978;  segmental  motor  localization  in, 
486  ;  segmental  sensory  localization  in,  500 ; 
surface  and  other  relations,  and  names  and 
functions  of  the  parts  of,  483 ;  syphilis  of, 
740 ;  systemic  diseases  of,  984 ;  tuberculo- 
sis of,  736  ;  tumours  of,  982. 
Spinal   hemorrhage,  981 ;  into  substance  of 

cord,  982;  meningeal,  981. 
Spinal  lepto-raeningitis,  acute,  991 ;  chronic, 
992. 


Spinal  meninges,  inflammation  of,  990;  e.x- 
ternal,  990;  internal,  991. 

Spinal  pia  mater,  acute  inflammation  of,  991 ; 
chronic,  992. 

Spine,  curvatures  of,  284;  posterior  curvature 
of,  283  ;  "  railway,"  949. 

Spinous  processes,  identifying,  805. 

Spirilla  of  relapsing  fever,  591. 

Spirochseta?  of  relapsing  fever,  591. 

Splanchnoptosis,  776. 

Splashing  sounds,  prsBcordial,  863. 

Splenomegaly,  primitive,  924. 

Splenoptosis,  776. 

Spleen  and  liver,  combined  enlargement  of, 
475. 

Spleen,  auscultation  of,  474:  causes  of  en- 
largement of,  474;  displacement  of,  475; 
effect  of  valvular  lesions  on,  316 ;  enlarged, 
to  distinguish  from  kidney,  472  ;  enlarged, 
to  distinguish  from  left  lobe  of  liver,  473  ; 
infarcts,  abscess  and  new  growths  of,  923; 
inspection  and  palpation  of,  471 ;  movable, 
923 ;  pain  in  disease  of,  51  ;  percussion  of, 
473 ;  rupture  of,  923;  tuberculosis  of,  736. 

Spondylitis,  1013. 

Spondylitis  rhizomelia,  285,  286. 

Spots,  Koplik's,  221. 

Sputum,  animal  parasites  in,  601 ;  red  blood 
cells  in,  597 ;  crystals  in,  600 ;  fibrinous 
casts  and  Curschmann's  spirals  in,  599; 
gross  (macroscopic)  characters  of,  259 ;  leu- 
cocytes, epithelium  and  elastic  fibres  in, 
598 ;  making  preparations  of,  596,  597 ; 
microscopical  examination  of,  596. 

Squint,  193. 

Stains,  Ehrlich's  triple,  573,  580;  Plehn's 
double,  574,  580. 

Stamps,  outline-,  for  history  keeping,  9; 
type-,  for  history  keeping,  10. 

Station,  32. 

Status,  epilepticus,  942;  lymphaticus,  29; 
prffisens,  5 ;  typhoid,  symptoms  and  causes 
of,  153. 

Steatozoon,  1032. 

Stenocardia,  894. 

Stenosis,  aortic,  880  ;  mitral,  883;  nasal,  215; 
of  pylorus,  768 ;  pulmonary,  886 ;  tricuspid, 
885. 

Steppage  gait,  34. 

Sterno-mastoids,  prominence  of  the,  264 

Sternum  as  a  landmark,  304. 

Stethoscope,  choice  of,  294  ;  diflfereutial,  295. 

Stiffness  of  shoulder  joint,  278. 

Stigmata  of  degeneracy,  507. 

Stomach,  anatomy  and  surface  relations  of, 
447  ;  auscultation  of,  452  ;  auscultatory  per- 


1056 


INDEX 


cussion  of,  451 ;  cancer  (carcinoma)  of,  765 ; 
dilatation  of,  examination  for,  456 ;  diseases 
of,  760 ;  eflect  of  valvular  lesions  on,  316 ; 
general  diagnosis  of  neuroses  of,  776. 

Stomach  contents,  chemical  tests  required  in 
examination  of,  60tj ;  determined  amount  of 
combined  HCl  in,  610 ;  determining  amount 
of  free  HCl  in,  608 ;  determining  amount 
of  organic  acids  and  acid  salts  in,  610;  de- 
termining the  presence  of  acetic  and  butyric 
acids  in,  611 ;  determining  total  acidity  of, 
609 ;  diagnostic  results  of  the  examination 
of,  614;  examination  of,  604;  methods  of 
testing  for  free  HCl  in,  607. 

Stomach  contents,  microscopic  findings  in, 
613;  mucus  in,  616;  obtaining  the,  453; 
reaction  of,  606  ;  results  of  examination  of, 
in  special  diseases,  617  ;  significance  of  the 
presence  of  lactic,  acetic,  or  butyric  acids 
in,  616 ;  testing  digestive  power  of,  609 ; 
tests  for  free  lactic  acid  in,  608;  test  for 
rennin  in,  612.  . 

Stomach,  dilatation  of,  768 ;  hour-glass  con- 
traction of,  764 ;  inflation  of,  453 ;  inspec- 
tion of,  448 ;  motor  neuroses  of,  775 ;  neu- 
roses of,  770 ;  ordinary  percussion  of,  450 ; 
pain  in  disease  of,  49 ;  palpation  of,  449 ; 
physical  examination  of,  448;  prolapse  of, 
examination  for,  456. 

Stomach,  relaxation  of,  776 ;  secretory  neu- 
roses of,  771 ;    sensory  neuroses    of,  773 
spasm  of,  775 ;  succussion  sounds  in,  449 
technic  of  obtaining  the  contents  of,  453 
test  for  motor  power  of,  612;  the  normal, 
455 ;  tumour  formed  by,  in  cirrhotic  gas- 
tritis, 763  ;  tumour  of,  449 ;  ulcer  of,  763. 

Stomach  cough,  258,  762. 

Stomach  disorders,  vertigo  from,  59. 

Stomach  tube,  contraindications  to  use  of,  455. 

Stomatitis,  aphthous  or  follicular,  750;  ca- 
tarrhal, 750  ;  gangrenous,  751 ;  mercurial, 
752 ;  parasitic  or  mycotic,  751 ;  subvarieties 
of,  752 ;  ulcerative  or  fetid,  750 ;  uraemic, 
931. 

Stone  in  the  kidney,  938. 

Stools,  consistence  and  colour  of,  133;  ab- 
normal contents  of,  134;  blood  in,  134; 
foreign  bodies  and  parasites  in,  138 ;  mucus, 
pus,  shreds,  fat,  and  gallstones  in,  136, 137 ; 
shape,  odour,  and  reaction  of,  132. 

Strabismus,  193. 

Strangury,  139. 

Strawberry  tongue,  231. 

Streptococcus  pneumonia,  718. 

Streptothrix  actinomyces,  745. 

Strongyloides  intestinalis,  1029. 


Strychnine  poisoning,  convulsion  of,  74. 

Stupor,  66. 

St.  Vitus's  dance,  950. 

Subconjunctival  hemorrhage  or  ecchymosis, 
184. 

Subphrenic  friction  sound,  362. 

Subphrenic  peritonitis  (abscess),  823. 

Subsultus  tendinum,  153,  517. 

Succussion  sounds  in  thorax,  421. 

Sudamina,  85. 

Sunstroke,  1026 ;  coma  from,  71. 

Suppuration,  iodine  reaction  in,  594. 

Suppurative  gastritis,  761. 

Suppurative  tonsilitis,  756. 

Suprarenal  capsules,  736 ;  tuberculosis  of, 
922. 

Sutures,  significance  of  abnormally  wide 
cranial,  160. 

Sweat,  amount  and  colour  of,  82.  • 

Sweating  of  head,  excessive,  175. 

Swelling  in  lumbar  region,  285. 

Sympathetic  nervous  system,  500. 

Symptom,  the  Komberg,  530. 

Symptom  group  and  causes,  of  internal 
hemorrhage,  150  ;  of  shock  or  collapse,  151 ; 
of  the  typhoid  status,  153. 

Symptom  group,  of  coma,  149 ;  of  dyspnoea, 
149;  of  fever,  149;  of  hyperpyrexia,  150; 
of  irritant  poisoning,  153;  of  jaundice,  153; 
of  obstructed  portal  circulation,  153;  of 
pyaemia,  153;  of  suppurative  (hectic)  fever, 
153;  of  syncope,  152;  of  tympanites,  153; 
of  weakness  or  debility,  152. 

Symptoms,  descriptive  terms  applied  to,  3; 
objective  and  subjective,  1. 

Syncope,  67,  70;  symptoms  of,  152. 

Synopsis  of  examinations,  xix. 

Syphilis,  737 ;  congeni  al,  739 ;  diagnosis  of, 
741;  haemorrhagica  neonatorum,  916;  he- 
reditary, facies  of,  163;  of  arteries,  741 ;  of 
heart,  741 ;  of  kidneys,  741 ;  of  larynx,  832 ; 
of  liver,  740 ;  of  lungs,  740 ;  of  nervous  sys- 
tem, 1004;  of  rectum,  741 ;  of  testicles,  741 ; 
visceral,  740. 

Syphilitic  ulceration,  head  and  face,  174. 

Syringomyelia,  984. 

Syringo-myelocele,  spinal,  981. 

Systole,  ineffectual,  882. 

Tabes     dorsalis,     985;     mesenterica,     735; 

pseudo-,  1017. 
Tache  cerebrale,  659. 
Taches  bleuatres,  659. 
Tachycardia,  paro.xysmal,  371. 
Tactile  (contact  and  pressure)  sense,  testing, 

528. 


INDEX 


1057 


Taenia,  echinococcus,  1030;  mediocanellata 
saginata,  description  of,  138;  solium,  de- 
scription of,  139 ;  symptoms  of,  1029. 

Tapeworms,  description  of,  138;  intestinal, 
1029  ;  symptoms  from,  1029 ;  visceral,  1030. 

Tapir  mouth,  971. 

Tarry  stools,  135. 

Tarsalgia,  959. 

Taste,  disorders  of,  282;  sense  of,  to  test, 
232. 

Tastes,  "  bad,"  233. 

Teeth,  223 ;  dates  of  eruption  of,  223 ;  grind- 
ing of,  225 ;  Hutchinson's,  224 ;  notched, 
dentated,  or  decayed,  224 ;  "  screw-driver," 
224. 

Temper,  irritable,  or  change  in,  63. 

Temperament,  61. 

Temperature  of  the  body,  diagnostic  indica- 
tions from,  105 ;  taking  and  recording  the, 
95. 

Temperature  sense,  disturbances  of,  534 ; 
testing,  529. 

Temperatures,  normal,  98 ;  abnormal,  99 ;  nor- 
mal surface  of  head,  chest,  and  abdomen, 
99 ;  subnormal.  111. 

Tenderness,  52 ;  in  head,  scalp,  thorax,  back, 
and  abdomen,  53 ;  in  extremities,  54. 

Tendinous  sense,  disturbances  of,  535 ;  test- 
ing, 529. 

Tenesmus,  37  ;  rectal,  132. 

Tension,  arterial,  310  ;  estimation  of,  368. 

Test,  for  acetic  acid,  612;  for  htemin,  123. 

Test  meals,  605. 

Testicles,  pendulous,  145 ;  syphilis  of,  741 ; 
tuberculosis  of,  734. 

Tests,  for  free  HCl,  607;  for  lactic  acid, 
608. 

Tetanus,  746 ;  convulsion  of,  74. 

Tetany,  518. 

Thermic  fever,  1025. 

Thermogenesis,  99. 

Thermolysis,  99. 

Thirst,  abnormalities  of  the  sense  of,  113. 

Thoma-Zeiss  counting  slide,  561,  562. 

Thomsen's  disease,  1007. 

Thoracometry,  297. 

Thorax,  anatomical  landmarks  of,  304;  bi- 
lateral deformities  of,  299;  characters  of 
the  normal,  296, 297 ;  describing  the  site  of 
lesions  in,  307  ;  oedema  of,  303 ;  increased 
rigidity  of,  acting  as  a  resonator,  303 ;  in- 
spection of,  296. 

Thorax,  local  depressions  of,  302 ;  miscella- 
neous signs  and  symptoms  connected  with, 
303 ;  mensuration  of,  297 ;  oedema  of,  303  ; 
pulsating  areas  of,  324,  325 ;  tenderness  on. 


53 ;  topographical  areas  of,  806  ;  unilateral 
contraction  of,  302;  unilateral  deformities 
of,  301. 

Threadworms,  133. 

Thrill,  hydatid,  442. 

Thrills,  329. 

Throbbing,  sensation  of,  57. 

Thrombosis,  cerebral,  997 ;  of  superior  mes- 
enteric artery,  797  ;  pulmonary,  843. 

Thrush,  751. 

Thymic  asthma,  928,  929. 

Thymus  gland,  diseaifes  of,  928. 

Thyroid  gland,  diseases  of,  925  ;  enlargement 
or  atrophy  of,  264. 

Tibia,  nodes  on.  and  periostitis  of,  281 ;  pain- 
ful enlargement  of,  280 ;  sabre-shaped,  280. 

Tic  douloureux,  962. 

Tic,  mimic,  951 ;  spasmodic,  with  coprolalia, 
953. 

Tics,  517. 

Tightness,  sensation  of,  68. 

Tinea  tonsurans,  165. 

Tingling,  burning,  numbness,  56. 

Tinnitus  aurium,  176. 

Tinnitus  cerebri,  177. 

Toison's  solution,  564. 

Tongue,  atrophy  of,  227  ;  beefy,  231 ;  colour 
and  pigmentation  of,  225  ;  diseases  of,  752 ; 
eczema  of,  752 ;  enlargement  of,  226  ;  gen- 
eral diagnostic  appearances  of  the.  230; 
geographical,  753 ;  leucoplakia  of,  230 ; 
scars,  fissures,  or  ulcers  of,  229 ;  paralysis, 
spasm,  or  tremor  of,  228 ;  psoriasis  of,  752 ; 
smoker's  patch,  230 ;  raspberry,  231 ;  straw- 
berry, '>31. 

Tonsil,  examination  of  lingual,  288. 

Tonsilitis,  chronic,  756;  follicular  (lacunar), 
755  ;  phlegmonous  (suppurative),  756. 

Tonsils,  diagnostic  appearances  of,  235 ;  dis- 
eases of,  765;  exudate  on,  236;  swelling 
and  ulceration  of,  235. 

Topfer's  test,  for  free  HCl,  607 ;  for  organic 
acids  and  acid  salts,  610. 

Tophi,  1011 ;  on  ear,  176 :  on  eyelid,  188. 

Topographical  areas  of  thorax,  306. 

Torticollis,  952 :  rheumatic,  1008 ;  spasmodic, 
166, 167. 

Toxaemia,  definition,  694;  causes  and  symp- 
toms, 695. 

Toxic  angina,  896. 

Toxic  gastritis,  761. 

Trachea,  displacement  of,  265. 

Tracheal  lugging,  265. 

Traube's  area,  dulne.^s  in,  402. 

Traumatic  hysteria,  949. 

Traumatic  neuroses,  949. 


1058 


INDEX 


Tremor,  diagnostic  associations  of,  575 ;  fibril- 
lary, 516 ;  varieties  of,  514,  515. 

Trichiniasis,  10-27. 

Tricocephalus  dispar,  1028. 

Tricuspid  incompetency  (regurgitation),  885 ; 
incompetence  and  stenosis,  direct  effect  of, 
upon  the  heart,  315 ;  stenosis,  885. 

Trismus,  225. 

Trophic  disturbances,  550. 

Trophoneuroses,  956. 

Tube  casts  in  urine,  642. 

Tubercles  in  choroid,  211.. 

Tuberculin  test  for  tuberculosis,  737. 

Tuberculosis,  acute  general  or  disseminated, 
723 ;  acute  miliary,  of  lungs,  725 ;  acute 
pulmonary  phthisis,  726 ;  acute  tuberculous 
meningitis,  724 ;  of  alimentary  canal,  735 ; 
of  bladder,  733 ;  of  brain,  736 ;  of  Fallopian 

■  tubes  and  ovaries,  734 ;  of  intestines,  736 ; 
of  kidney,  733. 

Tuberculosis,  of  larynx,  832 ;  of  liver,  736 ;  of 
lymph  glands,  734;  of  mammary  gland, 
736;  of  pericardium,  731;  of  peritoneum, 
732 ;  of  pleura,  731 ;  of  prostate  gland,  733 ; 
of  spinal  cord,  736 ;  of  spleen,  736  ;  of  su- 
prarenal capsules,  922;  of  testis,  734;  tu- 
berculin test  for,  737. 

Tuberculous  ulceration,  head  and  face,  175. 

Tugging,  tracheal,  265. 

Tumour,  '•  phantom,"  438. 

Tumours,  causing  general  abdominal  disten- 
tion, 438;  mediastinal,  867;  of  abdomen, 
examination  of,  439 ;  of  abdomen,  indica- 
tions from  situation  of,  443,  444 ;  of  abdo- 
men, mobility  of,  441 ;  of  abdomen,  which 
move  with  respiration,  439 ;  of  brain,  1001 ; 
of  kidney,  639 ;  of  spinal  cord,  982. 

Tympanites,  causes  of,  436 ;  symptom  group 
of,  153. 

Tympanitic  percussion  sound  over  lung, 
403. 

Typhlitis,  788. 

Typhoid  fever,  655;  complications  and  se- 
quelae, 661 ;  diagnosis  of,  664,  665 ;  facies 
of,  162 ;  varieties  of,  659. 

Typhoid  status,  facies  of,  162;  symptom 
group  and  causes  of,  153. 

Typhus  fever,  668. 

Tyrotoxismus,  1024. 

Uffelman's  test  for  free  lactic  acid,  608. 
Ulcer,  atheromatous,  900 ;  duodenal,  765 ;  of 

stomach,  763;  peptic,  763;  perforating,  of 

foot,  281. 
Ulceration,  syphilitic  or  tuberculous,  of  head 

and  face,  174. 


Ulcerative  stomatitis,  750. 

Ulcers,  of  cornea,  185;  in  pharynx,  236;  of 
intestine,  781 ;  stercoral,  782. 

Ulna,  swellings  or  nodes  over,  278. 

Umbilicus,  position  of,  424 ;  signs  relating  to,. 
429. 

Uncinaria  duodenalis,  1028. 

Uraemia,  convulsion  of,  73;  coma  of,  69; 
symptoms  of,  930 :  urine  in,  647. 

Ureter,  tuberculosis  of,  733. 

Urethra,  discharges  from,  144. 

Uridrosis,  82. 

Urina  spastica,  935, 1008. 

Urinalysis  card,  10. 

Urinalysis,  diagnostic  inferences  from  results- 
of,  621 ;  results  of,  in  special  diseases,  645,. 
648. 

Urinary  solids,  total,  624. 

Urination,  abnormalities  of,  139;  difficult  or 
frequent,  141. 

Urine,  acetone  in,  638;  albumin  in,  631  •„ 
blood  and  its  compounds  in,  634 ;  chlorides 
in,  626 ;  colour,  odour,  and  consistence  of,. 
623 ;  cystin  in,  638 ;  diacetic  and  oxybutyric 
in,  638;  diazo-reaction  in,  value  of,  639; 
elastic  fibres  and  tumour  fragments  in,  645 ;. 
epithelial  cells  in,  641,  642 ;  fat  in,  639. 

Urine,  in  acute  nephritis,  646  ;  in  amyloid 
kidney,  646;  in  chronic  diffuse  nephritis, 
646 ;  in  chronic  interstitial  nephritis,  646 ;. 
in  cystic  kidney,  647;  in  cystitis,  647;  in. 
diabetes  insipidus,  647 ;  in  diabetes  melli- 
tus,  647 ;  in  gout,  1010 ;  in  hydronephrosis,, 
647. 

Urine,  in  movable  kidney,  645 ;  in  pyelitis, 
646 ;  in  renal  cancer,  647 ;  in  renal  cal- 
culus, 647 ;  in  renal  hyperaemia,  646  ;  in 
renal  embolism,  647 ;  in  renal  tuberculosis, 
647 ;  in  uraemia,  6*7 ;  in  vesical  calculus,. 
647 ;  in  vesical  cancer,  648 :  in  vesical  tu- 
berculosis, 648. 

Urine,  incontinence  of,  141 ;  indiean  in,  629  ; 
naked-eye  deposits  in,  625 ;  oxalates  in, 
628 ;  parasitic  micro-organisms  in,  645 ; 
phosphates  in,  627  ;  prostatic  threads  and 
spermatozoa  in,  644 ;  pus  in,  640 ;  quantity 
of,  621 ;  reaction  of,  626. 

Urine,  results  of  analysis  of,  in  special  dis- 
eases, 645,  648  ;  retention  of,  142  ;  specific 
gravity  of,  624 ;  spermatozoa  in,  644 ;  sug- 
ars in,  6.37 ;  sulphates  in,  628 ;  suppression 
of,  143 ;  tube  easts  in,  642 ;  urea  in,  629 ; 
uric  acid  in,  630. 

Urticaria,  86. 

Uterine  headache,  44. 

Uvula,  swelling  of,  235. 


INDEX 


1059 


Vaccinia,  683. 

Vagabond's  disease,  1032. 

Vaginal  discharges,  causes  of,  147. 

Valeur  globulaire,  576. 

Valves,  direct  effect  of  lesions  of,  upon  the 
heart,  312. 

Valves,  position  and  areas  of  audibility  of, 
339,  340. 

Valvular  lesions,  chronic,  879 ;  defects,  com- 
bined, 886 ;  broken  compensation  of,  315, 
316 ;  indirect  or  peripheral  eflfects  of,  316. 

Varicella,  683. 

Varicocele,  145. 

Varicose  aneurism,  902. 

Variola,  679. 

Varioloid,  681. 

Vasomotor  angina,  890 ;  apparatus,  311 ; 
ataxia,  550 ;  irritation,  550  ;   paralysis,  549. 

Vater,  ampulla  of,  802. 

Vein,  portal,  thrombosis  of,  808. 

Veins,  auscultation  of,  366 ;  condition  of,  91 ; 
distended,  of  scalp,  175;  distention  of,  91 ; 
enlarged,  of  abdomen,  428;  evidence  of 
thrombosis  of,  365;  in  neck,  condition  of, 
267;  inspection  and  palpation  of,  365;  ju- 
gular, diastolic  collapse  of,  271 ;  of  chest, 
enlarged,  303 ;  of  neck,  condition  of,  267 ; 
of  scalp,  distended,  175  ;  phlebitis  of  deep, 
of  leg,  281 ;  pulsating  jugular,  269  ;  vari- 
cose, of  leg,  281. 

Venae  cavse,  effect  of  valvular  lesions  on, 
317. 

Venous  distention,  91. 

Venous  hum,  366 ;  pulsation,  269 ;  pulse, 
365. 

Ventricle,  left,  hypertrophy  of,  886 ;  right, 
hypertrophy  of,  887. 

Verruca,  181. 

Vertigo,  laryngeal,  60  ;  ocular,  195  ;  varieties 
and  causes  of,  58. 

Vesical  tenesmus,  139. 

Vessels,  relations  of  great,  to  chest  wall,  321. 

Vision,  double,  194 ;  minor  disorders  of,  202 ; 
red,  202. 

Visual  fields  for  light  and  colour,  contraction 
of,  207. 

Vocal  cords,  paralysis  of,  240. 


Vocal  fremitus,  394 ;  increase  or  absence  of^ 

395. 
Vocal  resonance,  amphoric,  418 ;    varieties 

and  significance  of,  417. 
Voice,  nasal,  245 ;  ventricular,  245. 
Volvulus,  792. 
Vomiting,  113,  114;   causes  of,  114;  fsecal, 

124 ;  indications  from  the  presence  of,  116  ; 

nervous  and  periodic,  775;  projectile,  1001. 
Vomitus,  indications  from  the  character  and 

amount  of,  122 ;  odour  of,  125 ;  parasites  in^ 

125  ;  pus  in,  125. 
Von  Graefe's  sign,  183. 
Von  Leube  and  Riegel  test  dinner,  606. 

Waddling  gait,  34. 
Wakefulness,  65. 
Water-brash,  121. 
Water-hammer  pulse.  880. 
"  Water-wheel  "  sounds,  363. 
Waxy  flexibility,  519. 

'Weakness,  sense  of,  58 ;  symptoms  of,  152. 
Weight,  25 ;   diagnostic  import  of  changes 

in,  27. 
"  Wet  brain,"  992. 
Whipworm,  1029. 
Whooping  cough,  677. 
Widal  test,  592. 

Williamson's  test  for  diabetes,  594. 
Wintrich's   phenomenon,  406 ;   interrupted, 

408. 
Wirsung,  duct  of,  819. 
Wool-sorter's  disease,  743. 
Wrist-drop,  512,  967. 
Writer's  cramp,  954. 
Wryneck,  952. 

X-ray,  uses  of,  654. 
Xanthelasma  of  eyelids,  183. 
Xerostomia,  113,  221 ;  causes  and  symptoms, 
753. 

Yellow  fever,  symptoms,  699  ;  diagnosis  and 
prognosis,  700. 

Ziehl-Neelsen  method  of  stwning,  for  the 
bacillus  tuberculosis,  601. 


THE   END 


/ 


DATE  DUE 

CAYLORO 

PRINTEO  IN  U.S.A. 

i 

A     000  510  463     3 

WBlUl 
B985d 
1901 
Butler,  Glentworth  R 

Diagnostics  of  internal  medicine 


WBll^l 
B985d 
1901 
Butler,  Glentworth  R 

Disgnostics  of  internal  medicine. 


MEDICAL  SCIENCES  LIBR/IRY 

UNIVERSITY  OF  CALIFORNIA,  IRVINE 

IRVINE,  CALIFORNIA  92661 


